Normal periodontium

• 1. The sulcus depth is 0.5-2 mm depth [average 1.8 mm]. It coincides

with arrangement of
• the supra-alveolar collagenous fibers running from the cementum into
the gingiva
The surface of marginal gingiva is smooth
The marginal gingiva is demarcated from the attached gingiva by an
indentation called the free gingival groove
 2. The intercellular spaces are wide and leukocytes are frequently
present between the epithelial cells.
 it may act as a semipermeable membrane Injurious bacterial products
endotoxins to penetrate the underlying tissue and tissue fluids pass from
the gingiva seep into the sulcus
3. WHAT IS THE PURPOSE OF THIS AND WHAT IS IN THE SULCULAR
FLUID?
This fluid contains WBCs____ and Ig enzymes, antibodies, etc
which have a specific defense mechanism\
The outward flow of the fluid cleans foreign material from the sulcus and
prevents the penetration of any bacteria,
contain plasma proteins that may improve adhesion of the epithelium to the
tooth

• 4. CAN YOU HAVE APICAL MIGRATION OF THE JE FROM THE

CEJ WITH GINGIVAL INFECTION?
• yes
5. Junctional epithelium
A Band Of Tissue At The Most Apical Portion Of The Sulcus That Attaches
The Gingiva To The Tooth.
 Can Occur On Enamel, Cementum, Or Dentin.
Initially It Occurs On The Cervical Area Of The Crown
• 6 Junctional epithelium . turn over is very high adheres to the tooth
surface at the bottom of the gingival sulcus and consists of
• 1-2 cell layers apical
• 10-29 cell layers coronal
• _nonkeratinized ___ cells.
• Attachment of the epithelium to the tooth surface and is called
epithelial attachment.
• very fragile due to wider intercellular space and less desmosomal
junction, thus it does not form a barrier against probing
• continuously renewed through cell division in
• the basal layer.
• In health it lies against enamel and extends to the cemento-enamel
junction
7. Attached Gingiva
It extends from the free gingival groove to the mucogingival junction
The attached gingiva is tightly bound to the underlying alveolar bone it is firm
and resilient because of the tight attachment of the fibers to the cementum
and periosteum of the alveolar bone.
The surface of the attached gingiva is stippled like orange peel. This stippling
varies more common on facial than on the lingual surfaces and is only present
in about 40% of adults
 8-The gingival margin consists of a core of
-fibrous connective tissue
-covered by stratified squamous epithelium
1-oral epithelium (OE), which faces the oral cavity
• 2-oral sulcular epithelium (OSE), which faces the tooth without being in
contact with the tooth surface
• 3-junctional epithelium (JE), which provides the contact between the
gingiva and the tooth

9. It takes 1 month for a keratinocyte to reach the outer epithelial

surface, where it becomes desquamated from the stratum corneum.
equilibrium between cell renewal & desquamation

10. Gingival connective tissue ground substance

Ground substances: The gingival connective tissue is made up of a mesh of
collagen fiber bundles running in a ground substance which contains cells,
blood vessels, nerves and lymphatic vessels.

Connective tissue cells and fibers, together with vessels and nerves are
embedded in a matrix which is synthesized by fibroblast and it is made
up of:
• Glycoproteins: it is a protein-polysaccharide molecule Glycoprotein like
fibronectin mediates attachment and migration of fibroblasts.
• Proteoglycans: it is a protein polysaccharide molecule in which
polysaccharide component is predominating. Example for
polysaccharide component is glucosaminoglycans (GAG).

11. The arrangement of these collagen fibers exists into five groups:
• Dentogingival fibers that are attached to cementum and fan out into the
gingiva.
• Alveolo-gingival fibers that arise from the alveolar crest and run
coronally into the gingiva.
• Periosteogingival fibers that attach gingiva to bone.
• Circular fibers which encircle the tooth in a ring like fashion in CT of
marginal and interdental gingiva.
• Trans-septal fibers which run from tooth to tooth coronal to the
interdental septum of bone and embedded in cemenum.

12. Fibroblast is the most predominant connective tissue cell (65% of

the total cell population). The fibroblast is engaged in the production of
various types of fibers and connective tissue matrix
13.

14.

15.Cemetum is avascular without innervation

16. Acellular cementum is important for attachment unit

 16.

17.

• 18.
 •
• Etiology
1. Dental plaque is defined as a structurally organized biofilm, it consists of
Clusters of microorganisms attached to the tooth surface. That are embedded
in a matrix of polymers of host and bacterial origin

2. Glycocalyx is the matrix: Composed of exopolysaccarides produced by

bacteria Biofilm contains waterchannels
Permit passage of nutrients and waste products.
Provides cell to cell communication and transfer of genetic information
Defense Against Host Protective Mechanisms As Well As Antimicrobial
Agents.

3. Based on relation with gingival margin plaque is differentiated into

-Supra gingival (coronal and marginal ) attached to the tooth surface contains
gram positive cocci and negative rods and influence sub gingival biofilm
Significance of subragingival if become mature will cause gingivitis
If persist will influence subgingival

-Subgingival (attached unattached) periodontitis gm negative

Tooth associated gm positive and some gm negative
Epithelium associated no matrix directly associated with epithelium causing
periodontitis Connective tissue associated ANUG and Aggressive periodontitis

4. biofilm life cycle

Free floating bacteria randomly present
Aggregate and form colonies
Dispersion of virulent bacteria to colonize other surface

5. nutrition is protein from GCF

6. quorum sensing is communication between bacteria in the bofilm trigger
expression of specific gene
6. phases of plaque formation
Pellicle glycoprotein from saliva gcf and bacterial product gm positive and
no clinical gingival reaction
Primary colonizer attracted to electrically charged surface by adhesion using
microbial adhesins after few hours of pellicle formation gm positive aggregate
Secondary colonizer, bacteria get attached to the surface as well as with each
other by secreting EPS (an extracellular polymeric substance) that entraps the
cells within a glue-like matrix. And shift to gm negative
Maturation The biofilm is formed of different bacterial groups, embedded in
a structured Polymermatrix
7. Non-specific plaque hypothesis Miller in 1890
entire microflora collectively is pathogenic (quantitiy)

8.Specific plaque hypothesis Loesche in 1976

bacterial species that were associated with cases with advanced periodontal disease
in deep pockets. Among these species were the porphyromonas gingivalis,
Tannerella forsythia and Treponema denticola which were described as the “Red
complex” and Aggregatibacter
actinomycetemcomitans
9. ecological plaque hypothesis
Any changes that would negatively affect the environment such as smoking, stress
or plaque accumulation would cause shift in the microbial population causing
anaerobic gram-negative bacteria to predominate
10.keystone pathogen hypothesis
Changing the commensal microorganisms present in the environment into
dysbiotic species
9.Inflammation mediated polymicrobial emergence and dysbiotic
exacerbation”
(IMPEDE). Van Dyke etal., (2020)
Stage zero= health= commensal biofilm =no inflamation
Stage1=gingivitis=commensal +diverse MO=inflamation
Stage 2=early periodontitis=polymicrobial diversity+dysbiosis= pathogenic
bacteria=inflamation
Stage 3 =established periodontitis=dysbiosis=uncontrolled inflammation
Stage 4 =late stage periodontits=polymicrobial infection
10. virulence factor = attack power of species causing damage
• Directly [Virulence/Survival Factors]
Attachment, Colonization, Invasion.
Production Of Substances That Can Cause Tissue Damage.
Evasion Of The Host Responses.
• Indirectly
By Triggering The Host Immune Responses
LPS= Potent Antigenic Properties.
production of multiple pro-inflammatory cytokines
Induce Bone Resorption.
Direct Toxic Effect On Tissues.
Activates Complement C3.
Chemotactic.
11. Virulence of porphyromonus gingivalis=gingipain
Decrease Opsonization and phagocytosis
Evasion of host
Degradation of specific antibody
Inhibition of phagocytosis
Decreased bacterial Killing
Apoptosis (programmed cell death) of PMN

12. A. actinomycetemcomitans
Killing of mature B and T cells;
nonlethal suppression of activity
arresting of lymphocyte cell cycle
Impairment of PMN response to bacteria
P. gingivalis
Impairment of PMN response to bacteria

13. Virulence in colors

• Aggregatibacteractinomycetemcomitans1 very high
• Porphyromonasgingivalis very high RED
COMPLEX
• /Tannerellaforsythia2 very high
• Treponema Denticola high
 • Prevotellaintermedia high
• Fusobacterium Nucleatum. Middle
Orange Complex
• Parvimonasmicra3 Middle
• Eubacteriumnodatum high
• Campylobacter Rectus high
• Eikenellacorrodens middle
GREEN COMPLEX
• Capnocytophagasp. Middle

14. Locallll forces

 The most complex type of force to which a tooth can be subjected is
jiggling force.
 When jiggling force is applied to a tooth, the periodontium is subjected
alternatively to both pressures and tensions in a very short period of time.
15. trauma from occlusion refers to the tissue injury
When the magnitude of occlusal forces is increased, the periodontium
responds with a widening of the periodontal ligament space, an increase in the
number and width of periodontal ligament fibers, and an increase in the
density of alveolar bone.
16.Diagnosis of TFO
 Clinical signs
 1. Attachment loss, Mobility
 2. Positive fremitus test
 Radiographic signs.
  Periodontal ligament widening, mostly with lamina dura thickening
along the root
 2. Angular bone defect.
 3. Radiolucency and alveolar bone condensation.
 4. Resorption of root.
 5. Migration of tooth.
 6. Tooth fracture.
 7. Thermal sensitivity.
17. In hypo function The periodontal tissues undergo degenerative changes
(tissue atrophy):
 Periodontal ligament is thin formed of unorganized fibers
 Alveolar bone proper is thin and undergoes atrophy.
 plaque retention
 gingival inflammation.
 Long term hypofunction results in increased tooth mobility.
18. Bruxism
1- Wear facets on the teeth.
2-Widening of periodontal membrane space
3-Hypertonicity of the muscles of mastication.
4-Tempromandibular joint discomfort.
 RG signs:
 1.Widened PDL space.
 2.Discontinuity of LD surrounding the tooth.
 3.Root rsorption. of the teeth
 Tongue thrusting cause Excessive lateral pressure causes
 periodontal trauma.
 Labial drifting of the anterior teeth.
 Tooth mobility due to Antagonistic forces created by the lip tend to direct
the tooth in inward direction .
- open bite,

19. Mouth breathing

 Signs of gingival inflammation in mouth breather is due to:
 Diminished normal cleansing action of saliva so that plaque
accumulates.
Impaired tissue resistance due to dehydration (Saliva contains
numerous defensive components as IgA, lysozyme
20. Faulty restoration
Providing ideal location for the accumulation of plaque which is
inaccessible for flossing.
ii- Changing the ecological balance of the gingival sulcus area to
favor the growth of pathogenic bacteria (gram-negative anaerobic
species).

*21. biological width It is the dimension of space occupied by JE and CT

attachment above the alveolar bone.
**It is recommended that there should be at least 2 mm between the
restoration margin and the bone crest to allow adequate biologic width.
*22. Extension of restorations margin too far subgingivally (2 mm or
less from the alveolar bone) will impinge on the attachment apparatus
leading to *gingival inflammation, *bone loss or *pocket formation
• 23. Prominent subgingival restoration margins
• The subgingival convexity and margin of a restoration is very important
in site-specific plaque control and is closely related to gingival health.
the concept that restoration margins placed apical to the gingival
margin are detrimental to gingival health has been confirmed by a 26-
year longitudinal study. Prominent subgingival restoration margins
promote gingivitis by increasing the local accumulation of bacterial
plaque. Thus, subgingival restoration margins need to be carefully
designed in order to minimize plaque retention.

Systemic modifying factors

24. Diabetes
 In the hyperglycemic state, numerous proteins and matrix molecules
undergo a non-enzymatic glycosylation, resulting in accumulated
glycation end products (AGEs).
influences on *vascular endothelium, *collagen metabolism and
*monocyte function
Collagen accumulation in the periodontal capillary basement
membranes, causing membrane thickening.
2- AGE-stimulated smooth-muscle proliferation
Atheroma formation and further narrowing of the vessel lumen.
A receptor for AGEs known as RAGE (receptor for AGE) has been
identified on the surface of monocytes/macrophages.
 Monocytes and macrophages in diabetic individuals are often hyper-
responsive to bacterial antigens. The AGE-RAGE interaction on
monocyte/macrophage leads to increased production of pro-
inflammatory cytokines and mediators such as *interleukin-1 (IL-1),
*tumor necrosis factor (TNF) resulting in collagen destruction and
bone resorption.
Defects in polymorphonuclear leukocyte (PMN) adherence,
chemotaxis, and phagocytosis

 in the formation of highly stable collagen macromolecules that are

resistant to normal enzymatic degradation and tissue turnover (less
normal repair or replace).
 The production of collagenase is increased in many diabetic patients.
Increased collagenase production degrades newly formed collagen
Capnocytophaya species, *porphyromonas gingivalis, *Prevotella
intermedia, and *Actinobacillus actinomycetemcomitans type 1
Prevotella intermedia, *porphyromonas gingivalis, type 2
1-Proper control of periodontal disease may reduce insulin
requirements.
2-Extensive periodontal treatment in patients with uncontrolled
diabetes is contraindicated .
3-Antibiotics and analgesics until diabetic control is attained.
antibiotic coverage for 2 weeks is recommended.
penicillin, tetracycline as doxycycline.
metronidazole is prescribed, the patients’ physician should be
consulted for adjustment of the antidiabetic oral drug .

25. Smoking
• Epidemiologic studies have revealed that smoking is one of the major
lifestyle-related environmental risk factors for periodontal disease.
•  Both the local and systemic effects of cigarette smoke should be
intrinsically considered.
• Inhaled cigarette smoke is absorbed from the capillary vessels via the
pulmonary alveolar epithelium and enters the systemic circulation,
• whereas direct exposure of inhaled cigarette smoke to periodontal
tissues causes vasoconstriction of the periodontal microvasculature and
gingival fibrosis, which is often observed in smokers.
• Although plaque accumulation and disease progression are exacerbated
in smokers, smokers have fewer clinical signs and symptoms of gingival
inflammation, and therefore smoking can mask an underlying
gingivitis.At the other end of the spectrum, the absence of clinical signs
of inflammation may not exclude the presence of an ongoing
inflammatory process evident at a histologic level. For example, during
cigarette smoking, the gingival inflammatory response to plaque
accumulation on teeth will be muted, despite distinct gingival host-
response patterns

resulting in an increase in the extent and severity of periodontal

destruction.
 Altered neutrophil chemotaxis, phagocytosis, and oxidative burst
 ↑ neutrophil collagenase and elastase in GCF,
 ↑ TNF-alpha and PGE2 in gingival crevicular fluid (GCF)

Reduce immunoglobulin G2
 ↑colonization of shallow periodontal pockets by periodontal pathogens
as Fusobacterium nucleatum, P. intermedia, T. forsythia, P. gingivalis ,
and Treponema denticola ↑ levels of periodontal pathogens in deep
periodontal pockets.
 ↓ GCF flow
• ↓ clinical response to scaling and root planing
• ↓ reduction in pocket depth
• ↓ gain in clinical attachment levels
26. Vitamin c deficiency
Low levels of ascorbic acid (Ascorbic acid deficiency )
 influence the metabolism of collagen within the periodontium, affecting
the ability of the tissue to regenerate and repair itself.
 interferes with bone formation, leading to loss of periodontal bone.
failure of the osteoblasts to form osteoid take place very late in the
deficiency state
27. stresss
The development of habits (grinding clenching etc.) that are injurious
B -The direct effect of the autonomic nervous system on the physiologic
tissue balance
Increased cortisol suppresses the immune response directly through
• major anti-inflammatory and immunosuppressive properties, inhibiting the
formation of lymphocytes
• antibody production is inhibited, marked decline in humoral immune
defense.
• inhibitory effect on the proliferation of fibroblasts in the inflammatory
granulation tissue.
synthesis of some pro-inflammatory cytokines will be suppressed
• 28. Plaque-induced gingivitis exacerbated by sex steroid hormones
• Evidence has accrued to show that tissue responses within the periodontium
are modulated by androgens, estrogens, and progestins at one time or
another in a person's life.
 •  For endocrinotropic conditions, plaque bacteria in conjunction with elevated
steroid hormone levels are necessary to produce a gingival inflammatory
response
• 29. Puberty
develop frank signs of gingival inflammation in the presence of relatively
small amounts of plaque during the circumpubertal period that are key to
distinguishing this condition
• 30. Menstrual cycle
• Gingival crevicular fluid flow has been shown to increase by at least 20%
during ovulation in over 75% of women tested,
• Most women with menstrual cycle–associated gingival inflammation will
present with clinically non-detectable signs of the condition
31. Pregnancy
During pregnancy, the prevalence and severity of gingivitis has been
reported to be elevated and frequently unrelated to the amount of plaque present.
And severity of gingival inflammation significantly higher in the pregnant vs the
post-partum patient, even though plaque scores remained the same between the
two groups.
gingival probing depths are deeper, bleeding on probing or bleeding with
toothbrushing is also increased,  and gingival crevicular fluid flow is elevated in
pregnant women.
The features of pregnancy-associated gingivitis are similar to plaque-
induced gingivitis, except the propensity to develop frank signs of gingival
inflammation in the presence of a relatively small amount of plaque during
pregnancy.
Pregnancy may also be associated with the formation of pregnancy-
associated pyogenic granulomas.
• 32. Oral contraceptives
• Oral contraceptive agents were once associated with gingival inflammation
and gingival enlargements.
 • increased gingival inflammation or enlargement was reversed when oral
contraceptive use was discontinued or the dosages reduced.
• The features of gingivitis associated with oral contraceptives in
premenopausal women were similar to plaque-induced gingivitis, except the
propensity to develop frank signs of gingival inflammation in the presence
of relatively small amounts of plaque in women taking these hormones.
• Current oral contraceptive concentrations are much lower than the original
doses that were reported in these early clinical studies, and it is known that
current formulations of oral contraceptive do not induce the clinical changes
in gingiva that were reported with high-dose contraceptives.

33. drug induced gingival enlargement

 a)Phenytoin (Dilantin) increase in the number of fibroblasts
 b)Dihydropyridine (Nifedipine) decrease the rate of cell death
c) Cyclosporines (Sandimmure)
 no increase in the fibroblast number
 increased protein, collagen and matrix macromolecules synthesis
 decreased collagenase activity(lack turn over)
 lesions become firm, fibrotic, pale pink and have no tendency to bleed.
 3-As the condition progresses the enlarged tissue unite and develop into a
massive tissue fold covering a considerable portion of the crown and
sometimes interfering with occlusion.
 4-The presence of the enlargement makes plaque control difficult, resulting
in secondary inflammatory process
34. Leukocyte neutrophil disorder
1-Defect in normal quantity
2-The impaired neutrophil function
3-The hyperactive neutrophil response.
a-diseases caused by quantitative leukocytes defect:
- neutropenia
- agranulocytosis
- cyclic neutropenia
b-diseases caused by qualitative leukocytes defect:
- Adherence (Leucocyte adhesion defect LAD life threatening )
- chemotaxis (in localized aggressive periodontitis yet hyperfunctioning in lost
direction)
- phagocytosis - degranulation and intracellular killing (Chediak Higashi )
• 1-Genetic disorders
• Chediak-Higashi Syndrome(It affects mostly the (melanocytes=
albinism, platelets=bleeding , and phago cytes) defective chemotactic
attraction, degranulation and intracellular killing of PMN’s.) aggressive
periodontitis

• Lazy Leukocyte Syndrome (defect in chemotaxis) gingivitis and

periodontitis
• Leukocyte Adhesion Deficiency(failure to *express normally an
important cell surface integrin, which is necessary for leukocytes to
adhere to the vessel wall at the site of infection). Aggressive
periodontitis
• Papillon-Lefevre Syndrome palmoplantar hyperkeratosis (on palms,
soles, knees, and elbows) and *aggressive periodontitis
• Neutrophil defects include decrease chemotaxis, phagocytosis and
intracellular killing.
 •
• Down’s syndrome (mongolism trisomy 21) The prominence of tongue
results in tongue thrusting that induce jiggling force on periodontium.
• Systemic modifying factors:
• defect in neutrophil function defective chemotaxis, phagocytosis and
intracellular killing.
• Defect in T cell maturation
• Poor circulation
• Gingivitis and periodontitis
• Localized aggressive periodontitis: LAP(defect in cheotaxis)

35. Leukemia enlargement, bleeding, infection due to immature wbcs

Classification of periodontal disease
36. Gingivitis
• Due to a loss of symbiosis between the biofilm and the host's immune-
inflammatory response, and development of an incipient dysbiosis .and
quorum sensing
• A. clinical signs and symptoms of inflammation that are
• B. confined to the free and attached gingiva and do not extend beyond the
mucogingival junction;
• C. reversibility of the inflammation by disrupting/removing the biofilm;
• D. the presence of a high bacterial plaque burden to initiate inflammation
and/or exacerbate the severity of the lesion (although this varies among
individuals);
• E. stable (i.e., unchanging) attachment levels on a periodontium, which may
or may not have experienced a loss of attachment or alveolar bone.
 • F. Systemic modifying factors (e.g., hormones, systemic disorders, drugs)
which can alter the severity of the plaque-induced inflammation
• 1) Introduction of the term “incipient gingivitis;” few sites are affected by
mild inflammation, expressed as mild redness and/or a delayed and broken
line of bleeding rather than edema or an immediate unbroken line of
bleeding on probing. Incipient gingivitis may be regarded as a condition that
is part of a spectrum of “clinical health,” but may rapidly become localized
gingivitis if untreated.
• The severity, or intensity of inflammation at a site, tooth, or the entire
dentition, would be reflected by the gingival index described by Loe (1967).

2) a description of the extent and severity of gingival inflammation;

3) a description of the extent and severity of gingival enlargement and;
• Mild gingival enlargement involves enlargement of the gingival papilla;
moderate gingival enlargement involves enlargement of the gingival papilla
and marginal gingiva, and severe gingival enlargement involves enlargement
of the gingival papilla, gingival margin, and attached gingiva

4) a reduction of categories in the dental plaque–induced gingival disease

taxonomy.
37. Classification of gingivitis
 A.Associated with bacterial dental biofilm only
 B.Potential modifying factors of plaque-induced gingivitis
o 1.Systemic conditions
 a)Sex steroid hormones
 1)Puberty
 2)Menstrual cycle
 3)Pregnancy
  4)Oral contraceptives
 b)Hyperglycemia
 c)Leukemia
 d)Smoking
 e)Malnutrition
o 2.Oral factors enhancing plaque accumulation
 a)Prominent subgingival restoration margins
 b)Hyposalivation
 C.Drug-influenced gingival enlargements
Causes of Recession
• Patients can lose attachment without the formation of periodontal pockets if
the gingival margin migrates apically at a rate similar to that of the loss of
attachment.
• Thin periodontium the B/L width of the alveolar housing is small
• Thin gingiva With minimal fibrous connective tissue between
• the oral epithelium and the sulcular epithelium, inflammation may
destroy the CT.
• Inflammation
• Trauma from oral hygiene procedures
• Anatomical factors
.

Continued
Gingivitis
Localized marginal gingivitis
Localized diffuse gingivitis
Localized papillary gingivitis:
Generalized marginal gingivitis
Generalized diffuse gingivitis= marginal gingiva + attached gingiva +
interdental papilla

Pathologic changes in gingivitis are associated with the presence of oral

microorganisms that cause destruction of epithelial and connective tissue cells.
The sequence of events in developing of gingivitis occurs in four different
stages:
Stage I: The initial lesion 2-4 days increase in gingival fluid PMN
Stage II: The early lesion.4-7 days bleeding on probing PMN and macrophage
Stage III: The established lesion.14-21 bleeding and blue hue of gingiva
plasma cells
Stage IV: The advanced lesion.21 days bone involved periodontitis
Principles of surgeries
What are the 3 key therapeutic endpoints of periodontal therapy?
eliminate or reduce inflammation
reduce probing depth
attachment gain
An adequate scaling and root planing can be rendered for a probing depth of
4mm

if a patient has 5-6 mm probing depths between #14 and #15, you will do as
much as you can for the SRP, however you will still miss a lot of calculus
=RESIDUAL POCKET
Can bleeding on probing (BOP) be used to predict the progression of
periodontitis yessss
How do you evaluate the periodontal condition following SRP and re-
evaluation?
- probing depth/ CAL

- bleeding on probing (BOP)

- progression of periodontitis

the final decision for surgery is not made until _

4 weeks of nonsurgical procedures have been done
A periodontal flap is a section of gingiva and or mucosa surgically elevated
from underlying tissues
To gain access to the bone and the root surface. to ensure removal of
calculus - Elimination or reduction of the depth of the periodontal pocket by
resection or regeneration/repair
Classification of periodontal flaps
A) According to bone exposure during reflection (thickness of the flap)
B)According to flap placement after surgery(displaced undisplaced)
C)According to the management of interdental
papilla(conventional/papilla preservation)

In order to displace the flap in any direction(apically)

1.The attached gingiva has to be totally separated from underlying
bone
2.reflection should extend to the level of alveolar mucosa.
3.Vertical incisions are performed at both ends of the flap.
N.B. Palatal flaps cannot be displaced owing to the absence of alveolar
Mucosa
Complete

.
rate of epithelium healing 
0.5 mm per day
time for blood clot and PMN cover wound
24 hrs
time of migration of oral epithelium
48 hrs
time for epithelium to cover wound reformation or crevicular epithelium
5 days
time for new junctional epithelium present
7 days
time for normal JE thicknes restored
14 days
alveolar bone healing: periosteum formed at ....****
3 mo
alveolar bone healing: bone maturation...***
6 mo
Resective pocket reduction surgeries
Gingivectomy Apically postiioned flap With/without osseous surgery
Gingivectomy: Pocket reduction by removing suprabony soft tissue (Must not have
a vertical bony defects) 
Solution to treat gingival enlargement with no adequate attached gingiva and
presence of pocket and attachment loss
IMPORTANT :Indication of reverse/internal bevel gingivectomy?
If gingivectomy will not eliminate the entire hyperplastic tissue.
If gingivectomy result in loss of all attached gingiva leading to a
mucogingival problem.
If gingivectomy leave a wide wound of exposed connective tissue which
will take long time to epithelialize and is painful
The only way to differentiate gingivitis and periodontitis is CAL and
Radiographic bone loss

For vertical defect you plan for scaling and root planning
Then flap for access if deep pocket
You choose internal bevel flap or undisplaced or modified widman flap
You choose regeneration according to bone architecture
3 osseous walls is the best We perform sulcular internal bevel insision and
regenerative materials
For horizontal defect
Access internal bevel flap if only (MWF or UNDISPLACED)
They used to perform resection of horizontal pocket by gingivectomy or apically
positioned but not common

Study by heart

Classification remember to classify gingivitis and

periodontits from the table what each include and the
rest of lecture
Staging / grading and their significance

Treatment plan
Periodontitis
Pocket
Principles of surgeries
gingivecomy
Internal bevel flap MWF, APF
Tips to remember
1/Diagnosis to differentiate gingivitis and periodonttis depend on CAL and
radiographic bone defect
2.Phase one therapy is the initial therapy with scaling and root planning
3.Suprabony pocket and infrabony pocket
4.Suprabony treated with access flap if deep than 5mm to remove biofilm
when deep
Or if shallow old treatment as resective treatment like gingivectomy or
apically positioned flap to eliminate the pocket
5.Infra bony pocket treated with access flap if deep than 5mm or regeneration
6.Gingivval enlargement treated with gingivectomy if the pocket is
pseudopocket and adequate keratinized tissue (resective treatment )
7.Gingival enlargement with pocket depth and inadequate keratinized tissue
the treatment is (internal bevel gingivectomy )
8.All surgeries should be preceded by initial therapy first reassessment after 4
weeks
9.Initial therapy is scaling root planning and oral hygiene maintenance and
check if sever cases or systemic disease need adjunctive use of antibiotics
10.Bleeding on probing is the monitor of inflammation after scaling
.Reduction in probing depth and clinical attachment gain is the key for
treatment success
12.Insicions which separate pocket lining are internal bevel (Undisplaced and
MWF)
13.Apically positioned flap treats inadequate keratinized tissue
14.Diabetic patients should be examined by glycosylated haemoglobin test to
check if controlled for 3 months For periodontal treatment needs scalling and
root planning and antibiotics surgeries are not indicated because of poor
wound healing
15. the dysbiosis of the biofilm is the cause of periodontal destruction
16. effect of smoking
17. causes of gingival enlargement
18. periodontitis chronic and aggressive and classification of pockets furcation
and recession
19. treatment plan phases
20. gingivitis chronic and incipient
21. flaps and classification
22. initial insicion is done by lancet, secondary(sulcular ) by lancet third by
buck or urban knife to remove collar and papilla
23. Suturing timing removal for wound healing to get maxmimum tensile
strength and delay removal occurs for delayed wound healing
24. partial thickness sharp disection and full thickness blunt dissection
25. causes of recession
26. old and new classification
27. defective neutrophil occur in aggressive periodontitis, down syndrome,
papillon le fever, chediak higashi……etc
28. smoking affect immunity and causes destruction and impaired healing
29. occlusal trauma clinical features
30. papilla management convential or preservation
40. indication of internal bevel gingivectomy
41. gingivectomy steps
42. supra and infrabony pockets
43. osseous walls and the best prognosis in 3 osseous
44. mild moderate sever gingival enlargement classification
45. repair and regeneration
46.tooth mobility
47. true and pseudo pocket
48. classification of furcation
49. gingivectomy remove gingival enlargement with pseudo pocket and it is
resective
48internal bevel remove gingival enlargement with true pocket and removing
inner lining and regeneration with grafts and membranes
49. resective pocket reduction includes gingivectomy and apically positioned
flap
50. MWF for access and removing inner lining and regeneration with grafts
and membranes
51. sulcular insision for access and regeneration with graft and membrane
52 apically positioned flap for attached gingiva and it is resective flap
53. treatment plan with the phases
54. surgical decision after 4 weeks of initial therapy
55. adequate scalling occurs when you have 4mm pocket
56. goals of internal bevel insision
57, paramarginal insision
58. healing of MWF is by primary intension , long junctional epthelium,
repair, crestal bone resorption, and soft tissue recession
59. choice of internal bevel depends on anatomical landmarks
60.timing of suture removal
61. healing of gingivectomy is by secondary intensions while periodontal flap
by primary intension because we approximate the flap by suture