Pathology I

2nd Semester
ORAL PATHOLOGY SY 2022-2023

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GENERAL PRINCIPLES OF ORAL PATHOLOGY
Lecture 1: Inflammation
Function of inflammation *not in the slide but discussed*
- To mobilize all the defenses of the body and bring them to  The pattern of increased vascular permeability varies,
the site of battle with the purpose of overwhelming the depending on the type of injury, animal species, and the
source of injury. intensity of the injury.
 Mild injury – lasts for only 15 to 30 minutes
The purposes of tissue change in inflammation
 More severe injury – delayed and lasts for hours
1. To bring to the area certain phagocytic cells which engulf  Very severe injury – immediate and lasts for
and digest bacteria, dead cells, or other debris. hours.
2. To bring antibodies to the site
3. To neutralize and dilute the irritant Starling’s hypothesis
4. To limit the spread of inflammation - Under normal circumstances the hydrostatic pressure
5. To initiate repair at the arterial end of the capillary is higher than the
Sequence of events following inflammation osmotic pressure in the surrounding tissues, so fluid
and nutrients
1. Arteriolar constriction followed by dilatation - escape from the circulation. At the venous end of the
2. Increased blood flow through arterioles, capillaries, and capillary
venules - the hydrostatic pressure falls below the osmotic
3. Venular and capillary dilatation and increased permeability pressure in the
4. Exudation of fluid or edema - surrounding tissues, and the fluid returns to the
5. Slowing or stagnation of blood How circulation.
6. Escape of leukocytes from the vessel wall
Exudate – the edema fluid in inflammation has a higher specific
gravity and a higher protein content than the edema fluid in
certain non-inflammatory conditions, and it is readily coagulable.
Transudate – that present in some noninflammatory conditions

(e.g. heart failure) has a low specifi gravity and a low protein
content.
2nd Semester
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Outstanding Feature of Inflammatory Process
Pavementing or margination
1. Serous inflammation - abundant extravascular fluid but
- the cells (particularly neutrophilic leuokocytes) then
few cells and little fibrinogen (e.g., acute inflammation of
leave the blood vessels, entering the surrounding
serous cavities, skin blister).
tissues, and move to the injured site by an ameboid
2. Fibrinous inflammation - Large amount of fibrin in
motion (emigration of leuocytes).
exudate (e.g., lobar pneumonia)
3. Purulent inflammation - Abundant pus in exudate.
Purulent or suppurative inflammation may be on the
Inflammation
surface or localized in the tissues (abscess), or may spread
 Body’s reaction to injury or invasion by disease producing diffusely through the tissue spaces (cellulitis or phlegmon).
organisms.
Sinus – when anabscess discharges on free surface, the tract
 To mobilize all the defenses of the body and bring them to
through which it drains is called sinus.
the site of battle with the purpose of overwhelming the
source of injury. Fistula – if the abscess discharges into two cavities, the tract
connecting the cavities is called fistula.
4 major types of inflammatory response
 Thus a periaplical abscess opens into the oral cavity via a
1. Acute inflammation
fistula or on the chin through a sinus.
2. Subacute inflammation
4. Sanguineous inflammation - Exudate containing blood
3. Chronic inflammation
(hemolytic streptococcal infections).
4. Chronic granulomatous inflammation
5. Catarrhal inflammation - Acute inflammation of mucous
membrane with abundant flow of mucus. (e.g., early stage
1. Acute Inflammation
of common cold).
 Microscopic characteristics:
6. Pseudomembranous inflammation - Acute inflammation
- Edema and polymorphonuclear leuokocytes
of mucous membrane with associated formation of
 Clinical characteristics
pseudomembrane, the latter consisting essentally of fibrin,
- Swelling, redness, heat and pain
necrotic epithelium, and white cells. (e.g., diphtheria).
 Last for few days to 2 or 3 weeks
2nd Semester
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Abscess - Acute inflammation localized within the tissues and 2. Subacute Inflammation
associated with tissue destruction and liquefaction as well as - A low-grade, prolonged, and proliferative type of
formation of pus. inflammation.
- An inflammatory process havig characteristics of both the
Cellulitis - Acute inflammation that spreads diffusely through tissue
acute and the chronic types is called subacute inflammation
spaces and along tissue planes; usually suppurative in nature. It is
- Generally extends over a period of weeks or months.
also called phlegmonous inflammation.
Chemical Mediators that sets into motion the process of 3. Chronic Inflammation
inflammation - Occurs when the irritant is of low virulence, when resistance
of the host is good, or when acute inflammation is in the
1. H substance - Histamine-like substance, that supposedly late reparative phases.
causes erythema due to vascular dilatation. - Extends over a period of months to years
2. Serotonin - Causes vascular permeability.  Microscopic characteristics
3. Polypeptides - Peptides, such as leukotaxine, bradykinin, - Presence of lymphocytes and plasma cells and by
and kallidin, that cause vascular permeability as well as fibroblastic proliferation.
emigration of leukocytes.
4. Proteases - Such as plasmin, Kallikrein, and globulin 4. Chronic granulomatous inflammation
permeability factor, produce vascular permeability. - Chronic inflammation may be of such a type that the tissue
5. SRS-A - Slow-reactive substance of anaphylaxis; produces response is characterized not only by lymphocytes and
vascular permeability. plasma cells but also by a prominent proliferation of
6. LPF. (leukocytosis-promoting factor) - Promotes histiocytes (macrophages). The latter may form diffuse or
formation of more leukocytes, in bone marrow. circumscribed masses.
7. Exudin - Promotes capillary permeability, - Seen in persons with tuberculosis, syphilis, sarcoidosis,
8. Necrosin - Causes proteolysis or tissue breakdown. fungal infections, foreign body reactions, and many other
9. Pyrexin - Causes fever. diseases.
10. Growth-promoting factors - Aid in repair.
Cytokines - powerful mediator that influence behavior of other
cells, transmit information or signal to send additional phagocytic
cell to the site of infection.
2nd Semester
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Prostaglandins- increase permeability and dilatation of blood
vessels, trigger osteoclastic activity, trigger over production of
destructive MIMP.
MMP or Matrix Metalloproteinases - enzymes that breakdown

connective tissue matrix.
Cellular Components of Inflammation
1. Neutrophilic polymorphonuclear leukocytes

2. Eosinophilic polymorphonuclear leukocytes
3. Mast cells and basophilic polymorphonuclear leukocytes
4. Lymphocytes and plasma cells
5. Monocytes and macrophages (histiocytes)
2nd Semester
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Lecture 2: Regeneration and Repair
 Regeneration 6. Local stimuli: Local stimuli, such as trephones or wound

- When a damaged tissue is replaced by cells that are hormones that are liberated by the proteolytic breakdown
similar or identical to those destroyed. of cellular debris, and certain wherjgals (e.g. urea) are
believed to stimulate tissue growth.
 Repair 7. Blood supply: Tissues with a sood vascular supply heal
- All-inclusive term that embraces both regeneration and faster than those in which the blood supply had been
those processes wherein the damaged tissue is replaced diminished due to disease or advanced age.
by dissimilar cells. 8. Mobility of tissues: Healing in both bone or soft tissues is
faster when the injured tissues are immobilized.
Factors affecting regeneration & repair
Regeneration
1. Species: As a rule, the lower and less differentiated
animals possess a greater ability for regeneration (e.g.,  PHYSIOLOGIC REGENERATION
certain amphibians can grow an entire limb, and the earth- - refers to replacement of cells, such as blood cells and
worm can regenerate a head). epithelium that are destroyed under normal
2. Tissue: Different tissues in the same animal vary in circumstances.
reparative potential (e.g., the mammalian liver cells can
regenerate rapidly, whereas a neuron, once destroyed, is  Regenerative Potentials in the Oral cavity
incapable of regeneration).  Oral epithelium – 4-6 days
3. Age: Young organisms can repair their damage faster than  Dorsum of the tongue
older ones.  Check
4. Nutrition: Certain nutritional deficiencies, such as protein  Palate
and vitamin deficiencies (e.g., vitamin C), prolong or hinder  Ventral surface of tongue
regeneration and repair.  Gingiva
5. Irritants: Whereas mild irritants enhance the reparative
process, excessive irritants (e.g., persistent infection, bone
sequestra, lack of rest) inhibit repair and regeneration.
2nd Semester
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Repair
 Five types of oral wounds repair

1. Wounds healing by first intention
2. Wounds healing by second intention
3. Wounds following tooth extraction
4. Transplantation and replantation of teeth
5. Jaw fractures
2nd Semester
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Lecture 3: Immunity and allergy
Immunity 2. Recognition of “nonself”

 The body’s immune system is able to distinguish
- The ability of an organism to resist infection. between its own self and nonself.
2 major groups 3. Immunologic memory
 Immunologic memory results from the host’s 1st
 Innate or species immunity – inherent in an entire come in contact with an antigen, which not only
species produce antibodies but also produce certain
 Acquired – attained by an individual. memory cells. And in second contact, the memory
 Natural – The first contact of the host with the cells assist the host in more rapid immune
organism may be as a result of getting a certain response.
disease, following which the host may resist
Allergy / Hypersensitivity
reinfection with the same organism (natural
immunity). - Immunologic reaction that are detrimental to the tissues of
 Artificial - the first contact may be artificially physiology of the host.
produced in the host by the injection of living or
dead organisms or their products with the resultant Types of allergic reaction:
immunity called active immunity, or by the
1. Type I, anaphylactic type, anaphylaxis, bronchial asthma.
introduction of antibodies prepared in another
Atopy – IgE
host, with the resultant immunity called passive
2. Type II cytotoxic, autoimmune hemolytic anemia,
immunity.
erythroblastosis fetalis, Ig G, M
3 Essential Elements of Immune Response 3. Type III – immune complex disease, arthus reaction, lupus,
antigen-antibody complexes
1. Antigenic specificity 4. Type IV – cell mediated delayed hypersensitivity, TB,
 Foreign proteins and large carbohydrate-lipid contact dermatitis, sensitized T lymphocytes.
complex may be able to stimulate the formation of
antibodies.
2nd Semester
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Immunoglobulin Anaphylactic shock - When an allergic response is stimulated
artificially. for example, in a laboratory animal or by an accidental
- Antibodies which are modified serum proteins of various
injection of a protein into a patient who is sensitive to the protein.
molecular forms.
Contact allergy – contact may be on the mucous membrane or the
Five major classes of immunoglobulin (Ig)
skin and lead to a local allergic reaction
 IgG
Bacterial allergy – the allergic response may be to a bacterial
 IgA
protein, such as seen in tuberculosis.
 IgM
 IgD 2 types of allergic reactions
 IgE
Immediate hypersensitivity – develops rapidly after
administration of the antigen
*not in the ppt but discussed*
Delayed hypersensitivity – the response occurs 24 to 48 hours
 Immunoglobulin or antibodies are produced by plasma later.
cells which are the progeny of B lymphocytes. These
cells manufacture and secrete antibodies. Cellular Aspect of Immunity and Allergy
 Macrophages of the lymphoid system “pick up” the
1. T lymphocytes
antigen, process it in some manner, and then “deliver” it
- Produce cells responsible for fixed (cellular) immunity and
to the plasma cells, where antibodies are then
delayed hypersensitivity.
produced.
2. B lymphocytes
 When an individual who has been previously exposed to
- Form plasma cells, chief source of antibody formation
an antigen is exposed to a second dose of the same
3. Macrophages
antigen, one of two things happens:
- Attack and engulf the antigen
(I) the antigen may be neutralized or destroyed in the
4. PML
bloodstream by the circulating antibodies, and the - Phagocytose and destroy the antigen-antibody complex.
person is immune to its untoward effects; or
(2) the circulating antibodies are not enough to
neutralize or destroy the antigen, and the latter reaches
the tissue cells, where it reacts with the fixed antibodies.
ORAL PATHOLOGY
PRELIMS - 2nd Semester, SY 2022-2023
DENTAL CARIES
- Microbial disease
- Is a disease of the hard dental tissue
where there is decalcification and
disintegration of the hard dental
tissues causing open lesions on
enamel, dentin and cementum
- Caries came from a latin word
means “dry rot”
- Demineralization of the inorganic
portion and destruction of the
organic substances of the tooth.
HYPERTHYROIDISM
A. Etiological Factors
Oral Manifestations:
General predisposing factors
• Enlargement of extraglandular
a. Race thyroid tissue (mainly in the lateral
b. Diet posterior tongue)
c. Heredity • Accelerated dental eruption
d. Nutrition • Burning mouth syndrome
e. Endocrine disturbance • Increased susceptibility to caries
f. Physical condition of the patient • Periodontal disease maxillary or
o Age incidence mandibular osteoporosis
o Somatic disease • Sjogren’s syndrome
o Pregnancy • Thyroid may be enlarged or
noticeably palpable (Grave’s disease)
DENTAL CONSIDERATIONS:
Medications:
DIABETES MELLITUS
• Anti-thyroid drugs – methimazole,
• Oral Manifestations: propylthiouracil
o Compromised periodontal • Radioactive iodine
health/worsen due to DM • Beta-blocker and iodides
o Candidosis (denture wearers)
o Dry mouth and sialosis ->
increased caries
o Glossitis
o Burning mouth syndrome
o Oral, facial dysesthesia
• Poor response/healing to periodontal
therapy
• Priority given to dental infections
ORAL PATHOLOGY
HYPOTHYROIDISM
Oral Manifestations:
• Delayed dental eruption

• Salivary gland enlargement
• Macroglossia
• Glossitis (swollen tongue)
• Compromised periodontal health –
delayed bone formation
• Dysgeusia (distortion of taste)
• Delayed wound healing
Medications:
• Synthroid
• Levothyroxine
• Armour thyroid HYPOPARATHYROIDISM
1. Dental abnormalities:
• Enamel hypoplasia in horizontal
lines
• Poorly calcified dentin
• Widened pulp changers
•
• Dental pulp classification
shortened roots hypodontia, and
delay cessation pf dental
development
HYPERPARATHYROIDISM
1. Dental abnormalities:
• Widen pulp chambers
• Development defects
• Alterations in dental eruption
• Weak teeth
• Malocclusions
• Loss of lamina dura on
radiographs
• Giant cells lesions
ORAL PATHOLOGY
B. Predisposing Factors fermentable carbohydrates after
• Structural quality they have been acted upon by
• Development defects enzymes of lactobacillus acidophilus.
• Malposition of teeth 2. Dietary Theory (James Shaw) –
• Attrition food consumed by the individual,
• Composition of saliva specially the CHO particularly
• Poor oral hygiene monosaccharides and disaccharides
• Physical oral hygiene of food are responsible for initiation and
• Occupational influences progress of carious lesion.
3. Proteolytic Theory (Bernhard
Development defect
Gottlieb) – caries is a proteolytic
process involving the invasion of
microorganisms into the tooth tissue
thru channels. Proteolytic bacteria
destroys first the organic substance,
followed by acidogenic bacteria
destroying the inorganic substance.
4. Proteolysis – Chelation Theory
(Schatz et al) – Calcium Phosphate
can be dissolved by numerous
substances capable of forming
soluble chelates and complexes.
When enamel surface is decalcified
C. Exciting Factors by substances which produces
• Acidogenic type – bacteria capable chelates or complexes, such will act
of producing acid on calcium resulting to erosion and
• Acidophilic type – bacteria capable the organic matrix is mechanically
of living in acid environment which is sloughed off.
strong enough to decalcify the 5. Theory od Dr. P. Pincus – enzyme
enamel. called sulphatase secreted by the
• Proteolytic type – bacteria capable gram negative bacilli present in the
of splitting protein into diffusible mouth acts on the polysaccharide
body, capable of digesting and releasing the sulfate ion which in
liquifying decalcified dentin. turn combines with water of the
• Protective type – bacteria capable of mouth forming sulfuric acid. This
producing filament to attach acid combines with calcium salts to
themselves on smooth surface. form CaSO4 – which is claimed to be
present in a carious lesion and
Theories on the Etiology of Dental Caries absent in healthy teeth.
6. Theory of l. l. de Vries – caries is
1. Miller-Black-Wiliams Chemico-
formed due to circulatory trouble, a
parasitic Theory (Acidogenic
lymphatic infarct is formed.
Theory) – dental caries result of
Circulatory disturbances causes
decalcification of tooth structure by
nutritional disturbance and the
acids derived from refined
ORAL PATHOLOGY
Bacteria
dentin and enamel become low in
resistance against bacterial attack.
Dextran,
7. Theory of Henrick Egyedi – Plaque amylopectin
sucrose
bacteria grows in the organic
substance of the enamel, and that Lactic Acid
the excess amount of CHO and
glycogen stored in the tooth tissue fructose Diet Caries
serves as nutrition for bacteria.
8. Atkinson and Matthew –
proteolytic enzymes elaborated most
likely by bacteria on tooth surface glucose
liberate aspartic and glutamic acid
from the tooth proteins as they pass • Bacteria in the mouth:
down through enamel lamella, prism 1. Streptococcus Mutans
sheaths and dentin through osmotic 2. Lactobacillus Acidophilus
and capillary forces. This acid cause • Lactic Acid – to decalcify the enamel
dissolution of enamel rods, thereby o 5.5 pH
freeing more proteins which will be • Amylopectin – intracellular
acted upon these free amino acids. polysaccharides
Bacteria
Mechanism of Development
3 conditions must be present: Lactic Acid

Plaque
1. Diet sucrose 5.5 pH
2. Plaque
3. Susceptibility of the enamel Dextran,
amylopectin
fructose Diet Caries
Carbohydrate from diet will contribute to
the formation of Plaque TIme
glucose Susceptibility
Dental Plaque – composed of bacteria,
of the
mucus, desquamated cells and food debris
enamel
Salivary glues: Dextran and Levan produced
by fermentation of dietary sucrose., makes
10% weight and 33% volume of plaque.
ORAL PATHOLOGY
Classifications of Dental Caries • According to nature of lesion
o Primary
• According to location
o Secondary – recurrent or
o Pits and Fissures
central
o Smooth Surface
Acute caries – deep penetrating and rapid

clinical destruction pulp easily involved and
pain is a constant symptoms. Common in
children and young adult.
Chronic caries – progresses slowly and

allows time for sclerosis and secondary
• According to the rapidity of the dentin formation, common in adult.
process
o Acute crown and root caries
– rampant Arrested Caries - from of caries which
o Chronic crown and tooth become static or stationary.
caries – arrested
Eburnated dentin – hard and polished
surface of decalcified dentin, burnished until
it takes a brown stain.
Recurrent caries – results from faulty

odonto therapy.
Marginal caries – poor marginial

adaptation or incomplete removal or soft
infected dentin.
ORAL PATHOLOGY
Central caries – worn out tooth exposing affected area may appear
the pulp. translucent than normal.
• Dark Zone – dense opaque zone
with little structure can be seen,
separated by a normal enamel from
the body, zone of active
demineralization and is
hypocalcified.
• Translucent Zone – lies deep to
the dark zone and is considered as
the inner recrystallization zone and
hypercalcified than normal enamel.
Pattern of Caries Development – pit and
fissure Zone of Enamel Caries
Pattern – smooth surface caries
Histopath Changes in Dentin
• Zone of complete decalcification

– the walls of dentinal tubules and
matrix become decalcified and later
decalcified matrix become
decomposed.
Histopathologic Changes in the • Zone of incipient decalcification
Enamel – there is beginning decalcification
of dentin.
• Body of the lesion – most severely
• Zone of Transparency –
demineralized are the bond of
obliterated dentinal tubules due to
Retzius, striations and prism core.
calcification of Tomes Fiber.
Occupies the greatest part of the
• Zone of Fatty Degeneration –
formation of fatty materials and
ORAL PATHOLOGY
beginning precipitation of calcium Preventive Measure
droplets in the protoplasm of Tome’s
• Flouride treatment
fiber.
• Antibiotic and antiseptics as
Protective Reactions mouthwash
• Prophylactic odontotomy, pit and
• Enamel – sclerosis of transparent
fissure sealant
enamel – non vital tissue,
• Oral hygiene
physiochemical activity, inorganic
substance, remineralization. Flouride
• Dentin – sclerosis, dentral tract –
calcification and degeneration of
dentinal tubules
• Pulp – secondary dentin,
inflammatory reaction
Dentin Caries
Pit and Fissure Sealant
Caries Susceptibility Test
• Lactobacillus count – increased

lactobacillus count in increase
quantity of sucrose/candies.
• Calcium dissolution test – mg of
powdered enamel dissolved in saliva
glucose mixture is incubated.
• Wach test – saliva glucose both
mixture is incubated, the amount of
acid produced is the measure of
caries activity.
• Synder’s test – assesses the
acidogenicity of the oral flora, using
a bromocresol green indicator
ORAL PATHOLOGY
Dental Caries Primary Modifying Factors of dental
Caries Formation
- Demineralization of the inorganic
portion and destruction of the 1. Tooth Anatomy
organic substances of the tooth.
(Viscarra – AvendaÑo)
- Is multifactorial, transmissible,
infectious oral disease caused
primarily by the complex interaction
of cariogenic oral flora (biofilm) with 2. Saliva
fermentable dietary carbohydrates
on the tooth surface over time. Functions of Saliva:
(Sturdevant 6th Ed. 2012) - Remineralization
- Is a biofilm-mediated, diet - Bacterial Clearance
modulated, multifactorial, non- - Buffer Action
communicable, dynamic disease - Antimicrobial Actions
resulting in net mineral loss of
dental hard tissues [Fejerskov 1997;
Pitts et al.,2017]
- Is a preventable, chronic, and
biofilm-mediated disease modulated
by diet, multifactorial, oral disease is
caused primarily by an imbalance of
the oral flora (biofilm) due to the
presence of fermentable dietary
carbohydrates on the tooth surface
over time. (Sturdevant 7th ed. 2019)
Four Primary Etiologic Factors of

Caries Formation:
1. Host
2. Cariogenic biofilm
3. Fermentable carbohydrates
4. Time
ORAL PATHOLOGY
3. Biofilm pH – dental plaque or plaque

biofilm, which has compositions (bio) and
structure (film). Biofilm is composed mostly
of bacteria, their by-products, extracellular
matrix, and water.
- Cariogenic bacteria in the biofilm

metabolize refined carbohydrates for energy
and produce organic acid byproducts. There
organic acids, if present in the biofilm
ecosystems for extended periods, can lower
the pH level in the biofilm to below a critical
level.
Demineralization – the result of a net loss

of minerals by the tooth caused by a low pH
that drives calcium and phosphate from the
tooth to the biofilm in an attempt to reach
equilibrium.
Remineralization – a process where

mineral can then be added back to partially
demineralized enamel when the pH in the
biofilm returns to neutral and the
concentration of soluble calcium and
phosphate is supersaturated relative to that
in the tooth.
ORAL PATHOLOGY
4. Use of Fluoride for preventing caries and periodontal
disease.
Anticaries Action of Flouride
7. Immune System – absence of systemic
- By reducing the enamel solubility
disease that has imoact on caries formation
- Improved crystallinity of dental
tissues - immunication/vaccine to
- Increased remineralization process
- probiotics
of dental tissues
- Lower the free surface energy of 8. Genetics Factors
tooth surface and prevent
desorption of protein and cariogenic - Physical form of the tooth
bacteria. - alignment and crowding due to
- Act as an antibacterial agent by small jaw and big teeth or vice versa
inhibiting bacterial enzymes.
Secondary Modifying Factors Dental
Caries Formation
1. Socioeconomic status
2. Education
3. Life style
4. Environment
5. Age
6. Ethnic Group
7. Occupation
5. Diet Specifics – frequent ingestion of

fermentable carbohydrates begins a series
of changes in the local tooth environment
that promotes the growth of highly
acidogenic bacteria and eventually leads to
caries.
- the metabolic product of cariogenic

diet is acid, and acid leads to the
development of caries.
6. Oral Hygiene – oral hygiene,

accomplished primarily by proper tooth
brushing and flossing. Etiology of Dental Caries
- biofilm-free tooth surfaces do The etiological agents of dental caries
not delay. Daily removal of plaque biofilm are pathogenic bacterial plaque.
by dental flossing, tooth brushing, and
rinsing is the best patient based sa measure
ORAL PATHOLOGY
Two basic hypothesis: - Role of Carbohydrates
o Frequency of ingestion –
1. Non-specific plaque hypothesis
higher frequency, more
- All plaques are pathogenic because
caries
pathogenic bacteria are universally
o Physical form – solid,
present in plaque
semisolid, sticky jelly like,
- The treatment of caries is total
liquid form
removal of plaque in all patients.
o Chemical composition –
2. Plaque and Caries – the carious
mono and disaccharide are
lesions started when specific
more cariogenic than
bacteria in plaque increased and
polysaccharides. Sucrose is
active pH is decreased.
most cariogenic.
- the plaque will become pathogenic
o Route of administration and
when signs of caries develop.
period of contact of
Theories of Etiology of Dental Caries: carbohydrate with the tooth
o Presence of other food
1. Acidogenic/Chemicoparasitic constituents (carbohydrate is
Theory less cariogenic in presence of
- It is themost accepted theory given high fat or protein level)
by Miller in 1980. - Role of Microorganisms
- Theory: Caries is caused by acids o On coronal surface initiation
produced by microorganisms of the of caries is caused by
mouth Streptococcus mutans and on
- Dental decay is a chemico-parasitic root surface mainly by
process consisting of two stages: Actinomyces viscosus.
o Decalcification of enamel and Presence of high
dentin (preliminary stage) Lactobacillus acidophilus
o Dissolution of the softened count in saliva designates the
residue (subsequent stage) occurrence of active carious
- Acids resulting in primary lesion.
decalcification are produced by the - Role of Acids
fermentation of the starches and o for initiation of dental caries,
sugar from the retaining centers of presence of acids (Lactic
the teeth. acid, butyric acid) on the
- Role of Dental Plaque: tooth surface is necessary.
o Dental plaque is also called 2. Proteolytic Theory
as bacterial plaque or - Theory: Organic or portion element
microbial plaque of a tooth are the initial pathway of
o Essential for initiation of invasion by microorganisms
caries because it provides the - Enamel lamellae are pathways for
environment for bacteria to organisms in the progress of dental
form acid, which causes caries
demineralization of hard - Microorganisms invade the enamel
tissue of teeth. lamellae and the acid produced by
ORAL PATHOLOGY
the bacteria causes damage to the - Macroscopically evidenced by the
organic pathways. appearance of an area of opacity –
3. Proteolysis-Chelation Theory white spot lesion
- Theory: Simultaneous microbial - Intact surface and the subsurface
degradation of the organic porosity – clinical characteristics
components and the dissolution of - Maybe reversed by remineralization
the minerals of the tooth by the - Mutans Streptococci – initiation of
process own as chelation (Schatz et enamel caries
al, 1955) - Actinomyces viscosus – organism to
- Chelation: process in which there is initiate root caries
complexing of the metal ions to form - Lactobacilli – progression of dentinal
complex substance through caries
coordinate covalent bond which
results in poorly dissociated/or
weakly ionized compound.
Clinical Sites for Caries Initiation
1. Pits and Fissures – found mainly

on the occlusal surfaces of the teeth
as well as in lingual pits of the
maxillary incisors
2. Smooth Enamel Surfaces – arises
on intact enamel surfaces
Zones of Incipient Lesion
3. Root Surface – involve any surface
of the root 1. Translucent Zone
- deepest zone; advancing front of the
enamel lesion
- structureless appearance
- pores or voids form along the
enamel prism boundaries
- pore volume is 1% 10 times greater
than normal enamel
2. Dark Zone
- Does not transit polarized light
- Total pore volume is 2-4%
3. Body of the Lesion
- Largest portion of the incipient
lesion while in a demineralizing
phase
- Has the largest pore volume varying
Incipient Lesion
from 5% at the periphery to 25% at
- First attack on a tooth surface the center
ORAL PATHOLOGY
4. Surface Zone - V shaped in cross section with a
- Unaffected by caries wide base at the DEJ and the apex
- Lower pore volume than the body of directed pulpally
the lesion - Caries advance more rapidly in
dentin then enamel because dentin
provides much less resistance to
acid attack because of less
mineralized content.
Zones of Dentinal Caries
1. Zone 1: Normal Dentin

- Deepest are which has tubules with
odontoblastic process that are
smooth and no crystals are in the
lumens
- Intertubular dentin has normal
cross-banded collagen and normal
dense apatite crystals
- No bacteria are in the tubules
- Stimulation produces pain
2. Zone 2: Subtransparent Dentin
- Zone of demineralization of the
intertubular dentin and initial
formation of very fine crystals in the
tubule lumen at the advancing front
- Damage to the odontoblastic
process; no bacteria are found in
this zone
- Stimulation produces pain; capable
of remineralization
3. Zone 3: Transparent Dentin
- Zone of carious
- Stimulation produces pain
Dentinal Caries
- No bacteria are present
- Dentin contains much less mineral 4. Zone 4: Turbid Dentin
and possesses microscopic tubules - Zone of bacterial invasion
that provide a pathway for the - Very little mineral present
ingress of acids and egress of - Cannot be remineralized
mineral 5. Zone 5: Infected Dentin
- DEJ has the least resistance to - Outermost zone
caries attack and allows rapid lateral - Consists of decomposed dentin that
spreading once caries has is teeming with bacteria
penetrated the enamel
ORAL PATHOLOGY
- No recognizable structure to the - Two cones, base to base, with the
dentin and collagen and mineral apex of the enamel cone at the point
seems to be absent of origin and the apex of the dentin
- Great numbers of bacteria cone directed toward the pulp
- Removal of infected dentin is
essential
- In x-section gross appearance of a pit and

fissure in an inverted V with a narrow
entrance and a progressively wider area of
involvement closer to the DEJ
Caries Terminology 2. Caries of enamel-smooth

surface origin
A. Location of Caries - form in a smooth area of the enamel
surface that is habitually unclean
1. Caries of pit and fissure origin - apex of the cone of caries in the
- Form in the regions of pits and enamel contacts the base of the
fissure cone of caries in the dentin.
- *pic
ORAL PATHOLOGY
- X-section shows a V shape with wide
area of origin and the apex of the V
directed toward the DEJ
4. Forward Caries
- Caries cone in enamel is larger or at
least the same size as that dentin
(pit and fissure caries)
5. Residual Caries
- Caries that is not removed during a
restorative procedure, either by
accident, neglect, or intention
3. Backward Caries
- When the spread of caries along the
DEJ exceeds the caries in the
contiguous enamel
ORAL PATHOLOGY
6. Root-Surface caries of Senile B. Extent of Caries
Carious Lesion
- Associated with aging process 1. Incipient Caries (reversible)
- May occur on the tooth root that has - First evidence of caries activity in
been both exposed to the oral the enamel
environment and habitually covered
with plaque
- Have less well defined margins tend 2. Cavitated Caries
to be U shaped in cross section and (irreversible)
progress more rapidly because of - The enamel surface is broken and
the lack of protection from enamel usually the lesion has advanced into
covering dentin.
C. Rate/Speed of Caries
1. Acute (rampant caries)
- Is when the disease is rapid in
damaging the tooth
- It is usually in the form of many,
soft, light – colored lesions in a
mouth and is infectious.
2. Chronic (slow of arrested)

caries
7. Secondary (recurrent) caries - Is slow or it may be arrested
- Occurs at the junction of a following several active phases
restoration and the tooth and may - Lesion is discolored and fairly hard
progress under the restoration - An arrested enamel lesion is brown-
to-black, hard, and as a result of
fluoride, may be more caries-
resistant than contiguous,
unaffected
- An arrested dentinal lesion is dark,
and hard this is termed as sclerotic
or eburnated dentin
ORAL PATHOLOGY
D. Cavities According to the

Number of Surfaces Involved
1. Simple Caries
- When the lesion is confined to a
single surface
- JOINED
2. Compound Caries
- When two surfaces are involved
- Compound caries lesion NOT
JOINED
1. Abrasion
- Abnormal tooth surface loss
resulting from direct friction forces
between the teeth and external
objects or from frictional forces
between contacting teeth
- compound caries lesion JOINED components in the presence of
abrasive medium
o Improper tooth brushing
o Habits – holding pipe stem
by the teeth
o Tobacco chewing
o Use of toothpicks
o Toothbrush abrasion – sharp
V. shaped notch in the
3. Complex Caries gingival portion of the facial
- When three or more surfaces are aspect of the teeth
involved
- NOT JOINED
ORAL PATHOLOGY
should not be confused with root
caries that appears brown and
leathery.
2. Erosion
- Is the progressive loss of dental pulp
- Clinical Features:
tissue by chemical means not
o Loss of tooth structure at site
involving bacterial actions; the wear
of wear
or loss of tooth surface by
o Sensitivity possible
chemicomechanical action
- Regurgitation of stomach acids
- Habitual sucking of lemons
- Etiology: repetitive mechanical habit;

using a hard toothbrush, improper
brushing technique along the
gumline, grinding or chewing hard
objects or food
- Treatment: prevention; restoration,
fluoride applications and tooth-
colored bonding
- Prognosis: once the gums begin to
recede, root surfaces become 3. Attrition
exposed and sensitivity to hot and - Mechanical wear of incisal or
cold temperatures soon follow. occlusal surface as a result of
- On dental radiograph, tooth brush functional or parafunctional
abrasion appears as a well-defined movements of the mandible
horizontal radiolucency along the - Affects the proximal contact areas
cervical region of a tooth.
- Clinically, the areas affected by
abrasion appear as hard, highly
polished defects in dentin and
ORAL PATHOLOGY
- Note that abfraction is different than
toothbrush abrasion with which it is
often confused
- Toothbrush abrasion is caused by
overbrushing with a hard bristle
toothbrush, while abfraction is
caused by excessive pressure
applied to the teeth by severe
brushing habits
- While abfraction tends to be a
*dished out* defect, toothbrush
abrasion tends to be a *notch* in
4. Abfraction the tooth surface just above the
- microfractures occur as the cervical gumline.
area of the tooth flexes under loads
- Clinical Features:
o Wedge-shaped notching at
cervical areas of involved
teeth
o Adults
5. Fractures
- Incomplete fracture not directly
involving vital pulp-greenstick
fracture
- Complete fracture not involving vital
pulp
- Fracture involving vital pulp
6. Nonhereditary Enamel
- Etiology: biochemical forces on teeth Hypoplasia
- Treatment: restoration; may not - Occurs when the ameloblasts are
require treatment injured during enamel formation
- Prognosis: once the enamel is gone, - Seen on anterior teeth and first
then dentin is exposed and the teeth molars; opaque white or light brown
are more susceptible to decay, areas with smooth intact hard
sensitivity and more wearing down. surface
ORAL PATHOLOGY
7. Amelogenesis Imperfecta
- Enamel is defective either in form of
calcification as a result of heredity
8. Dentinogenesis Imperfecta
- Hereditary condition in which dentin
is defective
G.V. BLACK CASSIFICATION OF 2. Class II – carious lesions that are

DENTAL CARIES located on the proximal surfaces of
premolars and molars
1. Class I – carious lesions that are located
in pits and fissures of the occlusal surfaces
of molars and premolars, occlusal 2/3 of the
buccal and lingual surfaces of molars, and
the lingual surface of the anterior teeth.
ORAL PATHOLOGY
3. Class III – carious lesions that are
located on the proximal surfaces of anterior
teeth that DO NOT INVOLVE the incisal
angle
6. Class VI – cavities on the incisal edges

and cusp tips.
4. Class IV – carious lesions that are

located on the proximal surfaces of anterior
teeth involving the incisal angle
INTERNATIONAL CARIES DETECTION

ASSESSMENT SYSTEM / ICDAS
- Visual system for caries lesion

detection and classification
5. Class V – carious lesions that are located - Developed to serve as a guide for
on the gingival 1/3 of the facial and lingual standardized visual caries
surfaces of both anterior and posterior teeth assessment that could be used for
clinical practice, clinical research,
education, and epidemiology.
ORAL PATHOLOGY
Two Minimum Conditions Required to 2 – distinct visual change in enamel
Properly Conduct Examination
1. Teeth must be sufficiently air-dried

so that the changes can be seen
properly
2. Biofilm or plaque must be
thoroughly removed from teeth prior
to the examination
Two Stages of ICDAS:
1. Code for the restorative

status if the tooth –
determined visually with
restorative/sealant code 0 to 8. 3 – enamel breakdown, no dentin visible
2. Code for the severity of the
caries lesion – statue of the
caries severity is determined
visually on a state of 0 to 6.
Caries Severity Code
0 – sound tooth structure
4 – dentinal shadow (not cavitated into

dentin)
1 – first visual change in enamel

ORAL PATHOLOGY
5 – distinct cavity with visible dentin International Caries Detection
Assessment System
6 – extensive distinct cavity with visible

Restorative/Sealant Code
dentin
0 – sound, surface not restored or sealed
1 – sealant, partial
2 – sealant, full
3 – tooth colored restoration
4 – amalgam restoration
5 – stainless steel crown
6 – porcelain or gold or PFM crown or

veneer
7 – lost or broken restoration
8 – temporary restoration
9 – used for the following conditions
96 – tooth surface can’t be examined;

surface excluded
97 – tooth missing because of caries (tooth

surfaces will be coded 97)
98 – tooth missing for reason other than

caries
99 – unerupted tooth
2ORAL
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PATHOLOGY
Semester
2nd sem SY 2022-2023

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Lecture 6: Diseases of pulp
Pulpitis results from: Hyperemia
 Bacterial - a subclinical condition characterized by

 Traumatic increased of blood in the blood vessels
 Chemical of the pulp. First sign of pulp distress.
 Thermal
Chronic pulpitis
 Electrical
 Systemic - Exhibit intermittent dull aching.
Sensitivity to heat and cold is less
Pulpitis - maybe acute, chronic or hyperplastic.
striking, tooth responds at higher level
Acute pulpitis to electric pulp tester than the normal
tooth.
- Characterized by severe pain that varies
from a continuous, throbbing type to Hyperplastic Pulpitis (Pulp polyp)
less severe and intermittent attacks.
- seen in children-tooth has a large cavity
- Severity of pain increases while the
usually on the occlusal surface, a red,
patient is in lying position and with
fleshy mass of tissue lies in the cavity or
changes in temperature.
projects beyond the occlusal area,
growth is not painful and tooth remains
 Acute serous pulpitis – pwede pa ma
vital.
reverse/ beginning or onset pa lang.
- Frequently involved the deciduous
 Acute suppurative pulpitis – ga damo
molar and first permanent molar.
ang pus. Irreversible.
 Why? – Because it has
 Abscess-breakdown of infected pulp
abundance blood supply, dako
Management/Treatment of acute pulpitis ang periapical opening.
1. Removal of the cause

2. Pulp capping (calcium hydroxide)
3. Root canal treatment (RCP)
Cracked tooth syndrome
- Condition in which pulpitis results

from a crack in the tooth. Patients
complain of ill-defined pain.
Although clinically usually invisible,
the crack in the crown extends into
the pulp; and the saliva and
organisms produce pulp
inflammation.
2ORAL
nd
PATHOLOGY
Semester
2nd sem SY 2022-2023

______________________________________________________________________________
with formation of foul smelling
The following sequence of events leads to the
incompletely oxidized products.
production of a pulp polyp. Caries produces
acute pulpitis; however, because of the wide Other pulp diseases
exposure, acute pulpitis does not lead to pulp
necrosis but gradually to chronic pulpitis,  Anachoresis - bacteria circulating in the
which is characterized by the formation of bloodstream settle in areas of
abundant granulation tissue (the latter inflammation or lowered resistance in
protrudes out of the exposure into the cavity). the pulp and produced pulpitis.
Then the desquamated cells from the oral  Aerodontaldia - high altitude flights
mucosa, many of which are viable, become produced pain in the teeth that are
implanted on the granulation tissue and by asymptomatic at ground levels, occurs
rapid prolifration and migration cover the in teeth with subclinical pulpitis.
surface. Microscopic sections of a pulp polyp  Reticular atrophy - is really an artefact
show vital pulp tissue with chronic but at one time believed to be a
inflammatory cells (plasma cells and regressive change of the pulp, micro,
lymphocytes) and young vascular connective seen as numerous spaces and
tissue (granulation tissue) that projects from intertwining bundles of fibers in the
the pulp into the carious lesion. pulp.
 Calcifications - diffused or scattered
Treatment consists, of surgical excision of the
calcification
polyp from the floor of the pulp chamber and
 Nodular - pulpstone, true denticles or
pulp capping. In successful cases this is
false denticles
followed by the formation of a dentin bridge
 Internal resorption - occurs from within
at the junction of the excised area and the
the pulp, cause is unknown,
pulp-capping material.
- trauma is contributory. Pink tooth
 Metaplasia - deposition of bone tissue
Terminal Stages of Inflammatory Process in the in the pulp.
Pulp
 Necrosis - death of the pulp without

bacterial infection-caseation necrosis,
liquefaction necrosis
 Gangrene -decomposition of the pulp
from bacterial infection. Pulp
mortification, moist-abundance of
serous exudates, dry-insufficient blood
supply.
 Putrifaction - anaerobic process of
splitting proteins by bacteria and fungi
2ORAL
nd
PATHOLOGY
Semester
2nd sem SY 2022-2023

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Lecture 7: Periapical lesions
Periapical diseases Radicular Cyst
 Dental granuloma  Usually asymptomatic, sensitive to

 Radicular cyst percussion, non-vital and may show a
 Residual cyst deep carious lesion or restoration
 Periapical (Dentoalveolar) abscess  History of pain and subsequent relief in
 Apical scar the tooth
 Cholesteatoma
 DO NOT produce gross deformity of the
Dental granuloma involved jaw
 Usually larger than a dental granuloma
 Apical extension of pulp inflammation
and may extend over the area of two or
 Clinically:
more teeth.
- asymptomatic or slightly painful on
percussion TREATMENT - Extraction and apical curettage,
 Appears as an area of radiolucency that RCT with apical curettage, RCT.
may be either a slight widening of the
periapical periodontal ligament or a RESIDUAL CYST
circumscribed lesion of varying size.
 A tooth associated is extracted but the
 Associated tooth is necrotic and the
cyst is left undisturbed, may persist
alveolar bone proper and periodontal
with in the jaw.
ligament in the periapical area is
 Microscopic feature is same with
replaced by granulation tissue.
radicular cyst
Process:
TREATMENT - Surgical enucleation.
1. Pulpitis from which the tooth failed to
PERIAPICAL (dentoalveolar) ABSCESS
recover
2. Leads to necrosis or it progresses  Acute onset, swelling, reddening of the
towards the apex overlying skin, elevation of the tooth in
3. Chronic inflammation extend to the the socket, extreme sensitivity on
periapical periodontal ligament percussion and elevation of
4. Formation of the granulation tissue, temperature (severe).
replaces the apical periodontal ligament  Usually has a deep carious lesion, a
5. Bone surrounding the granulation tissue fracture, restoration or inadequate root
undergo resorption. canal filling… but may be intact.
 Abscess point may be intraorally or
TREATMENT - Root canal treatment or
extraorally
Extraction
2ORAL
nd
PATHOLOGY
Semester
2nd sem SY 2022-2023

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 Sometimes. Periapical abscess may
appear as parulis or gumboil
TREATMENT - Drainage and RCT after acute

symptoms subside, Extraction.
APICAL SCAR
 Clinically the tooth is asymptomatic

 History of periapical lesion and root
canal filling or root canal filling and
apical curettage
 Circumscribed radiolucency
 Hyalinized apical scar
 Healing process has terminated in the
formation of dense collagen rather than
bone
 Remains ASYMPTOMATIC and requires
no treatment
CHOLESTEATOMA
 Radiolucency
 Same characteristic of dental
granuloma
 Consist of cholesterol crystal that
appear as cleft, also contains foam cells,
plasma cells and lymphocytes.
 Dental granuloma in which a great deal
of fatty degeneration has led to the
formation of abundant cholesterol
TREATMENT - Root Canal Filling and Apical

curettage
ORAL PATHOLOGY
REVERSIBLE AND IRREVERSIBLE

PULPITIS
Pulpitis – the inflammation of the
dental pulp tissue.
Irreversible Pulpitis – severe;

inflammation of the pulp, usually
progressing from reversible pulpitis.
FORMS OF ACUTE PULPITIS

1. Reversible
2. Irreversible
Reversible Pulpitis – mild inflammation of
the pulp tissue caused by the following:
1. Caries encroaching the pulp

2. Deep extensive fillings
3. Sudden physical trauma
4. Careless cavity preparation with
excessive heat production and
dehydration
- Hypersensitive to thermal and chemical
stimuli, which rapidly disappears when
the stimulus is removed
- produces pain that occurs spontaneously

or lingers for a few seconds after the
stimulus is removed.
ORAL PATHOLOGY
- pain may persists for several days after
removal or stimulus as result of pulpal
necrosis.
- the tooth become sensitive to pressure

and percussion.
TEST USED FOR ENDODONTIC DIAGNOSIS
• Thermal Test
o Cold test
o Hot test
• Cavity Test
• Electric Test
Percussion – indicates the condition of the

periodical ligaments and supporting
structures.
Palpation – indicates the periapical

involvement.
TREATMENT:
Reversible – removal of the caries of the

stimulus then restore.
Irreversible – Root Canal Treatment

(RCT)
ORAL PATHOLOGY
PERIODONTAL DISEASES a. Dysfunction Factors –

malposed, traumatic, loss of
- Involves the periodontal tissue, teeth
composed of gingiva, b. Systemic – hormonal,
periodontal ligament, and nutritional, hereditary
alveolar bone.
CLASSIFICATION OF PERIODONTAL
Plaque – the portion of the plaque that lies DISEASES:
in the vicinity of the gingival sulcus
produces gingival lesions. 1. Inflammatory
a. Gingivitis
a. Supragingival Plaque – mostly b. Periodontitis
attached to the tooth surface and is 2. Degenerative
composed mainly of gram-positive a. Periodontosis
aerobic organisms such as 3. Atrophic – periodontal atrophy
Streptococcus sanguis, S. mutans, S. 4. Hyperplastic
salivarius, and Actinomyces. a. Gingival hyperplasia
- It may be covered with a layer of 5. Traumatic
loosely attached plaque
- It is responsible for causing gingivitis Gingivitis – inflammation of the gingival
b. Subgingival Plaque – does not • Chronic Gingivitis – most common
extend to the bottom of the pocket form.
and is composed predominantly of o Edematous – glossy, loss of
gram-negative anaerobic rods and stipplings, bleeds easily.
cocci. Treatment consists of oral
- Subgingival unattached plaque prophylaxis, removal of the
lies between the attached plaque local cause by hand
and the lining of the pocket and also instruments or ultrasonic
extends to the bottom of the pocket. devices following which
- Because its location and recovery is rapid.
composition, this plaque is the most o Fibrous – latter stage of
pathogenic of all forms of plaque. It edematous type and is
consists primarily of gram-negative characterized by enlarged,
cocci and of rods and spirochetes. firm gingiva that may bleed
during toothbrushing. This
Etiology:
type of chronic gingivitis
1. Inititating Factors improves after ultrasonic and
a. Surface Irritants hand scaling, but
b. Faulty Dentistry gingivectomy may be
c. Mouth Breathing – gamala necessary in advanced
ang mouth muna mas prone disease.
sa caries formation kay wala • Hyperplastic Gingivitis –
protection halin sa saliva exuberant growth of gingival
2. Modifying Factors o Administration of drugs,
dilantin (epileptic patient),
ORAL PATHOLOGY
cyclosporine (organ presence of raw patches on the
transplant) attached gingiva and alveolar
o Genetic anomalies – mucosa.
hereditary fibromatosis o Resembles lichen planus,
gingivae pemphigus and erythema
o Idiopathic multiforme but confined to
- Since the gingiva is enlarged, It gingival
leads to the formation of a deep o In many cases gingival
sulcus, or a pseudopocket. epithelium can be separated
- The term pseudopocket is used to from the underlying tissue by
distinguish this “pocket” from the a moderate amount of finger
true pocket, which is associated with pressure (Nikolsky’s sign)
the loss of bone and periodontitis. o Treatment consists of
- Gingival hyperplasia without known improving oral hygiene, and
cause is called idiopathic symptomatic therapy.
fibromatosis and is essentially o In very painful conditions
identical to that just described. mouthwashes containing
- It may also occur in mouth diphenhydramine and
breathers and is usually limited to lidocaine prior to meals may
the anterior teeth. be of value.
• Acute Necrotizing Ulcerative
• Hormonal Gingivitis – Gingivitis (ANUG) – this disease
adolescents, pregnancy, has a strong correlation with stress,
menstruation smoking, and poor oral hygiene; it is
o Pubertal and pregnancy also common on winter months.
gingivitis o Symptoms are fever, cervical
o Puberty Gingivitis – gingivitis lymphadenopathy; malaise; a
occurring during puberty swollen, red, painful,
o Pregnancy Gingivitis – bleeding gingiva; and
gingivitis occurring during necrosis of the interdental
pregnancy papillae.
o patients who take oral o Treatment of ANUG consists
contraceptives often show of rest, fluids, aspirin, and
gingival lesions that are debridement of the area with
comparable to those seen in hand scalers or an ultrasonic
pregnancy. device. After debridement
o Treatment of hormonal the ulcer is covered with a
gingivitis consists of periodontal dressing or a
ultrasonic scaling and mildly anesthetic solution,
improved home care such as a mixture containing
procedures. equal parts of kaolin and
• Desquamated Gingivitis – pectin (Kaopectate) and elixir
unknown cause, desquamation of of diphenhydramine
the epithelium and subsequent (Benadryl)
ORAL PATHOLOGY
o Some cases of ANUG are formation, which are
associated with progressive therefore the two most
gangrenous lesions of the important clinical features of
cheeks called noma. the disease.
• Acute Recurrent Gingivitis – rare
Five distinctly different forms of
type that is characterized by a self-
periodontitis occur in humans
limiting, recurrent, painful, gingivitis
and these are:
that involves the interdental papilla.
o Oral hygiene is generally • Adult Periodontitis – by
good, and lesions resolve in far the most common
about 10 days. type.
o The cause of this disease is o it is caused by
not known, but like subgingival
necrotizing ulcerative plaque, of which
gingivitis, it is related to the unattached
stress. component plays
• Allergic Gingivitis – it is called a dominant role.
plasma cell gingivitis because o It is an almost
microscopically the lesions show universal disease;
dense plasma cell aggregates it is usually
o plasma cell gingivostomatitis, bilateral and
and idiopathic primarily
gingivostomatitis is a lesion interdental.
of the marginal and attached o Periodontitis ins
gingivae. adults has short,
o Most cases are an allergic rapid burst of
response to chewing gum, progression or
but reactions to animal “disease activity,”
epithelium have been which are
observed followed by
o Treatment consists of periods of
removal of the cause and inactivity,
improved oral hygiene. quiescence, or
• Miscellaneous Lesions – a even repair.
papillomatous, cobblestone • Periodontal Pocket – do
appearance of attached gingiva has not form or deepen in the
been reported in Cowden’s absence of bacteria.
syndrome. - The supragingival plaque
• Periodontitis – inflammatory leads to inflammation of
process, extends into the underlying the gingiva (gingivitis).
bone, the lesion is referred to as This inflammation
periodontitis. persists as long as the
o Accompanied by bone cause persists and is
destruction and pocket associated with
ORAL PATHOLOGY
degeneration of the o Progress of the disease is
gingival fibers of the slow
periodontal ligament o There may be function
immediately under the defects of neutrophils or
sulcus. monocytes (but not both)
- Periodontitis is treated by o Otitis media is an
scaling and surgical infrequent finding
elimination of the soft o The disease responds to
tissue and osseous scaling and antibiotic
defects. therapy.
• Juvenile Periodontitis
Two types of periodontal pocket are
(periodontosis) – is manifested
recognized:
clinically and radiographically by
➢ Suprabony Pocket – the deep periodontal pockets associated
bottom of the pocket is coronal with first permanent molars and/or
to the alveolar crest. It is the incisors that contain sparse bacterial
most commonly seen in anterior flora and manifest few or no clinical
teeth. signs of inflammation
➢ Intrabony or Infrabony - The bacteria consistently found
Pocket – the bottom of the in this type of periodontitis are
pocket is apical to the alveolar Capnocytophaga and
crest, occurs most frequently in Actinobacillus Actinomycetem-
the interproximal areas of the comitans – both of which
premolars and molars or on the produce exotoxins that inhibit
buccal and lingual areas of the the function of neutrophils.
molars. - It is associated with rapid initial
• Prepubertal Periodontitis – very bone destruction followed by
rare; it starts during or immediately slowing down or complete arrest
after the eruption of primary teeth. of the disease.
- In the generalized form - The treatment of oral lesions is
inflammation is extremely acute symptomatic. It is doubtful that
and destruction of gingiva and the oral lesions in this disease
alveolar bone is very rapid. are of infective origin.
- This disease involves all primary • Rapidly Progressive
teeth, may or may not involve Periodontitis – a rare form of
the permanent dentition, and is periodontitis that has its onset
not refractory to antibiotic between puberty and about 35 years
therapy. of age is rapidly progressive
- Characteristics of localized form periodontitis.
include the following: - Treatment is essentially the
o Only a few teeth are same as described for juvenile
affected periodontitis, but it may prove
o Gingiva may appear ineffective.
normal
ORAL PATHOLOGY
• Acute Necrotizing Ulcerative formation – the so-called gumboil or
Gingivoperiodontitis – very rare parulis.
form of periodontal disease that is - Clinically, this lesion appears as
associated with repeated, long-term a small, circumscribed boil on
episodes of acute necrotizing the gingiva of the affected tooth.
ulcerative gingivitis. - One of the most consistent
- It is characterized by formation organisms found in these lesions
of deep interdental craters in is the Bacteroides
some or all areas of the mouth. melaninogenicus.
- Treatment consists of local - Periodontal abscess is treated by
therapy and systemic antibiotics. incision, drainage, and surgical
elimination of the pocket.
• Occlusal Trauma – when the teeth

are exposed to excessive occlusal
forces, the resultant or occlusal
trauma.
- The causes of occlusal trauma
are essentially twofold:
o Because of malocclusion
or bruxism, there may be
absolute increase in the
occlusal force;
o Because of some
pathologic condition of
the supporting tissues,
such as periodontitis, the
normal occlusal forces
may become abnormally
intense for the reduced
supporting tissues.
- Occlusal trauma facilitates the
spread of inflammation from the
area of the periodontal pocket
into the underlying tissues.
- The treatment of periodontal
disease, not only should the
pocket be eliminated but also
any occlusal trauma present
should be alleviated.
• Periodontal Abscess (parulls) –
deep periodontal pockets are
sometimes associated with abscess
DEPOSITS AND STAINS
Deposits
- accumulation of mineral materials or sediments.
- Example: Calcium
Stains
- Any discolorations on tooth surface formed by foreign matter.
- Example: Cigarette
Concretions (Calculus)
- hard inorganic materials formed on hard surfaces.
Classi cation of Deposits

Soft deposits
1. Materia Alba -
2. Plaque
a. Mucinous plaque - from saliva composed of mucin
plus bacteria. Not visible kung ndi gamitan disclosing
solution/tablet.
b. Bacterial plaque - composed predominantly of
microorganisms/bacteria. More in cervical portion of
teeth. Composed of strep mutans, staphylococcus aureus, lactobacillus, and
actinomyces. Will eventually be dominated depends kung din sya nga area (ex. Kng ma
initiate na caries; strep mutans. Kung gingivitis; anaerobic microorganisms)
Hard deposits
Calculus
- latin (stones/pebbles) greek (lithus)
- Calci ed organic matter deposited in clinical crowns of
teeth
- Color: Brown, green, black
- Composition: food debris, bacteria, calcium salts
Disclosing solution/tablets
- color depends on maturity of calculus (matured - puple,
pathologic - blue)
INORGANIC (82.91%) ORGANIC (17.09%)
Calcium Phosphate Protein
Magnesium Phosphate Fats
Calcium Carbonate Water
Metals: Cu, Ag, Na, Sn, Cr

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Protein matters: Keratin, Mucin, Nucleoprotein
Note: Under radiograph makita man ang calcular deposits.
Types of Calculus
▪ Supragingival calculus (alivary calculus)
- much softer
- Cornal to gingival margin and makita usually sa lingual surfaces of
mandibular teeth kay dira ga excrete ang salivary ducts. Because our
saliva consists of calcium and phosphate ions that may also
contribute to the formation of calculus.
- Can be seen also at the buccal of maxillary tooth and also ang mga
wala opposing teeth. Also sa area nga may dentures because ga stuck
ang food.
- Much softer compare to subgingival. Color ranges from yellowish white or yellowish
o brownish.
- Pag na remove dasig mag redeposit.
▪ Subgingival calculus (serumal calculus)

- below the gingival margin
- serumal from the blood
- More di cult to remove compare to supragingival and very
adherent sa surface
- Color: Dark greenish brown or sometimes black
- Management: scaling and root planing
- Source: blood that is present in gingival area
▪ Pyogenic calculus
- calculus in periapical area or side of the root.
- Piorea (ga bleed, may susyo) forms the pyogenic calculus.
- Nag decompose and remnant sang pus then nag form pyogenic.
SCALING - insert sa hook then remove calculus

PLANING - removes also the cementum
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Theories on Calculus Formation
▪ Physico-chemical process
- alteration or change in the surface tension of saliva = equilibirum of colloidal solution
destroyed
▪ Enzymatic theory
- enzyme phosphatase hydrolyzes phosphoric ester
▪ Bacterial process
- lamentous type; Actinomyces
Requisites in order to have calculus formation

▪ Supersaturated solution where calcium salts can be taken (colloidal solution)
▪ Hard surface (tooth)
▪ Nidus (food and tissue debris, desquamated cells, bacterial)
▪ Film of organic matter (mucin)
Predisposing factors in the formation of deposits

▪ Nature of the diet (sticky, hard, brous) sticky; mas dasig maka form calculus.
Fibrous; less deposit and has the capacity to clean.
▪ Bacterial ora (Leptothrix buccalis)
▪ Roughness of tooth surface - there are surface nga kung nahuluman sang deposit,
naga ka decalcify and the surface started to get rough then dasig maka form deposits
▪ Récession of gingiva - recess ang gingiva dasig maka form deposits. Kung
exposed si cementum also dasig man maka form deposits.
▪ Lack of friction - if ang area wala opposing nga teeth or wala gina chew dira ga
form calcular deposits.
▪ Mal-alignment of teeth - kung crowded ang teeth ga increase ang susceptibility sa
caries because it is di cult to clean which leads to formation of deposits.
▪ Consistency of saliva - if malagkit ang or ropy ang saliva naga ka form calcular
deposits because it cant wash properly unlike watery saliva.
▪ Poor oral hygiene
Preventive Measures
✔ Maintain good oral hygiene and use the correct toothbrushing technique.
✔ Eat brous foods.
✔ Smoothen the rough surfaces by polishing them.
✔ Eat fruits that can induce watery saliva (less mucin).
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✔ Control protein intake.
✔ Employ vigorous mastication of foods
STAINS
- any discoloration that you can see in the surface of the teeth.
Extrinsic stains (outside)

- non metallic
- Metallic
Intrinsic stains (inside)

Due to:
- Blood-borne pigmentation
- Decomposition of RBC'S
- Drugs and metals
Extrinsic NonMetallic Stains

1. Green stain - children, gingival 3rd labial anterior
teeth, old person;poor oral hygiene
2.Black stain - 1mm above gingival line or premises on
feemales, non smoker, children with poor oral hygiene
and de cient nutrition.
3. Brown stain - gingival 3rd, pit and ssure and
maxillary posterior
4. Orange and red stain (rare) - chromogenic bacteria
ang cause. Poor oral hygiene.
5. Brown or black stain - tobacco stain. Lingual of
anterior
6. Bluish green stain - chromogenic bacteria due to poor oral hygiene.
Extrinsic Metallic Stains - inhalation of metal dust or from mouth

washes, medicines.
Greenish stain - Cu. Inhalation of copper especially in workers.
Metal workers. Adult
Green stain - nickel
Black stain - silver nitrate and manganese in mouth wash
Bluish stain - gold and contact with chlorine
Black or dirty green - mercury. Used as mouth wash or internal
administration of mercury.
Intrinsic stains
- Blood borne pigmentation
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- Decomposition of RBC's within the pulp
- Drugs and metals
Due to blood-borne pigmentation

🔘 Pink coloration of teeth
- typhus, cholera, acute exanthemata
🔘 Green or yellowish
- jaundice
🔘 Pink stains of teeth and bones
- hematoporphyria
🔘 Yellowish
- hypopituitarism
🔘 Milky white
- hypofunction of thyroid gland
🔘 Bluish white
- hyperfunction of thyroid gland
Stain due to decomposition of RBC's

▪ Traumatic injury
- From rapid pulpal hyperemia
- Blood pigments enter dentinal tubules
▪ Dental caries
- Pulpitis develops and leads to moist gangrene of the pulp
Derivatives of RBC's and their stains

▪ Hemoglobin - orange or pink
▪ Metahemoglobin - reddish-brown
▪ Hematoidin - orange
▪ Hemosiderin - brown
▪ Hematin - dark brown to black
▪ Heamin - bluish-black
▪ Sulphometahaemoglobin - reddish
Stains due to drugs and metals
✔ Bluish-green: copper albuminate of copper amalgam
✔ Black: discoloration of dentin from silver nitrate (AgNO.)
✔ Brown or black: discoloration from iodine and essential oils which
may penetrate tubules during RCT
Management of Stains
▪ Extrinsic - scaling and polishing (pumice and water)
▪ Intrinsic - external/ internal bleaching; Crowns
ORAL PATHOLOGY
MIDTERMS - 2nd Semester, SY 2022-2023
DEVELOPMENTAL ANOMALIES – JAW, - Wala collar bone (clavicle)
DENTINTION, AND TEETH - Paranasal surface are high
narrow (babalu)
• Developmental Disturbances
- Malocclusion
Affecting the Skull, Jaws, and
- Numerous supernumerary/
Teeth
impacted teeth
• Developmental Anomalies or
Disturbances Affecting the Jaws
• Developmental Anomalies of the
Teeth
o Disturbances during
initiation of tooth germs – 1
tooth germ = 1 tooth
o Disturbances during
Morphodifferentiation of
tooth germ – stage that
has shape 2. Craniofacial Dysostosis (Crouzon’s
o Disturbances during Disease; Maladie de Crouzon) –
Apposition of Hard Dental cranio = skull
Tissues – layer down - may collar bone (clavicle)
around 2.5mm of enamel; - the same condition as
form layer of matrix; kung cleidocranial dysostosis except
ano kadalumon ng that except that the clavicles are
enamel, dentin normal and the disturbance is
o Disturbances during limited to the skull, the upper
Calcification of Hard face, and the dentition.
Dental Tissues – deposit 3. Mandibulofacial Dysostosis
calcium/mineral to (Treacher-Colllin Syndrome;
calcified tissues Franeschetti’s Syndrome) – have
o Disturbances During congenital disorder
Eruption of Teeth – - it is characterized by hypoplasia
impaction, embedded of the facial bones, anomalies of
I. Developmental Disturbances the external ear and lower
Affecting Skull, Jaw, and Teeth eyelids, and marked hypoplasia
1. Cleidocranial Dysostosis (Sainton’s of the mandibular body – all of
Disease) – cleido = clavicle; cranial = which gives the patient a bird-
head face or fish-face appearance
- delayed closure of the
fontanelles and cranial sutures
and the presence of Wormian
bones.
- There is an absence or
hypoplasia of clavicles
- Delayed fontanelles
ORAL PATHOLOGY
4. Cleft Palate – result of lack of fusion of
two palatal processes with each other
or with the frontonasal process (primitive
palate).
- Varying in severity from the:
• Bifid uvula – cleft of the uvula to

a cleft involving the
Characteristics of Mandibulofacial: • Soft palate
• Hard palate
➢ Downward slanted eye –
• Alveolar ridges
absence of zygomatic
• Upper lip
➢ Micronaphia – small jaw
➢ Hearing loss - cleft lip is more common that cleft
➢ Underdeveloped ang zygoma palate and may be lateral (one side) or
(mandible) bilateral (both side)
➢ Absent ang ear
- it is represented by a defect in the
II. Developmental Disturbances
upper lateral incisor and canine areas.
Affecting Jaws
1. Macrognathia – large jaw; - cleft lip is hereditary.
condition is rare
5. Pierre Robin Syndrome –

2. Micrognathia – small jaw; extremely characterized by Micrognathia
rare
- glossoptosis
- cleft palate
Some condition that maybe present

together with other deformities:
- Mongolism – or trisonomy 21
3. Agnathia – failure development of the syndrome
jaw - Atresia of the ear
- Absent of the TMJ
- an extremely rare condition
ORAL PATHOLOGY
- Complete or partial anodontia of
both primary and permanent
dentition
- Malformation of any teeth
6. Cleft Mandible – extremely rare

condition in which a failure of fusion
between the right and left mandibular Clouston’s Syndrome or Hidrotic
processes leads to a defect in the Ectodermal Dysplasia – characterized
midline of the mandible by:
- Dystrophic thickened nails of

hands and feet
- Sparse brittle hair
- Hyperleratosis of the palm and
soles
- Thickening of the calvaria
- Pigmentation of skin over the
III. Developmental Anomalies of the axilla, elbow, knees, and
Teeth knuckles.
- Diffused white lesion in the
A. Disturbances during initiation of
mucosa
tooth germ
1. Ectodermal Dysplasia –
hereditary disease
- Hypotrichosis – absence or
reduction in amount of hair
- Anhldrosis – absence of sweat
glands
- Asteatosis – absence of
sebaceous glands
- Temperature elevation – due to
anhidrosis
- Dry skin 2. Anodontia
- Depressed bridge a. True Anodontia – absence
- Protrusion of the lip of teeth
- Defective mental development
ORAL PATHOLOGY
- It may be total involving both
primary and permanent
dentition.
- It may be partial or limited to
single tooth
b. False Anodontia – Pseudo
Anodontia – clinical
- Distomolar – accessory tooth
absence of tooth
distal to the 3rd molar
- impacted or ankylosed teeth
- Paramolar – one located buccal
that fail to erupt leave vacant
or lingual to the molars
places in the dental arch and
- Paramolar tubercle – fused with
represent fake anodontia.
permanent molar.
- false anodontia is seen in patients
with cleidocranial dysotosis, in
whom numerous teeth are
present in the jaws but do not
erupt.
Frequency of Missing teeth
1. Third Molar (most popular)

2. Lower 2nd Pre Molar - More common in maxilla than in
3. Upper Lateral Incisor mandible
4. Lower Central Incisor - More frequent sites are:
5. Lower Lateral Incisor o Between the maxillary
central incisors
o Distal to molars
3. Accessory and Supernumerary
But in mandibular:
Teeth – in excess of the normal
complement o Premolar region
- the term accessory (unique o Distal to the 3rd molar
shape) is used for teeth that do 4. Natal and Neonatal Teeth
not resemble than normal form. - Natal teeth – teeth present at
- Supernumerary – term for tooth birth
that mimic the normal shape - Neonatal Teeth – teeth that
- Mesiodens – accessory tooth erupts in the gingiva during the 1st
between the maxillary central month
incisors
- Peridens – tooth located buccal
or lingual to the arch
ORAL PATHOLOGY
5. Predeciduous Dentition – c. 8th nerve Deafness
extremely rare condition that - The alteration of the shape of the
implies the presence of teeth teeth is due to changes in the
preceeding the deciduous tooth germ during the stage of
dentition Morphodifferentiation maybe
- Consists of caps of enamel or due to inflammation in and
enamel and dentin. around the toth germ during the
6. Postpermanent Dentition – development.
extremely rare condition 2. Mulberry and Pfulger Molars – the
- Teeth may erupt after the loss of shape of the 1st permanent molar
permanent dentition is altered
- Usually impacted accessory or - 10-30% seen in patients with
supernumerary tooth that erupts congenital syphilis
after the insertion of dentures. - Occlusal surface is much
B. Disturbances during narrower than normal crown and
Morphodifferentiation of Tooth has pinched appearance
Germ - Shows hypoplasia of the enamel
1. Hutchinson’s Incisors – shape is - Pfulger Molar - identical to
altered 10-30% in children with mulberry molar but without
congenital syphilis hypoplasia of the enamel.
- Resemble a screwdriver – incisal
edges narrower than the middle
part of the crown
- May show NOTCHING on the
incisal edges
- Maxillary central incisors most
frequently involved.
3. Peg-shaped Lateral Incisors – an

example disturbance during
morphodifferentiation
Hutchinson’s Triad – pattern of

presentation for Congenital Syphilis
a. Interstitial Keratitis – inflammation

and scarring of the cornea
b. Hutchinson’s Incisor or Malformed
teeth
ORAL PATHOLOGY
4. Macrodontia – refers to a large - this invaginated epithelial organ
tooth then produces enamel and
- Can be proportional or dentin within the root.
disproportional – may involve a
single tooth
Etiology of Macrodontia:
a. Hormonal, gigantism in
hyperpituitarism
b. Cross inheritance
c. Over active odontogenesis
5. Microdontia – proportional or
siproportional or may involve a
single tooth
Etiology of Microdontia: 7. Dens Evaginatus – condition

occurs primarily in the mongoloid
a. Hypofunction of the
races
pituitary gland or dwarfism
- Hereditary trait
b. Cross inheritance
- Antithesis of dens invaginatus
c. Regression or atavism
- Presence of nipple-like
Two Forms: [rptruberance on the occlusal
surface of premolars.. rarely
a. Reduced number of cusp
canine and molars
b. Peg shaped tooth
- Evanginated odontoma is not
6. Dens Indente (Dens Invaginatus) – entirely appropriate for this
a “tooth within a tooth” malformation
Two Types:
a. Coronal Type – invagination of all

layers of enamel organ into the
dental papilla
- as the hard tissue are formed the
invaginated enamel organ
produces a small tooth within the
pulp Two Types of Dens Evaginatus:
b. Radicular Type – there is a folding a. Tubercle in the lingual ridge of
of the Hertwig’s sheath into the
the buccal cusp
developing root.
b. Tubercle in the center of the
occlusal surface
ORAL PATHOLOGY
11. Taurodontism – hereditary

8. Gemination (Twinning) – when a disturbance
single tooth germs splits or - The pulp chamber unusually
attempts to split to form two large and extended into the root
completely or partially separated canal
crowns – with single root rot canal - Teeth resemble those seen in the
with a single root. ungulates
- Can occur in primary and
permanent dentition, but most
common in permanent dentition
- Has long, rectangular body with
short roots, lacks constriction at
the cervix
9. Fusion – when two adjoining

tooth germs join to form a single
large crown
- Seen in the incisor area
- The single crown may have two
roots or a grooved root, but
usually have two root canals
C. Disturbances during Apposition of

Hard Dental Tissues
1. Enamel Hypoplasia – reduction in

the amount of thickness of
10. Dilaceration – twisting, bending enamel formed
or other distortion of the root. - Does not refer to the quality of
calcification
- Maybe due to local, hereditary,
and systemic factors
ORAL PATHOLOGY
- Teeth developing at this time of - Microscopically, dentin just below
systemic disease manifest defects the DEJ (mantle dentin) is normal
in areas of the crown - The remainder of the dentin
- Local enamel hypoplasia – shows reduction of tubules,
affects the tooth or a part of a cellular inclusion, and numerous
tooth and is due to a local cause resting lines, giving the
- Systemic enamel hypoplasia – appearance of stratification
abnormality is caused by a - Pulp chamber – progressively
generalized disease. It involves all obliterated and replaced by
teeth that are developing at this atypical dentin.
time and the defect is even seen
Dentinogenesis Imperfecta associated
in areas of the crown
with other developmental anomalies
- Hereditary enamel hypoplasia –
like:
involves the entire crowns. Both
permanent and deciduous a. Albinism
dentitions are involved. Since the b. Cardiac malformation
enamel thickness is reduced, the c. Osteogenesis imperfecta –
crowns may appear yellow and it characterized by atypical
is also called hereditary brown bone tissue, so that bones
teeth. fracture easily
d. Blue sclerae disease – a
congenital defect in
collagen synthesis causing
thinning of the schlera
which cause a bluish hue
on examination
2. Amelogenesis Imperfecta – ill-

defined term used to denote
hereditary enamel hypoplasia,
aplasia, or hypocalcification
3. Dentinogenesis Imperfecta
(opalescent dentin) – aa
hereditary disturbance that
affects the development of
dentin and maybe
accompanied by a similar 4. Dentinal Dysplasia – hereditary
disturbance in the bone disease
(osteogenesis imperfecta) - teeth appear clinically normal
- Teeth may appear opalescent or but are lost prematurely
gray. - radiographs show short pointed
roots, periapical radiolucencies,
ORAL PATHOLOGY
and obliteration of pulp
chambers and root canals
- microscopically, dentin is
whorllike, globular and
disorganized pattern.
7. Pigmentation of Enamel and

Dentin – the pigmentation is
caused by administration of
Tetracyclines during the period of
crown development.
5. Shell Teeth – modification of - Result from deposition of
dentinogenesis imperfecta Tetracycline in the dentin
- Root fail to form - Deposition in the enamel is
- Pulp chamber are very wide minimal
(shell)
- Enamel is normal
8. Cemental Hypoplasia –
6. Odontodysplasia – characterized characterized by significant
by defective dentin and enamel reduction in the amount and rate
formation of cementum formation
- Discolored, hypoplastic and - Clinically, teeth are lost
hypocalcified teeth with short prematurely and appear to be
roots shed off without apparent cause
- Usually fail to erupt, have wide - Usually found in hereditary
pulp chambers and maybe seen metabolic disease called
with radioluscent area around hypophosphatasia
the crown 9. Enamel Pearls – are round masses
- Radiographically, crowns of teeth of enamel that are attached to
have moth-eaten appearance the external surface of the tooth
ORAL PATHOLOGY
and are usually seen in the 2. Interglobular dentin – seen in
furcation of maxillary molar areas of uncalcified dentin
(external enamel pearl) - The dentin shows areas of
- Or may found within the coronal calcification with interspersed
dentin – called Internal Enamel irregular zones of uncalcified
Pearl dentin matrix
E. Disturbances During Eruption of

Teeth
1. Malocclusion – misalignment or
incorrect relation between the
teeth and the dental arches
D. Disturbances during Calcification
when they approach each other
of Hard Dental Tissues
as the jaw close
1. Enamel Hypocalcification – a Angle’s Classification of
condition in which the Malocclusion:
calcification of the enamel is
subnormal but the amount of Class I – Neutroclusion
the enamel is not changed Class II – Distoclusion
- Local hypocalcification – results
from local causes and affects Class III – Mesioclusion
only part of the tooth. Appears as
a white opaque area on the
crown.
- Systemic hypocalcification –
caused by some general
disturbance and affects a
number of teeth. Best example is
the Mottled Enamel
- Hereditary enamel
hypocalcification – affects the
entire crown 2. Concrescence – two
independently formed teeth
become fused
- Have separate pulp canals and
roots but fused to each other by
cementum or bone
- Both teeth may be erupted or
embedded or one tooth may be
ORAL PATHOLOGY
embedded and the other - Mandibular bicuspid
erupted - Maxillary bicuspid
- Maxillary central incisor
- Maxillary lateral incisor
3. Retarded Eruption/ Delayed

Eruption - teeth may be slow in
eruption.. may due to:
o Endocrine disturbances
o Vitamin deficiencies
o Local causes like lack of
space, dentigerous cyst,
eruption cyst, malposition
etc.
4. Shortened and Submerged Teeth
– both primary and permanent
teeth may be affected when Pell & Gregory Classification:
eruption ceased. - Relationship to anterior border of
- Ankylosis – fusion of the root to ramus;
the surrounding bone. o Class I – mesiodistal
5. Supraeruption – eruption of the diameter is completely
tooth beyond the occlusal plane anterior to the anterior
when the opposing tooth is lost border of the ramus
6. Embedded/Impacted Teeth – o Class II – ½ to 2/3
local causes: o Class III – more than 2/3 of
o lack of space the crown is within the
o dense overlying bone ramus
o retained or premature loss - Relationship to the Occlusal
of temporary teeth Plane/Relative Depth:
o systemic condition o Position A – highest point
(cleidocranial dysostosis, of the impacted tooth is
oxycephaly, progeria, level or above occlusal
achondroplasia, and cleft line of the 2nd molar
palate) o Position B – highest point is
below the occlusal plane
Frequency of Impacted Teeth:
but above cervical line of
- Mandibular 3rd molar the second molar
- Maxillary 3rd molar o Position C – below cervical
- Maxillary cuspid line of the 2nd molar
- Mandibular cuspid
ORAL PATHOLOGY
Relationship to the Maxillary Sinus:
Sinus Approximation (SA) – no bone or

very thin partition of bone exist
No Sinus Approximation (NSA) – 2mm or

Classifying: more bone exist
- Relationship to anterior border of

ramus
- Relationship to the Occlusal
Plane/Relative Depth
- Position of the long axis in relation
to the 2nd molar
Example:
Class I, Position B mesioangular

impacted 3rd molar
Classification of Maxillary 3rd Molar Classification of Maxillary Impacted

Cuspid:
Pell & Gregory Classification:
Class 1 – palate
- According to depth:
o Class A Class 2 – Labial/buccal of the maxilla
o Class B
Class 3 – crown palate and root buccal
o Class C
side or vise versa
Class 4 – vertically between incisors and

bicuspid
ORAL PATHOLOGY
Class 5 – edentulous maxilla Local Complications of eruption of
Deciduous Teeth
1. Acute Inflammation of the

Mucosa
2. Resistance of the tissue overlying
the erupting tooth
Anomalies of Teeth (Avendaño
Operculum – it cause pressure on the
Classifications of Anomalies of Teeth)
nerve trunk while cause pain and can
Anomalies in Size be relieved by incision of the mucosa
overlying the erupting tooth.
1. Macrodontia – (Megadontism,
Hyperpplasia of Teeth)
2. Microdontia – (hypoplasia of
teeth)
Anomalies in Numbers
1. Anodontia – hypoplasia of
dentition
- KINDS:
o Total Anodontia
(Complete) – failure of the
entire dentition to develop Pericorontitis due to erupting tooth
o Hypodontia (partial) – few
and specific teeth are are Operculectomy – removal of the
missing due to absence of operculum
anlage/tooth germ
o Oligodontia – many teeth
are missing and the
remaining are smaller
2. Supernumerary
Anomalies in Dentition:
a. Deciduous Dentition
aa. Premature Eruption
(Dentitia Precox) – early eruption
of deciduous teeth
bb. Delayed Eruption (Dentitia
Tarda) – retardation of eruption Eruption Cyst – a small circular bluish
deciduous teeth swelling over a tooth. It delays the final
emergence through the gums.
ORAL PATHOLOGY
a. Unusually or usually large
or small roots – due to
traumatic injuries or
systemic disturbances
b. Accessory roots
c. Concrescence – union of
fully formed teeth by
cementum only
cc. Premature Loss of Deciduous
- Synostosis – teeth united by bone
Teeth
to each other
- Ankylosis – teeth attach to
dd. Persistence of the Entire
alveolar bone
group of Deciduous Dentition
d. Enamel Pearls, enamel
drops, enameloma – small
b. Permanent Dentition
islands of enamel found at
aa. Premature eruption of permanent the roof surface or close to
teeth the CEJ frequently at the
bifurcation of root of
bb. Delayed or retarded eruption of molars and premolars
permanent teeth – impaction - Etiology: remnants of Hertwig’s
epithelial Root Sheath, that is
Anomalies in Shape and Form: when they persist to stay and fall
to be eliminated by resorption
Anomalies in Crown: - Talon’s Cusp – may developed in
maxillary incisors, a tubercle or
a. Fusion accessory cusp arising from the
b. Gemination cervicolingual ridge
c. Taurodontism e. Twisted roots – dilaceration
3 types:
- Hypotaurodont – mild form Enamel Defects:
- Mesotaurodont
- Hypertaurodont 1. White, opaque or chalky enamel
d. Dens Invaginatus/Dens In Dente – caused by total or partial
e. Supernumerary Cusp absence of interprismatic
f. Leong’s Premolar substance white spots due to
g. Peg tooth – aplasia of the mesial motting of enamel
and distal part of tooth 2. Corrrugated or Wrinkled enamel
h. Hutchinson’s teeth – grooves running across,
- Notched incisors surfaces are irregularly pitted. DEJ
- Mulberry molar-crown show very marked irregularly with
circular whorls and segments by
Anomalies in the root enamel protruding into the
dentin.
ORAL PATHOLOGY
3. Fissured Enamel – mild form, few a. Gastrointestinal
small grooves and fissures are on disturbances
the enamel surface. b. Infantile tetany – tetany of
4. Pitted Enamel – in more severe infants occurring usually in
cases it will show rows of deep pit association with rickets,
arranged horizontally across the due to dietary deficiency
surface, mild brownish of vitamin D
discoloration of enamel to severe c. Vitamin D, calcium and
pittings and irregularly of tooth phosphorus deficiency
crown. Very thin enamel maybe (Rickets)
worn out easily resulting to severe d. Vitamin C deficiency,
attrition. Infantile Scurvy
5. Gnarled Enamel/Enamel Whorl – e. Exanthemata – a skin
microscopically, the enamel rods eruption occurring as a
are twisted in form from DEJ to symptom of an acute viral
the surface, where there is or coccal disease, as in
twisting of enamel rods with scarlet fever or measles.
holes. D. Fluorosis
6. Turner’s Tooth – it is generally seen
in premolars resulting from Hypoplasia due to Congenital Syphilis
infection of deciduous teeth
(molar). It shows small crown, Oral Manifestation:
brown and irregularly shaped.
1. Hutchinson’s teeth
Enamel is lacking or present in
2. Moon’s Molar
zones or islands in some portion of
3. Mulberry Molar
the crown.
4. Bud Molars
7. Fluorosis – mottling, irregular
patches of white or brownish Moon’s Molar – may be present in one
pigmentation of teeth is due to or two shapes:
excessive consumption of fluoride
in water - Moon or bud molar – dome-
shape due to compression of the
Etiological Factors of Enamel and Dentin cusp so the mesio-distal
Defects measurement is less than the
bucco-lingual
A. Local Causes
- Mulberry molars – compression of
a. Trauma
occlusal which appears very
b. Infection
rough and pitted, presence of
B. General Causes
poorly developed nodules. Teeth
a. Disease of the genetic
are dull and muddy clear.
origin (Dentinogenesis
Imperfecta) Anomalies in the Position in the Dental
b. Syphilis Arch
C. Trophic Disturbances
ORAL PATHOLOGY
1. General Malalignment of teeth –
due to under developed
mandible resulting to crowding of
teeth
2. Diastema between the teeth –
maybe due to acromegaly,
hyperplasia of the jaw, or retain
deciduous or supernumerary
Types of Hypercementosis:
teeth.
3. Individual Malposition of the teeth a. Lateral – confined to one aspect
of the root
Individual Malposition of the teeth
b. Apical – seen in pulpless tooth,
especially in chronic infection
1. Labioversion – anterior teeth are
malposed towards the lip c. Diffused – develop around the
2. Buccoversion – malposed tooth, especially in funtionless
and embedded tooth
towards the cheek
d. Cementum hypertrophy –
3. Linguoversion – malposed
towards the tongue overgrowth with purpose of
improving the functional quality
4. Mesioversion – towards the
of the tooth
mesial
5. Distoversion e. Cementum hyperplasia – not
6. Torsoversion – rotated towards associated with increased
function but occurs in non
the long axis of the tooth
7. Supraversion – elongation of functioning tooth
tooth towards the occlusal f. Coronal cementum – cementum
8. Infraversion – associated with deposited in the crown
closed bite because of thet
decreased or arrested eruption
of the posterior teeth
9. Transposed teeth – interchange
of 2 teeth
10. Migration – tooth migrate to the
normal location like zygoma,
orbit, coronoid, etc.
Defects in the Cementum
1. Hypercementosis – overgrowth of
the cementum, localized or
diffused
Oral Pathology 3. Ethmocephaly
Lecture 3 – Midterm - mild form of cyclopia,
2 orbits and
rudimentary bulb
Congenital Anomalies of present. No nose.
the Head, Face and Oral Cavity
4. Synotia
A. Malformation of the Head and Face - failure of 1st
branchial arch to
1. Cyclops divide into maxilla
2. Cyclopia Hypognathus and mandible,
3. Ethmocephaly there’s union of
4. Synotia mouth and nose,
5. Archinencephaly/ Arhinencephaly fusion of ears in the midline and
6. Anencephaly (frog-like appearance) absence of the mandible.
7. Cebocephaly
8. Iniencephaly 5. Archinencephaly/ Arhinencephaly
9. Klippel- Feil Syndrome - a condition which is characterized
10. Microcephaly by malformation of the anterior
11. Macrocephaly part of the brain and skull and is
12. Hydrocephaly associated with ocular hypotelorism
13. Hydranencephaly and premaxillary agenesis. Nose
14. Oxycephaly maybe trunk-like rudiment.
15. Acrocephaly
16. Scapocephaly 6. Anencephaly (frog-like appearance)
17. Plagiocephaly - result from non closure
18. Dolichocephaly of the cerebral portion
19. Brachycephaly of the neural tube and
20. Trigonocephaly consist of complete
21. Kleeblattschadel Syndrome absence of cranial vault
22. Meningocele above the orbital ridge,
23. Aprosopus instead a soft, red,
24. Dignathus purple formless mass lying exposed
25. Hemifacial hypertrophy and atrophy base of the skull, composed largely
of thin walled vascular channels
1. Cyclops distended with blood.
- malformation in which the 2 eyes
fused into one.
- Premaxilla is absent and more How common is anencephaly?
processes grow together in the
Anencephaly is one of the most
median line, lie beneath the eye
and form high upper lip that replace common types of neural tube defect,
the external nose. affecting about 1 in 1,000 pregnancies.
2. Cyclopia Hypognathus However, most of these pregnancies
- single eye with small oral opening end in miscarriage, so the prevalence
and lack of nasal process. of this condition in newborns is much
lower. An estimated 1 in 10,000
infants in the United States is born
with anencephaly.
7. Cebocephaly 12. Hydrocephaly ( H2O in the brain)
- characterized with infant with - dilatation of brain cavity due to
single nostril associated with ocular cerebrospinal fluid inside the
hypotelorism, nose like in monkey. ventricles. The enlargement of the
CSF due to obstruction of the 4th
ventricle. The face appear shrunken
and small surrounded by dome-
shaped cranium. Bone of the
cranium is very thin.
8. Iniencephaly
- malformation of  Transillumination- will differentiate
the nape of the hydrocephaly from macrocephaly.
neck and the
brain. Head is Symptoms of Hydrocephaly
extended in the 1. Headache
face looks 2. Somnolence
upward. Skin of scalp is continuous 3. Irritability
with skin of the back. 4.Idiocy
9. Klippel- Feil 13. Hydraencephaly

Syndrome - complete or almost absence of
- basic defect cerebral hemispheres, the space
consist of being filled with CSF. The head is
shortening of normal size at birth. Percussion of
the neck as a the head give a tympanic note
result of (Macewen’s Sign) and
fusion and reduction is the number electroencephalogram reveals
of cervical vertebrae ( associated complete absence of electrical
with cleft palate). activity. Transillumination on one
10. Microcephaly side of the head, darkened room)
- condition characterized by an the glow often being transmitted
abnormally small skull with cranial through the pupil.
content about less than 1200 cc
instead of the normal 1,200 to 1750 14. Oxycephaly
cc. This is associated with feeble- - pointed head,
mindedness and idiocy. synonym for german
term which means
tower head, due to
premature closure of
transverse suture and
fissure which forces
the skull to develop
in an upward
direction.
11. Macrocephaly
- a condition characterized by large
skull circumference due to large
brain.
18. Dolicocephaly
15. Acrocephaly - long narrow skull without stenosis
- skull deformity of the sagittal suture.
which the frontal
bone bulges forward
due to premature
fusion of sagittal
sutures near the
bregma which
causes the bulging in
the frontal bone. 19. Brachycephaly
- round skull with short
16. Scapocephaly anteroposterior diameter. In severe
- convex shaped skull, which there is cases the skull is broad and
excessive development of shortened from the front to back.
length but diminished breadth due The face is flat, the eyes widely set
to premature closure of sagittal and orbits are shallow.
and parieto-temporal suture, which
causes inhibition in the
development of breadth. Frontal
ang occipital bones developed
prominently.
20. Trigonocephaly (Triangularity)

- Keel shaped forehead and
wide biparietal diameter of the
skull. The frontal protuberance is
produced by 2 halves of frontal
17. Plagiocephaly bone during fetal life associated
- slanting skull in which only 1⁄2 of with premaxillary agenesis and
the cranium is enlarged due pseudo-cleft of the upper lip.
to premature fusion of suture 1⁄2 of
the skull resulting to retarded
growth on the other half causing an
asymmetrical development.
21. Kleeblattschadel Syndrome
- skull is clover leaf in form (Trefoil 2. Prosopothoracopagus
Skull) combination of cranio- - twins fetus joined at
stenosis and hydrocephalus. the face, necks and
chest.
3. Prosoposternodymia
- double fetus joined at the face and
sternum
22. Meningocele 4. Diprosopus
- a defect on skull causing the dura - fetus with 2 faces
matter to herniate through the joined
opening. If the defect is large , the on the back of the head
brain substance as well as the 5. Dicephalus
meninges may protrude producing - with 2 completely
meningoencepholocele. separated heads
extending from one body.
C. Congenital Anomalies of the Jaws
1. Agnathia
23. Aprosopus - the maxillary or mandible or both
- development are missing completely
of the face is so
defective that a) Maxillary – the maxillary
it appears processes may have failed to
featureless. developed or only the
premaxilla is absent.
24. Dignathus b) Mandibular – due to absence of
- fetus with 2 lower jaws. the mandibular arch, maybe
seen in cyclops.
25. Hemifacial hypertrophy and atrophy b1. Agenesis of Ascending Ramus
 hemifacial hypertrophy- unilateral - resulting to small mandible and
enlargement of the facial and oral absence of chin.
structure. b2. Hemiagnathia
 hemifacial atrophy – slow progressive - congenital absence of half of the
atrophy of soft tissues of half of the mandible, maybe partial or
face. complete.
b3. Agenesis of Condyle
B. Malformation of the Head - absence of embryonic accessory
cartilage from which the condyle
1. Cephalothoracopagus developed, resulting to marked
- fetus joined by the micrognatha.
head and thorax
b4. Agenesis of mental protruberance 3. Macrostomia
- disturbance ofembryonic - complete fusion of the maxillary
cartilaginous skeleton ( symphysial and mandibular processes of the
cartilage) that takes part in the developing embryo resulting in an
development of symphysis menti. abnormal large oral aperture.
2. Micrognathia 4. Supernumerary mouth and /or jaws

- retarded development of one or - fetus with extra mouth which is
both jaws. smaller in size and generally ending
a. Maxillay - associated with mouth blindly, some has extra lips, tongue
breathing and jaw.
b. Mandibular –due to ankyloses of
condyle to glenoid fossa or agenesis of 5. Epignathus ( Oral Teratoma)
the condyle - teratoma arising in the region of
Rathkes’s pouch projecting into and
3. Macrognathia filling the pharynx or oral cavity
- large size of the protruding from the mouth.
jaw. If both jaws
are large it is
associated with
LEONTASIS OSSEA.
If mandible is large,
prognathic
asymmetry of the
jaw and face result.
a. Unilateral micrognathia E. Congenital Anomalies of the
- under development Tongue
b. Unilateral Ankylosis
- either due to overgrowth or 1. Aglossia
underdevelopment of section of the - congenital
face and jaw. absence of
the tongue
D. Congenital Anomalies of the Mouth
2. Ankyloglossia
1. Astomia
- Complete
union of
upper and
lower lip
2. Microstomia 3. Macroglossia
- usually acquired,
maybe associated
with operative
procedures or
stenosis of the
pharynx.
4. Microglossia 9b. Tongue Curling – ability to curl
up the lateral border of the tongue.
5. Lobulated tongue
- ( cleft tongue-cleft or bifid tongue)
9c. Tongue up folding – ability to

extend the tongue beyond the lips and fold
6. Fissured tongue ( scrotal tongue) the lip back upon the body of the tongue,
without the aid of the teeth.
7. Median Rhomboid glossitis

9d. Tongue rolling – ability to roll the tongue
from side to side
9e. Ability to place the tip of the tongue behind

the palate
9f. Ability to touch the tip of the nose with the

tip of the tongue
8. Supernumerary tongue
- tongue like structures projecting
from the tonsillar pillar
F. Congenital Anomalies of the Oral

Mucosa
1. Fordyce’s Disease
9. Abnormal tongue movements: - characterized by appearance of
9a. Trefoil tongue – ant. Portion discrete yellowish spots on mucosa
of the tongue can be deformed at will of lips, cheek and palate. First
into clover leaf pattern. described by Fordyce corresponding
to the opening of sebaceous glands.
2. Fissural Anomalies of the cheek 2. Labial Cleft ( cleft of the Lip) cleft lip
- absence of union of maxilla and or lagoschisis or lip-like hare.
mandibulae part, presence of 2a. Labial cleft of upper lip
groove line of the teeth. - due to failure of margins of globular
and maxillary process to unite.
3. Congenital pits and fistulas of the lips 2b. True median cleft of upper lips
- occurs in upper and lower lips, - due to failure of 2 globular
secretes mucus and therefore processes to unite.
spoken as fistulas. 2c. Lower lip
- failure of the mandibular processes
to unite in the median line
producing a cleft in the lower lip.
3. Lateral Nasal Cleft

4. Lateral Clefts of the upper lip
4. Double lip - Unilateral
- fold of mucosa of upper lip may - bilateral
give the impression of double lip 5. Oblique facial cleft ( meloschisis)
due to sucking the lip or drawing it - cleft that passes
between the incisors. through upper lip to
lower eyelid. Failure
of median nasal ,
lateral nasal and
maxillary process to
unite.
5. Abnormal labial frenum 6. Transverse Facial Cleft (cheek cleft)

- hypertrophy of labial frenum with - cleft extending from corner of the
thickening of the fibrous strand mouth to masseter muscle or in
exting down to the alveolar crest severe cases to the tragus of the
where it crosses the palatal side ear to embryonal tissue separating
forming between two incisors. the maxilla and the mandibular
processes.
b) Cleft of Internal Parts of the Face

extending or involving the maxilla
and mandible
1. Median Palatal Cleft
G. Cleft of the Face: 1a. Hard palate
a) Cleft on the outer surface of the - due to failure of 2 palatine
face: processes and nasal septum to
1. Median Nasal Cleft unite.
– cleft separating 1b. Soft Plate
the median nasal - failure of 2 palatine processes to
process from unite.
lateral nasal
process.
2. Lateral Cleft of Maxilla ( alveolar
process or gnathoschisis)
condition may either be:
i. Unilateral
ii. Bilateral
3. Median cleft of Mandible

- Failure of 2 mandibular processes
to unite.
ORAL PATHOLOGY
FINALS - 2nd Semester, SY 2022-2023
Dental Alveolar Trauma (Traumatic Sex
Injuries to the Anterior Teeth)
- in primary dentition, the
ETIOLOGY prevalence of injuries ranges
from 31-40% in boys and from 16-
- Trauma to the teeth and
30% in girls.
orofacial structures continues as
- In permanent dentition, the
a frequent dental problem. As
prevalence of dental trauma in
long as young children remain
boys ranges from 12-33% as
active, accidents will occur,
opposed to 4-19% in girls.
requiring careful and
conscientious care. Age
- The management of a dental
- The most common age for
emergency requires a rage of
trauma in the primary dentition is
skill, judgement, and experience
from 1.5-2.5 years, when the child
unequaled by any other
is learning to walk
challenge in dental practice.
- In the permanent dentition, the
Trauma to the Primary Dentition peak age ranges from 8-10 years.
- Traumatic injury to the primary Occlusion

dentition is a common
- Increased overjet with protrusion
occurrence. Anterior teeth are
of upper incisors and insufficient
the most commonly traumatized,
lip closure are significant
with 71% of cases involving the
predisposing factors to traumatic
maxillary central incisors.
injuries.
- this is three times more frequent
- “Accident Prone Profile”
than the involvement of the
- Mc Ewen and Mc Hugh in their
maxillary lateral incisors
study found out that as overjet
The Most Common Cause of Dento- increased, the incidence of
alveolar Trauma are: fractured maxillary incisors also
increases.
• falls in infancy
- they estimate that boys with
• child physical abuse (50% of
overjet of 1mm or less, the
injuries are to face and orofacial
chance of fracture is 1 in 25,
area)
whereas boys with 10 mm or mor
• falls and collisions
overjet, there is a chance in four
• sports and related injuries
of sustaining fracture before age
• automobile accidents
13. (Clinical Pedodontics, Finn)
Predisposing Factors:
Diagnosis and Assessment
Several factors play a role in
- careful diagnosis and case
predisposing children to dental trauma,
documentation is the first step in
the frequency of which varies
considerably.
ORAL PATHOLOGY
the treatment of any traumatic Garcia and Godoy’s Classification
injury.
- Is also a modification of the WHO
Diagnostic steps following Dental system. This classification differs
Trauma from others mainly because it
separates dental fractures into
➢ medical and health history
those which involve cementum
➢ history of the dental injury and
and those which do not.
immediate care provided
Moreover, there are no groupings
➢ neurologic evaluation
for subluxation or alveolar injuries
➢ clinical examination of the head
and mandible or maxilla
and neck
fractures.
➢ oral examination of soft and hard
tissues Ellis and Davey’s Classification
➢ radiographic examination
- Is another modification of the
➢ photographic documentation
WHO system. This system is
Classification of Injuries to the Anterior simplified classification which
Teeth groups many injuries and allows
for subjective interpretation by
WHO Classification
including broad terms such as
- describes injuries to the internal “simple” or “extensive” fractures.
structures of the mouth and Injuries to the alveolar socket and
incorporates a broad group of fractures of the mandible and
other injuries including laceration maxilla are not classified here.
of oral soft tissues - “May classification have been
suggested for dental injuries with
Andreasen’s Classification some classifications were
- is a modification of the World excessively complex. As
Health Organization’s (WHO) and suggested earlier, there is a need
contains 19 groups that include for reappraisal of tooth fractures
injuries to the teeth, supporting and any such classification
structures, gingiva, and oral should be applicable to both
mucosa. primary and permanent
- Unlike the WHO classification, the dentition.” (K Loomba, Journal of
socket and fractures of the Oral Science, Vol. 52, 2010)
mandible or maxilla are not
grouped under oral injuries, but
rather are classified separately as
fractures of facial bones. It is very
comprehensive system which
allows for minimal subjective
interpretations.
ORAL PATHOLOGY
Ellis and Davey’s Classsification of • Class 3 – extensive fracture of
Anterior Teeth (1960) the crown, involving
considerate dentin and
exposing the pulp
Classification of Dental Injuries

• Class 4 – traumatized tooth
• Class 1 – simple fracture of becomes non vital (dead),
the crown-with little or no with or without loss of crown
dentin involvement. structure
• Class 5 – complete loss of
tooth
• Class 2 – extensive fracture of

the crown-involving
considerable dentin but not
the pulp
ORAL PATHOLOGY
• Class 6 – root fracture, with or
without loss of structure
Avulsion
- Complete displacement of the

tooth out of its socket.
• Class 7 – displacement of tooth

without crown or root fracture
• Class 8 – fracture of the crown en
masse
• Class 9 – injuries involving primary
dentition
Soft Tissue Trauma
Concussion
- Injury to the tooth supporting Intrusive Luxation

structure without abnormal
- Displacement of the tooth into
loosening or displacement of the
the alveolar bone
tooth, but with reaction to
percussion
Subluxation (loosening)
- Injury to the tooth supporting

structure with abnormal
loosening, but without
displacement of the tooth.
Lateral Luxation
- Displacement of the tooth in a

direction (mesial, distal, lingual, Extrusive Luxation
labial) usually accompanied by
- Partial displacement of the tooth
fracture of alveolar component.
out of its socket
ORAL PATHOLOGY
Treatment of Hard Tissue Fractures
Hard tissue fractures are present

Management of Injuries to the Primary in about 60% of all injuries involving
Teeth primary teeth. The treatment of a tooth
fracture is determined by the extent of
Color changes subsequent to trauma: the fracture.
- Reddish-brown or pink ➢ If pulp is exposed, perform pulp
discoloration is indicative at therapy restoring the tooth with resin
pulpal hemorrhage which may or SSC.
turn to Bluish-black color ➢ If extensive pulpal exposure is
indicating pulpal necrosis. Treat present, extraction is usually the best
with extraction or pulp therapy. choice.
➢ If no pulp exposure exists, smoothen
sharp edges and continue to
observe at future appointments.
➢ Alert parent to watch for color
changes and infection.
➢ Follow up with radiographics.
➢ If trauma is associated with root
fracture, extract all fracture
- grayish-yellow discoloration indicates
segments without damage to
pulp canal obliteration. Since this does
developing permanent tooth bud.
not interfere with physiological root
DO NOT chase apical third
resorption, no treatment is necessary.
fragments.
Intrusion Injuries
- Assess permanent tooth bud

damage with radiographs. If the
primary tooth is displaced into
the permanent tooth bud,
EXTRACT the primary tooth. If the
tooth is labially intruded, which
ORAL PATHOLOGY
occurs in 80% of the cases, allow Sequelae to Developing Permanent
it to spontaneously re-erupt. Teeth
Anatomically, the permanent

anterior teeth develop in close proximity
to the apices of the primary incisors.
Thus, periapical pathology that is due to
necrotic pulp, intrusive injuries, or over
instrumentation of primary root canals
can irreversibly damage permanent
teeth
• Trauma to the primary tooth can

There are different approaches to the
disturb enamel formation in the
management of an intruded tooth. The
underlying permanent tooth,
child usually suffers no discomfort, and
especially on the labial surface. This
treatment involves a “wait and see
condition is referred to as Turners
policy”. – J. Vitug, Oct-Nov.2003, PDA
Hypoplasia.
Journal
➢ If the displaced tooth is very loose in

its socket or if it interferes with
occlusion, extraction is the best
choice.
➢ Do not stabilize primary teeth with
any of the techniques used to
stabilize permanent teeth.
➢ Advise a soft diet for two weeks.
Avulsed Primary Teeth

• Small to large opacities of
- Are not reimplanted due to hypocalcification in the enamel are
possible injury to the developing thought to be caused by periapical
permanent tooth infection
• Root dilaceration occurs in 3% of

injuries to the primary dentition. Root
ORAL PATHOLOGY
dilaceration appear as marked Class III Fracture
curvatures of the root usually
- Evaluate the size of pulp
involving permanent central incisors.
exposure to determine whether
pulp capping or pulp therapy is
necessary. If exposure is less than
1mm, perform a direct pulp cap.
If exposure is 2mm or greater,
pulpectomy is recommended.
Concussion
- Percussion or pressure produces

Management of Injuries to the
sensitivity
Permanent Anterior Teeth
- Relieve occlusion
Class I and Class II Crown Fractures - Perform vitality tests
- Observe periodically with
- If dentine is exposed place
radiographs for up to a year
adequate dentinal protection
- Advise soft diet for two weeks
and follow with composite
“band-aid” restoration. Subluxation
- If minimal, leave alone, monitor

tooth with vitality tests, and adjust
occlusion if necessary.
- If extensive, place a flexible splint
(monofilament fiber or light
orthodontic wire) bonded to the
tooth with acid-etch resin for one
to two weeks.
- Evaluate the tooth for clinical
signs of pulpal degeneration
- Allow up to four weeks of
using vitality tests and
recovery, then restore the tooth
radiographic follow-up.
with aesthetic resin restoration
ORAL PATHOLOGY
Intrusion Injuries - Monitor with radiographs for up
to five years
- The optimal treatment of
- Poor prognosis
intruded teeth has not yet been
determined. Immediate Extrusion Injuries
repositioning has been shown to
- Asses the position of the tooth
increase the incidence of
radiographically. Then, reposition
complications such as external
tooth to normal position and
root resorption and loss of
splint with a non-rigid, acid-etch
marginal bone support.
splint for two to three weeks.
Therefore, the treatment of
- Monitor pulp vitality every few
choice is orthodontic
weeks. If pulp necrosis occurs,
repositioning over a period of
perform endodontic therapy.
three to four weeks as shown in
Choice of root canal filling
the photos below.
material depends on the maturity
of the tooth.
Avulsion Injuries
Factors affecting the prognosis of

an avulsed permanent tooth include:
- Orthodontic extrusion should be - Stage of root development

performed as soon as possible for - Physiologic status of the
two reasons – to gain access to periodontal ligament
pulp chamber should - Length of extra-oral time
endodontic treatment become If parents call the dental office to report
necessary and to minimize the that their child’s tooth has been
chances of external root avulsed:
resorption.
- Place the tooth in a moist
environment if they cannot
replant the tooth into its socket.
- Stored in milk (liquid) or contact
lens solution until replacement.
- Storage in tap water or saliva is
NOT recommended, since the
- Pulp necrosis will occur hypotonic conditions will result in
- Begin orthodontic extrusion within rapid lysis of PDL cells.
two weeks - The extra-oral time (EOT) the
- Access root canal within three to tooth is out of its socket is critical
four days and perform to the success of the replantation
endodontic treatment procedure. Success compared
with time shows:
ORAL PATHOLOGY
o Less than 30 mins – 90% line and restore endodontically.
success
o 30 to 90 mins – 43%
success
o More than 90 mins – 7%
success
Treatment Protocol:
- Gently rinse tooth in a steady

stream of saline. DO NOT
manipulate root surface.
- Place tooth in OSE (optimal
The methods of root healing have been
storage environment) for 30 mins
described by Andreasen and
while obtaining medical history,
Michanowiczs and co workers, the
injury history, neurologic
integrity of the periodontal ligament is
assessment, and radiographic
essential requirement for root healing to
assessment.
occur, while the presence of vital pulp is
- Flush socket and replant tooth
not necessary.
with light pressure.
- Splint tooth with a flexible, Three Categories of Root Repair
passive splint for two to three
weeks. 1. Healing of the fractured area
- If apical foramen is closed, with dentin surrounded by
perform root canal therapy (RCT) cementum and cementoid.
one week following the trauma. 2. Healing of the fractured area by
filling in of the connective tissue.
Root Fracture 3. Healing of the fractured area by
interposition of bone and
- Root fracture tend to be more
connective tissue.
common after age 10 years. To
identify the fracture, change
radiograph angulation 10—15
degrees apically or coronally to
see the fracture.
- Treatment involves the
application of a rigid splint for up
to six weeks. Careful monitoring
with radiographs and pulp vitality
tests are important. If pulp
necrosis is becomes evident,
remove pulp tissue to the fracture
SYSTEMIC DISEASES WITH 3. Xeropthalmia
ORAL MANIFESTATIONS 4. Follicular Keratitis
3 MAIN GROUPS OF LESIONS IN THE 5. Squamous metaplasia

MOUTH
2. VITAMIN B DEFICIENCY
• GROUP A
 VITAMIN B - found liver, yeast,
- includes those disease that occurs milk and green leafy vegetable.
exclusively in the oral tissues  Vit B1 (Thiamine) - prevent
Beriberi
• GROUP B
 Vi B3 (Niacine) - prevent Pellagra
-disease that are generalized but become  Vit B2 (Rivoflavin) - prevent
manifest in the oral cavity before Angular Cheilosis
anywhere else.
3. VITAMIN C DEFICIENCY
• GROUP C
 VITAMIN C - for production of
-become apparent in the mouth only in
the late stage of their development. ground substance of all connective
tissue, bone, cartilage and blood
VITAMIN DEFICIENCY vessels.
 prevent scurvy.
 VITAMIN A DEFICIENCY  Deficiency shows:
 VITAMIN B DEFICIENCY  petechia and ecchymosis in
 VITAMIN C DEFICIENCY the mucous membrane
 VITAMIN D DEFICIENCY  hyperemia and edema
 enlargement of the gingiva
with increase bleeding
1. VITAMIN A DEFICIENCY tendency.
 VITAMIN A 4. VITAMIN D DEFICIENCY

 fat-soluble and colorless alcohol  VITAMIN D - aid in the
derived from the carotene Found absorption of calcium and
in fish oil, butter and eggs. phosphorus thru the
Maintenance and function of the mucous membrane of the
specialized pith of photosensitive intestine and promote
pigments used by the cone and calcification of bone and
rods of the eyes and also for the cartilage.
maintenance of skeletal growth.  Deficiency causes:
 Rickets in children
 DEFICIENCY CAUSE  Osteomalacia in
adult
1. Night blindness - both are failure of calcification of
cartilage and bone
2 Bitot's spot
BLOOD DISORDERS 3. Atrophy of the oral mucosa and gastro
intestinal mucosa,
 Leukemia- applied to those
malignant tumor of WBC that 4. Hemorrhages of the skin and oral
extend into the blood stream. In mucosa.
some instances, patients WBC
count maybe normal or below Plummer vinson syndrome or
normal. sideropenic dysphagia
 oral findings include enlargement, - is a symptom complex that occur
bleeding and necrosis of the oral almost exclusively in middle aged
mucosa. Tooth extraction followed female associated with stomatitis
by profuse bleeding. pharyngoesophageal ulcerations,
 Agranulocytosis- reduction in the dysphagia and changes in nails.
granular leukocyte chiefly Oral lesions includeleukoplakia
neutophils. Oral lesions include with dyskeratosis, angular chilitis,
gangrenous ulceration in the atrophic glositis and xerostomia as
gingiva, tonsils, soft palate, lips, seen in iron deficiency anemia.
buccal mucosa, and pharynx
(agranulocytic angina) Erythroblastosis fetalis
Anemia-deficiency of erythrocytes and - hemolvtic disease in new born

hemoglobin caused by blood group
incompatibility between mother
1. Iron deficiency anemio- result from and child. Mother develop
defilency of iron antibodies against the RH factor of
the fetus.
2. pernicious anemia-result from
- These antibodies pass to the fetus
deficiency of anti pernicious anemia
and destroy the RBC.
factor or vit b12
- Result to hemolysis, jaundice and
3. Folic acid deficiency anemia- caused by anemia. Oral manifestation result
diseases of gastrointestinal tract such as to black, brown or bluish
sprue, celiac disease and fish tapeworm pigmentation of the teeth.
infestation.
Thalassemia (Cooleys Anemia)
4. Hemolytic anemia- excessive
- congenital familial disease that is
destruction of red cells, particularly in
predominant among persons of
erythroblastosis fetalis, thalasemia and
mediterranean origin and is
sickle cell anemia.
caused by defect in the rate of
 Characteristics common to all synthesis of hemoglobin A. the
types of anemias include: head is enlarged and radiograph
shows thickening of diploe and a
1. Pallor of the mucosa,skin and muscle, “hair on end appearance”,
protrusion of the upper anterior
2. Fatty change in the heart and liver, teeth and honeycombed
appearance of bone trabeculae.
DISEASES OF THE BONE
 Pagets disease or ostitis

deformans
- generalized bone disease of
unknown cause.
- Major involvement occurs in the
skull and weight bearing parts of
the skeleton. Oral involvement
includes enlargement of the
alveolar ridge in edentulous
patient, teeth may migrate, loosen,
and diastema may develop.
Microscopic appearance is
pathognomonic, consist of mosaic
or jig saw pattern due to
successive bone destruction and
bone apposition.
 Fibrous dysplasia
- disease of childhood and
adolescence, sometime associated
with hypergonadism and with
brown spot on the skin, café au lait
spots.
- Radiograph shows enlargement of
the jaw, expansion of cortex,
radiolucency or mottled enamel.
 Leontiasis ossea
- a form of fibrous dysplasia,
primarily affects the upper face. It
is essentially a hyperostosis.
Lesions are characterized by dense
area of radiopacity in the maxilla,
nasal bones, frontal bones,
temporal bones and zygomatic
bones.
 Caffeys disease (infantlike

cortical hyperostosis)
- characterized by enlargement of
the affected bone commonly the
mandible, the ulna and clavicle.
Patient is usually 6 months of age.
ORAL PATHOLOGY
Metal Poisoning - Microscopically, the lead line

consists of a granular pigment
A number of metallic salts act
deposit in the perivascular
as systemic poisons. The most
areas of the submucosa and
prominent among these are arsenic,
the basement membrane. This
lead, bismuth, mercury, silver, and
pigment is called lead sulfide.
phosphorus.
- Used in paints, ceramics,
• ARSENIC gasoline, batteries, cosmetics
- Arsenic poisoning consists of - Can cause coma
gingivitis and stomatitis, other - In children, it can exhibit
clinical features including behavioral disorder and
vomiting, diarrhea, affects intellectual activity
hyperkeratosis, hyper
other manifestations of lead
pigmentation, and neurologic
poisoning:
disturbances,
➢ Inorganic Arsenic – soil, - Gastrointestinal upset
sediments, ground water, - Convulsive seizures
smelling, industrial use - Neuritis
- Production of pesticides - Anemia
- Wood preservatives - Peculiar basophilic stippling of
➢ Organic Arsenic – fish, ocean, erythrocytes
shellfish - Osteosclerotic lines in the
- Natural occurring metaphyses of long bones
• BISMUTH
Expose:
- Bismuth poisoning was
- Intake of drinking water with common when metal was
arsenic content used for treatment of syphilis,
manifestation consist of
Long term exposure:
metallic tase, burning
- Skin disorder sensation of the oral mucosa
- Diabetes and a bismuth line.
- High blood pressure - Microscopically, granular
- Several types of cancer deposits of black pigment
• LEAD (bismuth sulfide) are seen in
- Lead poisoning manifest in the the submucosa.
oral cavity as excessive - The bismuth salt is believed to
salivation, metallic taste, react with hydrogen sulfide
swelling of the salivary glands, that is produced from the
and a dark line along the degradation of food debris in
gingival margin the mouth and to produce
ORAL PATHOLOGY
bismuth sulfide, which in turn o Discoloration of the skin

deposits as an insoluble (ashen gray)
precipitate. • MERCURY
- Used for anti-diarrheal and - Acute and chronic poisoning
antacid medication with metallic mercury leads to
- Pigment on cosmetics, disturbances in the central
catalyst in rubber production, nervous system and the
fire alarm, glass gastrointestinal tract.
- Neurotoxicity, hepatoxicity, - Oral manifestation include
increase viscous blood salivation, stomatitis, glossitis,
➢ Bismuth salt – cause toxicity swelling of salivary glands, and
- Consumption of medication a dark line on the gingival
• PHOSPHORUS similar to bismuth
- Follows prolonged inhalation - Seafoods
of phosphorus compound, - Industries that process
most remarkable oral mercury, thermometer, etc.
manifestation is persistent and batteries,
progressive swelling of maxilla sphygmomanometer
and mandible. - blood mercury level = 100
- White phosphorus = toxic nanogram/mL
o Manufacture of - mas delikado ma inhale and
explosive bombs, mercury kesa ma intake
artificial fertilizers ➢ forms of mercury
• SILVER - Elemental
- Due to prolonged contact - Inorganic – occupational
with organic and inorganic (industries)
silver, the skin and oral mucosa - Organic – metal mercury (fish,
acquire an ashen gray hue, if ihaboy sa dagat ang
presence of fine black mercury then gin kaon ka isda
granular pigment in the sub ang mercury, gin kaon mo
epithelial connective tissue man ang isda)
- The granules are an insoluble ➢ Factors that determine Severity:
albuminate of silver and give a - Dose
permanent pigmentation to - Age – pila ang edad ang
the tissue. maapektuhan to consider na
- Component of amalgam may toxic effect
- high level toxicity of silver in o kids – very toxic
the air can cause lung and o developmental – if sa
breathing irritation tiyan pa, 1st trimester ma
- Silver poisoning = “ARGYRIA”
ORAL PATHOLOGY
apektuhan na ang
baby
- Duration of exposure – kung
ano kalawig ang exposure
- Route of exposure – na inhale
or nakaptan ang mercury
• MINAMATA DISEASE
- Is a methylmercury poisoning
with nerurological symptoms
and caused by the daily
consumption of lagre
quantities of fish and shellfish
that were heavily
contaminated with the toxic
chemical generated in
chemical factories and then
discharged into the sea.
• DOH ADMINISTRATIVE ODER 2008-
21
- Gradual phase out of mercury
in all Philippine Health Care
facilities and institutions
ORAL PATHOLOGY
• RA 6969
- Toxic substances and
hazardous and nuclear waste
control act of 1990,…
Regulation for manufacture,
sale, and distribution of HG.
ENDOCRINE SYSTEM • Increase bone mass – given to
postmenopausal to increase and
- Gland produces hormones for a specific prevents osteoporosis.
function.
- Sleep, mood Pituitary Gland
- Chemical messenger systems causing
• Master gland
feedback loops.
• Influences most endocrine organs
• controls the function of most other
• Hypothalamus
endocrine glands and is therefore
• Pituitary gland – growth hormone
sometimes called the master gland.
• Pineal
• Thyroid
• Barathyroid
• Adrenals
• Pancreas
• Gonads
Hypothalamus
• is the neural control center for all

endocrine systems.
• makes ADH and oxytoxin – controls Disorders that result from overproduction
uterus during pregnancy. of pituitary hormones include:
• Brain and stored in pituitary gland
• Tells kidney how much fluid to restore • Acromegaly or gigantism: Growth
• Balance and regulates water in blood. hormone
• Cushing disease: Adrenocorticotropic
Pineal Gland – release melatonin hormone (ATH)
• Galactorrhea (the secretion of breast
• a small, pea-shaped gland in the brain.
milk by men or by women when not
• it produces and regulates some
pregnant): Prolactin
hormones, including melatonin.
• Erectile dysfunction: Prolactin
• Last brain organ to be discovered
• Infertility (particularly in women):
• House of the soul “rene des cartes”
Prolactin
Melatonin – sleep hormone
Disorders that result from underproduction of
• is best known for the role it plays in pituitary hormones include:
regulating sleep patterns. Sleep
• Central diabetes insipidus: Vasopressin
patterns are also called circadian
• Hypopituitarism: Multiple hormones
rhythms.
• Large in children and shrinks in adults
Disorders of pituitary gland: Thyroid Gland
Overproduction – excessive growth - is a gland below the Adam's apple in the

gigantism children front of your neck. Glands make and
release hormones. Hormones stimulate
Tumor in pituitary gland acromegaly other cells or tissues into action. The
adult thyroid makes thyroid hormones.
OM: hoarse and swelling, overgrowth of - How fast you burn your calories
mandible (jaw bone) - Heart beat
- Body temperature
• Adrenocorticotropic hormone (ACTH)
(high) 2 Types of Thyroid Hormones
- Cushing disease 1. Tetraiodothyronine (thyroxine, T4)
• Cortisole
- Natural steroids of the body 2. Triiodothyronine (T3)
- Stress hormone
Thyroid-stimulating hormone (TSH)
- Helps maintain blood pressure, blood
measurement
glucose
- Turns food into energy - TSH measurement is the best means of
• Steroids determining thyroid dysfunction.
- Double-edge sword - Normal result essentially rule out
- Inflammatory Hyperthyroidism or hypothyroidism,
- Immunosuppressant except in patients with central
• Galactorrhea hypothyroidism due to disease in the
- The secretion of breast milk by men or hypothalamus or pituitary gland or in
by women when not pregnant:prolactin rare patients with pituitary resistance
- Leuteotropin to thyroid hormone.
➢ Erectile dysfunction : prolactin
- Hyperprolactenemia – ❖ Hyperthyroidism (Thyrotoxicosis)
hypergonadism - Hyperthyroidism may result
➢ Infertility – prolactin from increased synthesis and
secretion of thyraid hormones
Disorders of underproduce pituitary production:
(thyroxine [T41 and
• Central diabetes insipidus : vasopressin triiodothyronine [T3]) from the
(excessive production of urine) thyraid, caused by thyroid
- Inherited/caused by other stimulators in the blood or by
disorder/unknown autonomous thyroid
• Hypopituitarism – multiple hormones hyperfunction.
- -The most common causes
overall include
1. Graves disease
2. Multinodular goiter
3. Thyroiditis SIGNS OF HYPERTHYROIDISM
4. Single, autonomous,
hyperfunctioning “hot” 1. warm,
nodule 2. moist skin;
3. tremor;
❖ Graves disease (toxic diffuse goiter) 4. tachycardia;
- the most common cause of 5. widened pulse pressure;
hyperthyroidism, is characterized by 6. atrial fibrillation
hyperthyroidism and one or more of SYMPTOMS OF HYPERTHYROIDISM
the following
1. Goiter 1. nervousness,
2. Exophthalmos 2. palpitations,
3. Infiltrative ophthalmopathy 3. hyperactivity,
4. increased sweating,
❖ Toxic solitary or multinodular goiter 5. heat hypersensitivity,
(Plummer disease) 6. fatigue,
- sometimes results from TSH receptor 7. increased appetite,
gene mutations causing continuous 8. weight loss,
thyroid activation. 9. insomnia,
- Patients with toxic nodular goiter have 10. weakness,
none of the autoimmune 11. frequent bowel movements
manifestations or circulating antibodies (occasionally diarrhea).
observed in patients with Graves 12. Hypomenorrhea may be present.
disease.
THYROID STORM
❖ Inflammatory thyroid disease
(thyroiditis) - an acute form of hyperthyroidism that
- includes subacute granulomatous results from untreated or inadequately
thyroiditis, Hashimoto thyroiditis, and treated severe hyperthyroidism.
silent lymphocytic thyroiditis, a variant - occurring in patients with Graves
of Hashimoto thyroiditis. disease or toxic multinodular goiter
❖ Single, autonomous, hyperfunctioning • It may be precipitated by:

"hot" nodule
1. infection,
- refers to any abnormal growth that
2. trauma,
forms a lump in the thyroid gland.
3. surgery,
- If the nodule produces thyroid
4. embolism,
hormone in an uncontrolled manner
5. diabetic ketoacidosis,
(without regarding the body's needs),
6. or preeclampsia.
the nodule is referred to as
autonomous, the nodule may produce
signs and symptoms of too much
thyroid hormone (hyperthyroidism)
Thyroid storm causes abrupt florid symptoms of 4. Dermatologic manifestations
hyperthyroidism with one or more of the 5. Ocular manifestation
following: 6. Gastrointestinal manifestations
7. Gynecologic manifestations
1. fever, 8. Cardiovascular manifestations
2. marked weakness and muscle wasting,
3. extreme restlessness with wide
• Primary hypothyroidism
emotional swings,
- is most common; it is due to
4. confusion,
disease in the thyroid, and
5. psychosis,
thyroid-stimulating hormone
6. coma,
(TSH) levels are high.
7. nausea,
8. vomiting,
• Secondary hypothyroidism
9. diarrhea,
- is less common; it is due to
10. hepatomegaly with mild jaundice.
pituitary or hypothalamic
11. patient may present with cardiovascular
disease, and TSH levels are low.
collapse and shock.
Myxedema coma
Thyroid storm is a life-threatening emergency
requiring prompt treatment - is a life-threatening
complication of
❖ Treatment of hyperthyroidism depends hypothyroidism, usually
on cause but may include: occurring in patients with a long
o Methimazole or history of hypothyroidism.
propylthiouracil - Its characteristics include coma
o Beta-blockers with extreme hypothermia
(temperature 24° to 32.2° C),
Hypothyroidism (Myxedema) areflexia, seizures, and
respiratory depression with
- is thyroid hormone deficiency.
carbon dioxide retention.
It is diagnosed by clinical
- Severe hypothermia may be
features such as a typical facial
missed unless low-reading
appearance, hoarse slow
thermometers are used.
speech, and dry skin and by low
- Rapid diagnosis based on
levels of thyroid hormones.
clinical judgment, history, and
- Management includes
physical examination is
treatment of the cause and
imperative, because death is
administration of thyroxine.
likely without rapid treatment.
Symptoms and Signs Precipitating factors include

1. Metabolic manifestations
2. Neurologic manifestations 1. illness,
3. Psychiatric manifestations 2. infection,
3. trauma, turn increases the absorption of calcium
4. drugs that suppress the central nervous from food in the intestines.
system
5. exposure to cold. Hypercalcemia
- is a condition in which the calcium level

❖ PARATHYROID GLANDS in vour blood is above normal. Too
- are four tiny glands, located in much calcium in your blood can weaken
the neck, that control the your bones, create kidney stones, and
body's calcium levels. Each interfere with how your heart and brain
gland is about the size of a grain work.
of rice (weighs approximately
30 milligrams and is 3-4 There are many causes of hypercalcemia, but
millimeters in diameter). The the most common are:
parathyroids produce a
1. Hyperparathyroidism
hormone called parathyroid
2. Cancer
hormone (PTH).
3. Vit. D toxicity
✓ Parathyroid hormone (PTH).
❖ ADRENAL GLANDS
- PTH is produced by four button-
- also known as suprarenal glands, are
sized parathyroid glands that
endocrine glands that produce a variety
are located in the neck behind
of hormones including adrenaline and
the thyroid gland.
the steroids aldosterone and cortisol.
- Normally, these glands secrete
They are found above the kidneys. Each
PTH into the bloodstream in
gland has an outer cortex which
response to low blood calcium
produces steroid hormones and an
levels.
inner medulla.
The hormone works in three ways to help raise
blood calcium levels back to normal (two are
direct and one is indirect): The Adrenal glands consist:
1. PTH directly promotes the release of • Cortex
calcium from bones into the • Medulla
bloodstream.
2. It directly acts on the kidneys to reduce ❖ ADRENAL CORTEX
the elimination of calcium in the urine The adrenal cortex produces:
while promoting the elimination of • Glucocorticoids (primarily
phosphorus in the urine. cortisol)
3. The indirect effect stimulates the - Hydrocortisone
kidneys to convert vitamin D from the - Corticosterone
inactive to the active form, which in • Mineralocorticoids (primarily
aldosterone)
• Androgens (primarily - progressive hypofunctioning of the
dehydroepiandrosterone and adrenal cortex. It causes various
symptoms, including hypotension and
❖ ADRENAL MEDULLA hyperpigmentation, and can lead to
- is composed of chromaffin cells, which adrenal crisis with cardiovascular
synthesize and secrete catecholamines collapse.
(mainly epinephrine and lesser amounts
Symptoms and Signs
of norepinephrine).
- Most adrenal deficiency syndromes • Weakness
affect output of all adrenocortical • fatigue
hormones.
• orthostatic hypotension
- Hypofunction may be primary or
• Hyperpigmentation
secondary
• Anorexia
Most Common Disorders and Diseases of the • nausea
Adrenal Glands • Vomiting
• Diarrhea
• Addison's Disease - Primary or Chronic • Decreased tolerance to cold
Adrenocortical Insufficiency • hypometabolism
• Adrenal Virilism - Adrenogenital • Dizziness and syncope
Syndrome • Weight loss
• Cushing Syndrome - excess pituitary • dehydration
production of ACTH
• hypotension
(adrenocorticotropic hormone)
Symptoms of Adrenal Insufficiency ❖ Adrenal crisis

- Adrenal crisis is characterized by
• Weakness 1. Profound asthenia (weakness)
• Fatigue 2. Severe pain in the abdomen, lower
• abdominal pain back, or legs
• nausea 3. Peripheral vascular collapse
• weight loss 4. Renal shutdown with azotemia
• low blood pressure Treatment of Addison's
• darkened skin (in the case of Addison's Disease
disease) o Hydrocortisone or
• salt craving (in the case of Addison's prednisone
disease) o Fludrocortisone
• dizziness upon standing o Dose increase during
• depression intercurrent illness
o Addison's Disease Clinical Consequences of

Prolonged Use of Excessive
Corticosteroids
1. Suppressed inflammatory response 1. Type 1 Diabetes – insulin production
2. Delayed wound healing absent because of autoimmune
3. Osteoporosis pancreatic beta-cell destruction, insulin
4. Capillary fragility dependent
5. Tendency for candidiasis 2. Type 2 Diabetes – resistance to
insuling, non insulin dependent
Endocrine Disorders, Hepatic Diseases and its 3. Miscellaneous types of Diabetes
Dental Correlations a. Genetic defects affecting beta-
cell function, insulin action,
Pancreas and mitochondrial DNA – ex.
- Is an organ located in the abdomen. It Maturity-onset diabetes of
plays an essential role in converting the youth
food we eat into fuel for the body’s b. Pancreatic Diseases – ex. Cystic
cells fibrosis, pancreatitis,
- hemochromatosis,
pancreatectomy
c. Endocrinopathies – cushing
sundrome, acromegaly
d. Toxins – the rodenticide
pyriminyl (Vacor)
e. Drug-induced diabetes – most
notably due to glucocorticoids,
The pancreas has two main functions: beta-blockers, protease
inhibitors, and therapeutic
1. Exocrine – function that helps in doses of niacin
digestions f. Gestational Diabetes –
2. Endocrine – function that regulates pregnancy causes some insulin
blood sugar resistance in all women, but
only a few
Two Main Pancreatic Hormones (with
endocrine function) Symptoms and Signs
1. Insulin – which acts to lower blood 1. Polydipsia – permi nauhaw

sugar 2. Polyphagia – permi gakaon/nagutom
2. Glucagon – which acts to raise blood 3. Polyuria – frequent nga pag ihi
sugar 4. Blurred vision
5. Vascular disease
Diabetes
6. Peripheral neuropathy
- Is impaired insulin secretion and 7. Nephropathy
variable degrees peripheral insulin 8. Predisposition to infection
resistance leading to hyperglycemia
Diagnosis Hepatic Diseases
1. Fasting plasma glucose (FPG) levels Hepatitis – is the name given to a general
2. Glycosylated Hb (HbA1C) infection of the liver, and viruses, toxins, or an
3. Sometime oral glucose tolerance testing autoimmune response can cause it. It is
characterized by an inflamed liver. In may cases,
the liver can heal itself, but liver failure can
occur in severe cases.
Types of Hepatitis:
1. Hepatitis A
2. Hepatitis B
3. Hepatitis C
4. Hepatitis D
5. Hepatitis E
Common Types of Hepatitis

Liver
1. Hepatitis A – or infectious hepatitis
- Is the largest solid organ and the largest - Hepatitis A is a liver disease caused by
gland in the human body the hepatitis A virus. The virus is
- Is situated above and to the left of the primarily spread when an uninfected
stomach and below the lungs (and unvaccinated) person ingests food
- The roles of the liver include or water that is contaminated with the
detoxification, protein synthesis, and faeces of an infected person
the production of chemicals that helps - The disease is closely associated with
digest food. unsafe water, inadequate sanitation
and poor personal hygiene.
The major functions of the liver include: 2. Hepatitis B – is a potentially life-
threatening liver infection and puts
1. Bile production
people at high risk of death from
2. Absorbing and metabolizing bilirubin
cirrhosis and liver cancer.
3. Supporting blood clots
- the virus is transmitted through contact
4. Fat metabolization
with the blood or other body fluids of
5. Metabolizing carbohydrates
an infected person
6. Vitamin and mineral storage
- it is a major global health problem
7. Helps metabolize proteins
3. Hepatitis C – is a liver disease caused by
8. Filters the blood
the hepatitis C virus; the virus can cause
9. Immunological function
both acute and chronic hepatitis
10. Production of albumin
infection, ranging in severity from a
11. Synthesis of angiotensinogen
mild illness lasting a few weeks to a
serious, lifelong illness.
- it is a bloodborne virus and the most • Erythroplakia and Squamous Cell Carcinoma
common modes of infection are - Erythroplakia is a general term for red,
through unsafe injection practices; flat, or eroded variety lesions that
inadequate sterilization of medical develop in the mouth. In this image, an
equipment in some health-care settings exophylic squamous cell carcinoma is
and unscreened blood and blood surrounded by a margin of erythoplakia
products
Measures that protect the Dentist from contact

with the source of Virus
• use of rubber gloves as barrier

• rubber dams
• goggles and facemask
• proper sterilization to prevent transfer
of serum hepatitis
- Leukoplakia is a general term for white
Alcohol Cirrhosis hyperkeratotic plaques that develop in
the mouth. About 80% are benign.
- is advanced liver disease characterized However, in this image, squamous cell
by extensive fibrosis the disrupts the carcinoma is present in one of the
normal liver architecture leukoplakic lesions on the ventral
- hypoprothrombinemia and delayed surface of the tongue.
drug metabolism may occur
Oral Feature of Chronic Alcoholism:
- generalized erythema of the oral

mucosa
• Oral Squamous Cell Carcinoma
- This photo shows a close up of the
inside of the mouth in a patient with
squamous cell carcinoma of the oral
mucosa.

Pathology I

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Pathology I

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2nd Semester

ORAL PATHOLOGY SY 2022-2023

Transudate – that present in some noninflammatory conditions

MMP or Matrix Metalloproteinases - enzymes that breakdown

Cellular Components of Inflammation

1. Neutrophilic polymorphonuclear leukocytes

Lecture 2: Regeneration and Repair

 Regeneration 6. Local stimuli: Local stimuli, such as trephones or wound

 Five types of oral wounds repair

Lecture 3: Immunity and allergy

Immunity 2. Recognition of “nonself”

• Delayed dental eruption

3 conditions must be present: Lactic Acid

Acute caries – deep penetrating and rapid

Chronic caries – progresses slowly and

Recurrent caries – results from faulty

Marginal caries – poor marginial

Pattern – smooth surface caries

Histopath Changes in Dentin

• Zone of complete decalcification

Pit and Fissure Sealant

Caries Susceptibility Test

• Lactobacillus count – increased

Four Primary Etiologic Factors of

3. Biofilm pH – dental plaque or plaque

- Cariogenic bacteria in the biofilm

Demineralization – the result of a net loss

Remineralization – a process where

5. Diet Specifics – frequent ingestion of

- the metabolic product of cariogenic

6. Oral Hygiene – oral hygiene,

Clinical Sites for Caries Initiation

1. Pits and Fissures – found mainly

Zones of Dentinal Caries

1. Zone 1: Normal Dentin

- In x-section gross appearance of a pit and

Caries Terminology 2. Caries of enamel-smooth

2. Chronic (slow of arrested)

D. Cavities According to the

- Etiology: repetitive mechanical habit;

G.V. BLACK CASSIFICATION OF 2. Class II – carious lesions that are

6. Class VI – cavities on the incisal edges

4. Class IV – carious lesions that are

INTERNATIONAL CARIES DETECTION

- Visual system for caries lesion

1. Teeth must be sufficiently air-dried

Two Stages of ICDAS:

1. Code for the restorative

Caries Severity Code

0 – sound tooth structure

4 – dentinal shadow (not cavitated into

1 – first visual change in enamel

6 – extensive distinct cavity with visible

3 – tooth colored restoration

5 – stainless steel crown

6 – porcelain or gold or PFM crown or

7 – lost or broken restoration

9 – used for the following conditions

96 – tooth surface can’t be examined;

97 – tooth missing because of caries (tooth

98 – tooth missing for reason other than

2nd sem SY 2022-2023

 Bacterial - a subclinical condition characterized by