Perio Exam, Diagnosis

PERIODONTICS: Examination, Case
Assessment, & Treatment Planning
Dr Kevin Nicholson
Study & management of disease
General Pathology Periodontal disease
Case Assessment Treatment Plan

General Pathology:
Detailed study of disease
Definition Diagnosis
Classification Prognosis (sequalae)
Clinical features Treatment
Aetiology
Risk factors
Pathogenesis
Pathology:
macropathology,
micropathology, ie
histopathology
Aetiology of disease
Inherited/acquired
Simple causes,
multifactorial
Developmental
Trauma; physical,
chemical
Inflammation
Infection
Degeneration
Neoplasia
Aetiology of disease
Immune-mediated
disease
Autoimmune disease
Pathology associated
with systemic disease
(nutritional, hormonal,
metabolic)
Psychological factors
Iatrogenic disease
Idiopathic disease
Diagnosis of disease
●
History
●
Medical History
●
Personal, social & Diagnosis
family history Aetiology
●
Clinical examination
●
Additional/special
investigations
Diagnosis of Oro-dental disease
History Additional/special
investigations:
Medical History
Dietary analysis
Personal, social &
family history Plaque analysis
Blood/urinalysis
Clinical examination
Immunological assays
Additional/special Biopsy
investigations:
Radiographs/imaging
Clinical photographs
Diagnosis
Study casts Aetiology
Treatment/Management of disease
Preventive Recall/review
Palliative Maintenance
procedures
Medical
Surgical
Radiotherapy
Chemotherapy
Combined therapies
PERIODONTAL DISEASE
Aetiology: primary factors
Plaque/bacteria
Non-specific theory – accumulation
Specific pathogen theory
Direct effect
Endotoxins
Exotoxins
Metabolic waste products
Enzymes
Tissue invasion
Indirect effect
Host response/inflammation
PERIODONTAL DISEASE
Aetiology: primary factors
Plaque/bacteria
Non-specific theory –
accumulation
Specific pathogen theory
PERIODONTAL DISEASE
Aetiology: secondary factors
Secondary factors - Local
Increase plaque accumulation/prevent removal
Calculus
Carious lesions
Inadequate restorations; form, contour
Dental morphology
Open contact areas; food impaction
Tooth position; imbrication
Mucogingival factors
frenal attachments, recession
PERIODONTAL DISEASE
Increase plaque accumulation/prevent removal
Calculus
Carious lesions
PERIODONTAL DISEASE
Root surface hypersensitivity
Restoration margins
Poorly designed prostheses
Orthodontic appliances
Tobacco smoking
Occlusal factors
Lack of lip seal/Mouthbreathing
Xerostomia
PERIODONTAL DISEASE
Secondary factors – Systemic
Modify host response/healing response
Smoking
Diabetes mellitis
Genetic
Down syndrome
Nutritional, metabolic, hormonal
Haematological; neutrophil abnormalities, immune
dysfunction
PERIODONTAL DISEASE
Secondary factors – Systemic
Modify host response/healing response
Osteopenia, osteoporosis?
Arthritis?
HIV/AIDS
Drugs/medication
Dermatoses
Stress
PERIODONTAL DISEASE
Risk factors
“Any aspect of personal behavior or life style,
environmental exposure, inborn or inherited
characteristics, which is known to be associated
with disease-related conditions”
“ An action or event that is related statistically in some
way to an outcome & is truly causal”
Smoking
Diabetes mellitis
Genetic factors
Specific microorgansms
HIV infection
PERIODONTAL DISEASE
Risk predictors/indicators
“A characteristic that is associated with elevated risk, but is not
a direct cause”
“An attribute or event that increases the probability of
occurrence of disease”
Age
Race
Gender
Oral hygiene status
Socioeconomic & educational status
Previous dental history/use of dental services
Angular bony defects, periapical pathology
Malocclusion
PERIODONTAL DISEASE
Host susceptibility: gingivitis
Rate of development & degree of inflammation
varies between individual with similar plaque
accumulation
13% of individuals represent a “resistant’ group
Some modifying factors produce an increased
inflammatory response, others a reduced response
PERIODONTAL DISEASE
Increased gingival response; greater susceptibility,
greater risk for disease
Metabolic/hormonal; puberty, pregnancy
Genetic; Down syndrome
Nutritional; Vit C deficiency
Systemic drugs; Dilantin
Systemic disease; leukemia, immune deficiencies,
diabetes mellitus, stress
Genetic polymorphism; IL-1 gene cluster
Susceptible patients require more stringent plaque control
PERIODONTAL DISEASE
Reduced inflammatory response
Smoking; anti-inflammatory drugs
Muted response with smoking may mask underlying
attachment loss
Complete periodontal examination required
PERIODONTAL DISEASE
Host susceptibility: periodontitis
10% individual highly susceptible, 10% highly
resistant
50% of the risk for chronic periodontitis due to
heredity (Michalowicz, Diehl, & Gunsolley, 2000)
Significant risk factors
Smoking
Diabetes mellitis
PERIODONTAL DISEASE
Smoking & host susceptibility
Smoking, in a dose-dependent manner,
Greatly increases the risk for chronic periodontitis
& generalised aggressive periodontitis
Smokers have deeper probing depths, more

attachment loss, greater bone loss, more rapid
disease progression, more tooth loss
Smokers respond less well to periodontal therapy
More prone to lose teeth during maintenance

PERIODONTAL DISEASE
Smoking & host susceptibility
Smoking as a risk factor:
Negative effects on PMN functions
Reduced humoral & cellular immune responses
Reduced fibroblast function
Reduced vascular bed activity
Smoking is a modifiable risk factor
PERIODONTAL DISEASE
Diabetes & host susceptibility
Diabetes increases susceptibility to periodontitis &
other infectious diseases via:
Non-enzymatic glycation of proteins & lipids,
resulting in formation of advanced glycation end
products (AGE’s)
AGE’s alter the functionality of the target cells of
diabetes (eg endothelial cells & monocytes)
through specific cell surface receptors
Altered functionality of endothelial & monocytic
cells results in vascular changes & increased
inflammatory responses, including increased levels
of inflammatory cytokines eg TNF- and matrix
degrading enzymes such as collagenase
PERIODONTAL DISEASE
Genetic defects
50% of the risk for chronic periodontitis due to
heredity (Michalowicz, Diehl, & Gunsolley, 2000)
Specific genes not determined
Susceptibility to periodontitis may be linked to
susceptibility to gingivitis Tatakis & Trombelli, 2004)
PERIODONTAL DISEASE
Genetic defects
Genetic diseases associated with periodontitis
Down syndrome
Pappilon-Lefevre syndrome
Cyclic neutropenia
Congenital neutropenia
Chediak-Higashi syndrome
Leukocyte adhesion deficiency
Cohen syndrome
SPECIFIC MICROORGANISMS
ASSOCIATED WITH PERIODONTAL
HEALTH & DISEASE
Role of specific organisms in disease causation &
progression?
Different periodontal diseases have unique profiles
of associated bacteria
Gingivitis
Streptococcus spp (Gr+ve facultative)
Actinomyces viscosus, Peptostreptococcus micros
(Gr+ve anaerobe)
Fusobacterium nucleatum, Prevotella intermedia,
Veillonellaparvula (Gr-ve anaerobe)
Pregnancy gingivitis (Prevotella intermedia ^ )
HEALTH & DISEASE
Chronic periodontitis
–
Peptococcus micros (Gr+ve anaerobe)
–
Porphyromonas gingivalis (Gr-ve anaerobe)
–
Tanneralla forsythia (Gr –ve anaerobe)
–
Prevotella intermedia (Gr-ve anaerobe)
–
Campylobacter rectus (Gr-ve anaerobe)
–
Fusobacterium nucleatum (Gr-ve anaerobe)
–
Actinobacillus actinomycetumcomitans (Gr-ve anaerobe)
–
Treponema spp ( Gr-ve anaerobe)
●
Clinical resolution of disease following treatment is
associated with a decrease in level of these species
HEALTH & DISEASE
Localised aggressive periodontitis
AA (Gr-ve anaerobe)
AA predominant cultivable species in up to 90% of
sites
Porphyromonas gingivalis (Gr-ve anaerobe)
Campylobacter rectus (Gr-ve anaerobe)
Eikenalla corrodens (Gr-ve anaerobe)
Epstein Barr virus, human cytomegalo virus?
HEALTH & DISEASE
Necrotising ulcerative gingivitis
Treponema spp (Gr-ve anaerobe)
Prevotella intermedia (Gr-ve anaerobe)
Rothia dentocariosa (Gr-ve anaerobe)
Fusobacterium spp (Gr-ve anaerobe)
Achromobacter spp (Gr-ve anaerobe)
Propionibacterium acnes (Gr-ve anaerobe)
Capnocytophaga spp (Gr-ve anaerobe)
HOST DEFENCE MECHANISMS
IMPLICATED IN PERIODONTAL TISSUE
DESTRUCTION
Dental plaque has potential to cause tissue damage
directly, eg matrix degrading enzymes & molecules
that impair host cell functions
Plaque elicits most periodontal tissue damage through

indirect mechanisms dependent on initiation &
propagation of inflammatory host tissue reactions
Complex interactions between host defence cells &

periodontal structural elements
DESTRUCTION
Inflammatory infiltrate of periodontitis
PMN’s, macrophages, lymphocytes, plasma cells,
loss of collagen
Cellular structural elements of the periodontium

epithelial cells, periodontal ligament, gingival
fibroblasts, alveolar bone cells, osteoblasts,
osteoclasts
DESTRUCTION
●
Molecular structural elements of periodontium
●
extracellular matrix ie collagen, non-collagenous
proteins (elastin, connective tissue proteoglycans)
●
Interaction between plaque, inflammatory & structural
elements
●
determines clinical pathogenesis of gingivitis
alone or irreversible periodontal attachment
destruction
HOST CELLS & MOLCULES
IMPLICATED IN PERIODONTAL
DISEASE
Neutrophils
Role of host inflammatory reaction is to contain or
eliminate the injury causing agent (eg bacterial
lipopolysaccharide) & to initiate events that result in
repair of tissue damage
Proper PMN function is essential for adequate host
response
In LAP PMNs show defects in chemotaxis or
phagocytosis
Genetic disease characterised by quantitative or
qualitative defects in PMNs & associated
periodontitis indicates protective role of PMNs
DISEASE
PMNs & host defence mechanisms may also play a
role in tissue destruction, eg gingival epithelial cells,
periodontal ligament fibroblasts
Neutrophil elastase & collagenase can degrade
several components of the extracellular matrix,
destroying the 3-dimensional scaffolding needed
for tissue organisation
Neutrophils may release toxic oxygen metabolites
degrading periodontal matrix molecules
LAP studies show role of “hyperfunctional” PMNs
may cause enhanced tissue damage (Kantarci,
Oyaizu, Van Dyke, 2003)
DISEASE
Macrophages
Mononuclear cells initiating early, non-specific
defence against microorganisms
Specific immunity via antigen-presenting function
No quantitatve increase in macrophages
comparing healthy, gingivitis & periodontitis sites
Macrophages in periodontitis show varied
phenotypes; significance unknown
DISEASE
Natural killer cells
A lymphocyte subset involved in the innate immune
response
Ability to recognise & kill infected & malignant
cells
NKC levels increase in diseased periodontal
tissues
Impaired NKC function in various systemic
conditions associated with periodontitis, eg
Papillon-Lefevre syndrome, Chediak-Higashi
syndrome, smoking
NKCs serve protective function in periodontium?
DISEASE
T lymphocytes (Helper & Cytotoxic T cells)
Mononuclear cells essential for cell-mediated
immunity
Helper (CD4+) T cells proliferate & activate other
lymphocytes
Cytotoxic (CD8+) T cells act as destroyers of
target cells, eg infected or cancerous cells that
express specific antigens on their surface
CD4+ & CD8+ cells are present in periodontitis
lesions, their numbers reflecting regulatory status
of the local immune response
T cell direct involvement in bone resorption?
DISEASE
B cells
Lymphocyte subset essential for humoral immunity
B cells programmed to recognise specific
antigens, give rise to plasma cells that produce
specific antibodies when triggered by the antigen
& other regulatory cells
B cells increase in number from health to
gingivitis to periodontitis
Significantly higher B cell levels in active
periodontitis lesions suggests that B cell
activation contributes to disease progression
DISEASE
Host molecules regulating the inflammatory
response
Categorised as proinflammatory &
antinflammatory
Balance determines tissue response & the
initiation or progression of disease
DISEASE
Proinflammatory cytokines & lipid mediators
Interleukin-1
Role in alveolar bone loss & periodontal disease
IL-1 produced by monocytic, epithelial, osteoblastic
& other cells, is a potent stimulant of bone
resorption & inhibitor of bone formation
Several periodontopathogens can stimulate IL-1
production by host cells
IL-1 levels are elevated in diseased periodontal
tissues, both gingivitis & periodontitis
Periodontal therapy significantly reduces IL-1 levels
DISEASE
Tumor necrosis factor-α
TNF-α cytokine with similar biological activity to IL-1
TNF inhibitors combined with IL-1 inhibitors
decrease inflammation & tissue destruction in
non-human primates
TNF-α may be significant in periodontal destruction
associated with diabetes
DISEASE
Prostaglandins & thromboxanes
Prostaglandin E2 & Thromboxane B2 are lipid
molecules produced by many host cells
prostaglandin E2 & thromboxane B2 contribute to
the redness & bleeding of gingivitis & alveolar
bone loss of periodontitis
DISEASE
Anti-inflammatory cytokines & lipid mediators
Interleukin-10
Potent anti-inflammatory mediator that regulates
humoral & cellular immune responses & production
of several pro-inflammatory cytokines such as IL-1 &
TNF
Gingival tissue IL-10 levels are greater in healthy
compared with periodontitis sites
DISEASE
Lipoxins
Lipoxins are produced through the lipoxygenase
pathway
Lipoxin A4 can modify the host response to
promote resolution of inflammation in response to
periopathogens
SYSTEMIC EFFECTS OF
PERIODONTAL DISEASE
Some studies suggest an association between
Periodontal disease &
Cardiovascular disease
Pulmonary disease
Diabetes
Pregnancy complications
SYSTEMIC EFFECTS OF
PERIODONTAL DISEASE
History of Focal infection hypothesis
Localised chronic infection may contribute to
various systemic diseases?
Chronic, localised (focal) infection can
disseminate microoranisms or toxic microbial
products to contiguous or distant tissues?
Sites of focal infection tonsils, sinuses, bronchi,
GIT, urinary tract, lymph nodes?
Focal infections lead to systemic disease eg
arthritis, nephritis, conjunctivitis, iritis, otitis
media, endocarditis, anaemia?
By 1950’s focal infection theory discounted
SYSTEMIC EFFECTS OF
PERIODONTAL DISEASE
Current studies of localised infection and
systemic disease
Bacteria from dental plaque may enter the blood
stream via discontinuities of oral tissues
(ulcerated sulcular epithelium, infected root
canals), & travel through the blood stream to
cause infection at a distant site?
Periodontal disease bacteria stimulate release of

pro-inflammatory cytokines or acute-phase
proteins at a distant site, eg liver, pancreas,
skeleton, arteries?
SYSTEMIC EFFECTS OF
PERIODONTAL DISEASE
●
Products may initiate or intensify a disease
process eg atherosclerosis, diabetes?
●
Bacteria may travel from oral sites to other
mucosal surfaces (lung, gut) causing
inflammation & infection, eg pneumonia, gastric
ulcers?
Association of PDD with
atherosclerosis, CVD & stroke
Atherosclerosis
Narrowing of arteries due to deposition of cholesterol,
cholesterol esters on surface of blood vessel walls
Cholesterol rich plaques also contain cells, including

fibroblasts & immune cells
Risk factors include chronically elevated blood levels

of cholesterol & triglyceride, hypertension, diabetes,
mellitus, tobacco smoking
Atherosclerosis
Cholesterol uptake is reduced in some people with
excess cholesterol accumulation in the blood,
forming atherosclerotic plaques
Blood-flow occlusion; stroke, myocardial infarction
Vascular wall inflammation, infection, and

autoimmune mechanisms involved in
atherosclerosis?
Atherosclerosis
Infectious agents appear to be associated with
atherosclerosis, eg Chlamydia pneumoniae
Chlamydia pneumoniae DNA & proteins detected in

arteries of patients with giant-cell arteritis,
endarectomy samples
Elevated levels of antibody against Chlamydia

pneumoniae found in patients with coronary heart
disease compared with controls
Several case control studies report a positive association
between indicators of poor dental health & CVD (Mattila,
Valle, Niemenin, 1989; Mattila, Asikainen, Wolf, 2000)
Alveolar bone loss >4mm significantly greater in patients
with a history of recent myocardial infarction (Renvert,
Ohlsson, Persson et al, 2004)
Studies support a positive association between PDD &
prevalence of CV events?
Association observed between atherosclerosis-induced
disease & PDD may be the result of common aetiologic
factors eg smoking
Studies have shown a modest positive association between
PDD & stroke?
Association of PDD with pneumonia
Pneumonia; inflammation of the lungs caused by

fungal, viral, parasitic, or bacterial infection
Bacterial pneumonia classified as either community-
acquired or hospital acquired (nosocomial) pneumonia
Community-acquired pneumonia typically caused by
aspiration of bacteria that normally reside in the
orophaynx, eg Streptococcus pneumoniae, Haemophilus
influenzae, Mycoplasma pneumoniae
Nocosomial pneumonia caused by different set of bacteria
including Staphylococcus aureus, & Gram–ve bacteria
such as Pseudonmonas aeruginosa, & the enteric species
Klebsialla pneumoniae
Oral cavity may serve as a reservoir for respiratory

pathogen colonization & infection
Colonization of dental plaque or oral mucosa by
potential respiratory pathogens shown to be greater
(65%) in intensive care unit patients compared with
regular out patients (16%) attending dental school
clinic (Scannapieco, Stewart, Mylotte, 1992)
Oral colonization by respiratory pathogens was
associated with antibiotic usage
Other studies show an association between poor oral
health status & onset of pneumonia in ICU patients
In nursing home populations a greater percentage of

dentate patients develop aspiration pneumonia
compared to edentulous patients
Dental plaque scores significantly higher in nursing
home residents than in outpatient controls
Oral bacteria in dental plaque/saliva may serve as a
reservoir for lung infections, ie Porphyromonas
gingivalis in dental plaque, Staphylococcus aureus in
saliva
Oral intervention trials to prevent pneumonia

Improved oral hygiene measures can reduce the
incidence of ventilator-associated pneumonia in
nursing home orally intubated patients
In ICU patients, topical application of antibiotic paste

(polymixin B sulfate, neomycin sulfate, vancomycin
hydrochloride) to retropharynx every 24 hours &
swallowed reduced tracheobronchial colonisation by
Gram-ve respiratory pathogens & Stapylococcus
aureus & reduced the rate of pneumonia fivefold
compared with control treatment (5% dextrose)
In ventilated patients following cardiac surgery,

0.12% chlorhexidine gluconate applied twice daily to
oral mucosal & tooth surfaces together with oral
hygiene procedures reduced the incidence of
respiratory tract infections by 69% compared with
placebo
Evidence that topical antimicrobials reduce the risk of

pneumonia in ICU/nursing home patients
Association of PDD with chronic
obstructive pulmonary disease (COPD)
COPD defined as a spectrum of conditions
characterised by chronic obstruction to airflow due
to emphysema and/or chronic bronchitis
Statistical analysis has shown that poor oral hygiene

& smoking status were associated with chronic
respiratory disease
PDD (measured as alveolar bone loss assessed from

periapical radiographs) shown as an independent
risk factor for COPD in adult men
Association of PDD with chronic
obstructive pulmonary disease (COPD)
Cigarette smoking is a cofactor in the relationship
between PDD & COPD
Oral colonisation by respiratory pathogens appears

to be a risk factor for lung infection in high risk
subjects
Further studies are required to verify the apparent

association between PDD & COPD
Adverse pregnancy outcomes & PDD
Preterm low birth rate (PTLBW) is a significant cause

of infant morbidity & mortality
Risk factors that appear to contribute to adverse

pregnancy outcomes include low socioeconomic
status, race, multiple births, mother’s age, history of
preterm birth or delivery of low birth weight infant,
drug & alcohol abuse, systemic maternal infection
Adverse pregnancy outcomes & PDD
Possibility that infectious processes occurring elsewhere in

the body may contribute to neonatal morbidity & mortality?
Several studies support the contention that women with

PDD have a greater risk of having preterm or low birth
weight children
Intervention studies show that periodontal therapy before 28

weeks of gestation may significantly reduce the incidence of
PTLBW children
Association of PDD with diabetes
mellitus
Diabetes mellitus is a metabolic derangement
characterised by impairment in glucose use
Type I diabetes is the result of a reduction in or the
elimination of insulin production by beta cells in the
pancreas
Individuals with type I diabetes require daily insulin
supplementation to properly regulate glucose use
Type 2 diabetes is characterised by a deficient

response to insulin by target cells, although insulin
response is typically normal or even enhanced in
these individuals
mellitus
Type 2 diabetes
●
Target cell impairment may be due to changes in the
structure or number of the cell receptors for insulin
●
Type 2 most common form of diabetes (85%-90% of
all diabetes)
●
Incidence of diabetes increasing each year, probably
reated to concomitant increase in obesity in the
population
●
Many acute & chronic complications related to
chronic elevation of blood glucose levels in
peripheral blood (hyperglycaemia)
mellitus
Complications of diabetes
Coronary vascular disease
CVD (stroke)
Peripheral vascular disease
Retiinopathy
Nephropathy
Neuropathy
mellitus
Reduced fibroblast proliferation

Reduced collagen synthesis
Hyperglycaemia effects would healing?
Diabetics have more severe PDD:
More severe pocket depths
More alveolar bone loss
Frequent abscess formation
Poor healing following therapy
mellitus
Mechanisms for more aggressive PDD in
diabetics
Non-enzymatic glycation of proteins & lipids,
resulting in formation of advanced glycation end
products (AGE’s)
AGE’s alter the functionality of the target cells of

diabetes (eg endothelial cells & monocytes)
through specific cell surface receptors
mellitus
Altered functionality of endothelial & monocytic
cells results in
Vascular changes & increased inflammatory
responses, including
Increased levels of inflammatory cytokines eg TNF-

and matrix degrading enzymes such as collagenase
History & Examination in Periodontal
Disease
Medical History
Dental History
Personal, social, family history
The clinical examination/ Data collection
Dental examination & charting
Periodontal examination & charting
Occlusal examination
Additional Investigations
Radiographic examination/report
Disease
Aetiology; primary & secondary factors
Risk factors; risk predictors
Pathogenesis
Pathology (macroscopic/microscopic)
Diagnosis
Prognosis (Sequelae)
Treatment risk factors
Disease
Medical History
Current & past medical history
Systems review
Medication review
Disease
Personal, social, family history
Marital Status
Occupation
Family
History of mental illness
Previous care for mental illness
Current medication
Specialist/Consultant
Disease
●
Antibiotic cover required for any reason?
●
Does medical history affect diagnosis?
●
Does medical history affect treatment in any way?
●
Does current medication require change for dental
treatment?
●
History of blood pressure problems?
●
Will medical consultation be required?
Disease
Dental History:
Presenting complaint
Record in patient's own words
Additional complaints?
Disease
History of presenting complaint
How?
What?
Why?
Who?
When?
Where?
Disease
Past Dental History
Preventive
Oral hygiene procedures
Periodontal treatment
Extractions/Oral Surgery
Endodontics
Orthodontics
Restorative/Prosthetic/Implant
Clinical Examination & data recording
Recording clinical information

Clinical Notes
Odontogram
Clinical Examination in Periodontal
Disease
Extra Oral Intraoral
●
General morphology Soft tissues/oral
mucosa
●
Skeletal base
Underlying bony
●
Skin lesions
structures
●
Lymph nodes
Masticatory muscles
●
Neck & facial muscles
Oral hygiene/Saliva
●
Lip support/seal
Dental examination
●
TMJ
Periodontal examination
Occlusal examination
Existing prostheses
Disease
Oral hygiene
●
Halitosis
●
Tongue surface
stains/debris
●
Dental plaque
●
Dental calculus
Saliva
●
Quality
●
Quantity
Disease
Dental
●
Teeth present/missing
●
Attrition
●
Abrasion
●
Abfraction
●
Erosion
●
Caries
●
Coronal fracture;
enamel/dentine
Disease
Dental
●
Hypomineralisation
●
Staining/discoloration
●
Gingival recession,
exposed root surfaces
●
Dentine hypersensitivity
●
Enamel faceting
●
Dentine cupping
Disease
Dental
Restorations;material,
surfaces restored
Adequate/inadequate
Failed, lost
Overhangs
Open contact
areas/food impaction
Plunger cusps
Pulpal response CO2
Disease
Periodontal
●
Oral hygiene procedures
●
Calculus deposits
●
Plaque deposits
Plaque index
Plaque deposits; 4 sites
per tooth
O’Leary PI (% of total
surfaces)
Disease
Gingival tissue
Colour
Form, contour,texture
Swelling
Bleeding
spontaneous, on
gentle palpation?
Ulceration
Exudate
Suppuration
Disease
Gingival recession; 6
sites per tooth
Gingival biotype
Attached gingivae
Attached gingiva
Adequate width
Diminished width
Mucogingival lesion
Disease
Frenal attachments,
vestibular depth
Gingival line
Gingival recession
Dentine hypersensitivity
Residual ridge; gingivae
& bone loss
Disease
Pocket probing depths
●
6 sites per tooth
●
Bleeding/suppuration on
probing
●
CAL
●
Gingival (bleeding)
index
●
Psuedo-pocketing
Disease
Bone loss
●
Bone loss at furcation
sites; site & extent
●
Horizontal, vertical
●
Localised bone defects
Disease
Occlusion
●
Mobility (Miller Index)
●
Fremitus
●
Tooth migration;
drifting, tilting
●
Premature contacts;
ICP/RCP
●
Occlusal interferences;
working, non-working,
protrusive
Disease
Existing prostheses
Removable
Fixed
Implant retained prostheses
Provisional prostheses
Occlusal splints
Disease
Existing prostheses
General comments; hygiene
Design, finish, form, contour
Fit
Retention
Extensions
Stability
Occlusion/occlusal analysis
Aesthetics
Comfort/function/speech
Disease: additional investigations
Pulpal response tests Dietary analysis
Plaque/gingival indices Referral to
physician/medical
Radiographic
specialist
examination
Referral to
Study casts
dentist/dental specialist
Clinical photographs
Medical investigations
Biopsy procedures
Additional Investigations
Radiographic examination
Radiographic report
Panoramic
BW's
Periapical
Radiographic interpretation/assessment
Additional Investigations:
radiographic examination/report
Dental
●
Teeth present/absent
●
Restorations
●
Restoration
overhangs/deficiencies
●
Caries; coronal, root
●
Calculus
Dental
Pulp chamber
size/morphology
Pulp canal
size/morphology
Root canal treatment
Adequate
Inadequate
Dental
Root formation
Apical development
Root fractures
Root resorption
Supporting structures
Periodontal ligament
space
Periapical radiolucencies
Loss of crestal/alveolar
bone
Localised/Generalised
Horizontal/Vertical
Irregular
Furcation sites
Adjacent structures
Jaw radiolucencies
Cysts
Tumours
Jaw radiopacities
Unerupted teeth
Retained roots
Foreign bodies
Maxillary sinus
proximity of roots
Adjacent structures
TMJ
Condyles
Position
Form; size, shape
Cortication
Joint space uniformity
Radiographic report
Structured report
Patient details; film details
Dental
Supporting tissues
Adjacent structures
Radiographic/provisional diagnoses
Additional radiographs/further investigations
Clinical implications of findings
Periodontics: case assessment &
treatment planning
●
CASE ASSESSMENT
●
TREATMENT PLANNING
CASE ASSESSMENT:
Evaluation of information obtained
Evalulation of:
Medical history
Dental history
Results of additional investigations
●
Consideration of:
–
Existing problems? (Diagnosis)
–
Aetiological/risk factors evident?
–
Long term outcome both with & without
treatment? (Prognosis)
CASE ASSESSMENT:
Evaluation of information obtained
Considering treatment goals
Overall treatment goals
Goals of individual treatment procedures
Considering treatment risk factors

Considering treatment options
Concept of the phased treatment plan
Concept of the provisional treatment plan
CASE ASSESSMENT:
Diagnosis
Consideration of:
Gingivitis &/or periodontitis?
Acute or chronic?
Localised or generalised?
Mild, moderate, severe?
Slowly progressing, aggressive or associated with
underlying systemic (medical) condition?
CASE ASSESSMENT:
Classification**/Diagnosis
1999 American Academy of Periodontology**
I Gingival disease
Dental plaque induced gingival disease
Non-plaque induced gingival disease
II Chronic periodontitis
Localised
generalised
III Aggressive periodontitis
Localised
Generalised
CASE ASSESSMENT:
IV Periodontitis as a manifestation of systemic
disease
V Necrotising Periodontal Diseases
VI Abscesses of the Periodontium
VII Periodontitis associated with Endodontic lesions
VIII Developmental or Acquired Deformities &
Conditions
Localised tooth-related factors
Mucogingival deformities around teeth
Mucogingival deformities on edentulous ridges
Occlusal trauma
CASE ASSESSMENT:
References**
Armitage GC (1999). Development of a classification
system for periodontal diseases & conditions. Ann
Periodontol; 4 (1).
American Academy of Periodontology
<www.perio.org> refer Parameters of Care
Plaque-induced periodontal disease:
goals of treatment
Gingivitis:
–
To establish gingival health & prevent progression
to periodontitis
Periodontitis:
To arrest progression of the disease,
preserve the dentition in a state of health,
comfort, function & aesthetics;
To prevent recurrence of the disease
To maintain patient well-being
TREATMENT PLANNING:
the phased treatment plan
Provides for:
appropriate sequential order of treatment
procedures
effective & efficient treatment needs
customized & optimal treatment needs
TREATMENT PLANNING:
Allows the patient to participate in:
their own treatment needs & dental health
maintenance
flexibility within and between phases of
management
not all patients require treatment within all
phases of management
TREATMENT PLANNING:
●
Phase 1 (Preliminary phase)
●
Phase 2 (Interim phase)
●
Phase 3 (Restorative/prosthetic phase)
●
Phase 4 (recall/review/maintenance)
The phased treatment plan:
preliminary phase
Phase 1 treatment procedures
Relieving pain & discomfort
Infection control
Elimination of active carious lesions
Extraction of teeth with hopeless prognosis
Instituting effective plaque control
Additional home care procedures
Initial periodontal therapy
Scaling & root planing
Removal of plaque retentive factors
preliminary phase
Home care procedures
Interdental & subgingival cleaning
floss, tape, interdental brushes, wood points
Additional aids
–
Disclosing tablets
–
Home use mouth mirror
–
Non-abrasive toothpaste, desensitising paste
–
Fluoride MW, F application gels
–
Mouthwashes
preliminary phase
Scaling & root planing
Scaling: removal of plaque & calculus deposits
from root surface
Root-planing: removal of “diseased” cementum,
producing a hard & smooth root surface
Subgingival curettage: removal or epithelium &
granulation tissue from pocket wall
Tooth polishing: rubber cup & mild abrasive paste
to produce a smooth tooth/root surface,
facilitating daily plaque removal by the patient
preliminary phase
Reassessment of Phase 1
Addressed patient's presenting complaint?
Comfortable, stable dentition?
Control of risk factors; systemic, local?
Tissue response to initial periodontal treatment?
Patient motivation to continue treatment?
Review phase 2 & 3 treatment goals
preliminary phase
6-8 weeks after last scaling appointment
Review medical history/medication changes,
smoking, stress factors
Patient concerns re oral hygiene, eg difficult
access
Gingival/teeth sore or sensitive?
Changes in gingival bleeding?
Gum swelling or shrinkage?
Food impaction sites?
Other patient concerns?
preliminary phase
–
Plaque index, bleeding index
–
Gingival tissue tone?
–
Presence of plaque or calculus?
–
Reduction in probing depths?
–
Bleeding/suppuration on probing?
–
Recession
–
Mobility
–
Furcation sites
preliminary phase
Decisions following Phase 1 reassessment
Degree of resolution of inflammation, reductions
in probing depths, changes in attachment levels,
OH status?
Resolution of signs & symptoms?
Is further treatment required?
preliminary phase
Reassessment & further management options
Maintenance therapy
Re-do SRP
Re-do SRP with systemic antibiotics
Open debridement (flap surgery for access)
Pocket elimination surgery
Other surgery, eg root resection
GTR techniques
Mucogingival surgery to cover areas of recession
Other procedures, eg tooth splinting
Interim phase
Direct (non-complex) restorations
Repairs/relines to existing prostheses
Oral surgery, complex extractions eg 8's
Endodontics
Orthodontics
Interim phase
Periodontal, osseous & mucogingival surgery
GTR, bone grafting/ridge augmentation
Crown-lengthening procedures/gingivoplasty
Implant placement procedures
Occlusal analysis/therapy
Provisional restorations/prostheses
Interim phase
Active disease sites?
Plaque score acceptable to proceed to Phase 3?
Acceptable gingival contours/aesthetics?
Patient interest/motivation?
Review Phase 3 treatment goals
Restorative/Prosthetics phase
Occlusal analysis/diagnostic wax up
Direct & indirect restorative procedures
Fixed prosthodontics
Removable prosthodontics
Implants/prostheses
Restorative/Prosthetics phase
Reassessment on completion of Phase 3
Phase 3 treatment goals met?
Review treatment outcomes Phase 1, 2, 3
Recall/Review/Maintenance
Phase 4 management goals
Disease free long-term maintenance
Control of inflammation
Maintain stable clinical attachment level
Preservation of periodontal bone support
Ongoing reinforcement of home care
Long term comfort, function, aesthetics
Occlusal stability
Overall patient well-being
Phase 4 management procedures
Check appointments
Address current concerns
Short term
Short term recall, review/reassessment
Longer term
Longer term recall, review/reassessment
Maintenance program
Maintenance therapy
Review medical/dental history
Comprehensive oral examination
Plaque control review
Scaling, root-paling, tooth polishing
Application of fluorides
Evaluate further treatment needs
Antibiotics in periodontal
treatment *
Antibiotic therapy
Local antimicrobial therapy
Sub-gingival irrigation
Controlled local release delivery
Topical agents
mouthrinses
Gels
*Ref: Dr Ivan Darby (2006). OTC lecture program Semester 1.

treatment
Systemic antibiotics
Advantages
Manage deeply penetrating bacteria
Adjunct in treatment of widespread disease
Considerations
Complications & side effects, allergy, resistance,
drug interactions eg oral contraceptives
Basic principles
Appropriate drug, contact with organism,
therapeutic level, required contact time
treatment
Penicillin
Inhibit cell wall synthesis
Penicillin V ; Gram +ve organisms
Ampicillin; broad spectrum, Gran +ve/-ve
Amoxycillin; higher serum levels than Ampicillin,
mainly active against Gram -ve oral anaerobic
bacteria
All 3 penicillins susceptible to β-lactamase
producing organisms
Augmentin: Amoxycillin plus Clavulanic acid (β-
lactamase blocker)
treatment
Tetracyclines
Broad spectrum antibiotics with activity against
Gram +ve & Gram -ve bacteria, as well as
Mycoplasmas, Rickettsial& Chlamydial infections
Bacteriostatic unless in high concentrations
Inhibit protein synthesis
Achieve higher levels in GCF than in serum
Also inhibit collagenase activity & enhance
reattachment/regeneration
treatment
Doxycycline
Suppress Gram -ve pathogens
Concentrates in GCF X3 that of serum
Bind to tooth surface, slow release
Non-antimicrobial properties
Promote fibroblast & CT attachment
Anti-inflammatory properties
Inhibit some enzymes & osteoclast function
Periostat; 20 mg Doxycycline bid
treatment
Metronidazole
Affects nucleic acid synthesis
Good against anaerobes, poor versus aerobes
Sometimes used in combination with
Augmentin/Amoxycillin esp. in AA associated
periodontitis
Taste?
Alcohol?
treatment
Clindamycin
Inhibits protein synthesis
Good against Gram +ve, but most Gram -ve
aerobes are resistant
Works well against Gram -ve anaerobes
Penetrates well into GCF & maintains
concentration above MIC
Stomach upsets?
treatment
Use of Systemic Antibiotics
Sole means of therapy
Combination therapy
Advantages
Broader antimicrobial spectrum
Synergistic effect
Reduced resistance
Disadvantages
Increased adverse reactions
Antagonistic reactions
treatment
Single antibiotic regimes
Penicillin; good against AP, Refractory & RPP
Augmentin; similar to penicillin
Tetracyclines ; good results in AP & RPP
Petronilla's; good against all forms of PDD
Clindamycin; inconclusive in AP, poor in RP
treatment
Combination antibiotic regimes
Tetracycline & Metronidazole works well in RP
Augmentin & Tetracycline, or

Augmenting or Amoxycillin & metronidazole good
results in RP, LJP & RPP
treatment
Case selection for systemic therapy
Consider use in:
Refractory cases with continual breakdown
Aggressive/early onset disease
Patients with medical conditions that predispose
to PDD
Acute periodontal infections
Use to manage no-oral periopathogen associated
periodontl disease
treatment
Case selection for systemic therapy
Use in AA related periodontitis, LJP, LEOP
S/RP inadequate for controlling infection &
disease progression
Can use Tetracycline +/- surgery to eliminate AA
Rationale:
AA probable pathogen for LJP
AA is sensitive to several antibiotics; ? use of
combined therapy
AA is present in soft tissue
AA is not eliminated by mechanical treatment
treatment
Local antimicrobial therapy
Advantages
–
Site specific applications
–
Sub-gingival concentrations greater than can be
achieved systemically with fewer complications
Options
Oral mouthrinse; supragingival effect only
Subgingival irrigation fails to penetrate entire
pocket; rapid clearance or inactivation
treatment
Options
Controlled release
Reservoirs, no rate control
Rate control systems (gels & matrices)
Actisite (25% tetracycline in ethylene vinyl
acetate)
Dentomycin (2% Minocycline in lipid gel)
Elyzol (25% Metronidazole in lipid gel)
Periochip (CHX in gelatine)
PERIODONTICS: Aetiology, Case
Assessment, & Treatment Planning
References
Tatakis, DN & Kumar, PS (2005). Etiology &
Pathogenesis of periodontal Diseases. Dental
Clinics of North America, 49 (3), pp 491- 516.
Albandar, JM (2005). Epidemiology & Risk Factors of
Periodontal Diseases. Dental Clinics of North
America, 49 (3), pp 517- 532.
Scannapieco, FA (2005). Systemic Effects of
Periodontal Diseases. Dental Clinics of North
America, 49 (3), pp 551 - 572.

Perio Exam, Diagnosis

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Perio Exam, Diagnosis

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PERIODONTICS: Examination, Case

Assessment, & Treatment Planning

General Pathology Periodontal disease

Case Assessment Treatment Plan

Smokers have deeper probing depths, more

Smokers respond less well to periodontal therapy

More prone to lose teeth during maintenance

Plaque elicits most periodontal tissue damage through

Complex interactions between host defence cells &

Cellular structural elements of the periodontium

Periodontal disease bacteria stimulate release of

Cholesterol rich plaques also contain cells, including

Risk factors include chronically elevated blood levels

Blood-flow occlusion; stroke, myocardial infarction

Vascular wall inflammation, infection, and

Chlamydia pneumoniae DNA & proteins detected in

Elevated levels of antibody against Chlamydia

Pneumonia; inflammation of the lungs caused by

Oral cavity may serve as a reservoir for respiratory

In nursing home populations a greater percentage of

Oral intervention trials to prevent pneumonia

In ICU patients, topical application of antibiotic paste

In ventilated patients following cardiac surgery,

Evidence that topical antimicrobials reduce the risk of

Statistical analysis has shown that poor oral hygiene

PDD (measured as alveolar bone loss assessed from

Oral colonisation by respiratory pathogens appears

Further studies are required to verify the apparent

Preterm low birth rate (PTLBW) is a significant cause

Risk factors that appear to contribute to adverse

Possibility that infectious processes occurring elsewhere in

Several studies support the contention that women with

Intervention studies show that periodontal therapy before 28

Type 2 diabetes is characterised by a deficient

Reduced fibroblast proliferation

AGE’s alter the functionality of the target cells of

Increased levels of inflammatory cytokines eg TNF-

Recording clinical information

Considering treatment risk factors

*Ref: Dr Ivan Darby (2006). OTC lecture program Semester 1.

Augmentin & Tetracycline, or

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