Transcript Pathobiology of the Periodontal Tissues

Pathobiology of the Periodontal
Tissues
Mark C. Herzberg
Department of Oral Sciences
A classification of periodontal diseases
Diagnosis
• gingivitis
• periodontitis
– juvenile
• localized
• generalized
– adult
Characteristics
Infection -> inflammation
Loss of alveolar bone
Clinical considerations
age of onset
rate of progression
severity
sites affected
Epidemiology of periodontal diseases
• Estimated 20 to 60%
of adults affected in
US
• Prevalence and
severity
– unrelated to dental
caries history
– inversely related to
education, urbanization,
economic status
– increases with age
(NO C-E relationship)
• Principally associated
with quality of oral
hygiene
• Juvenile and rapidly
progressive lesions
seen before age 40
• Risk factors vs. cause
(etiology)
Transition from health to periodontitis
• Periodontitis is
typically a chronic
infection
• Loss of epithelial
attachment and
resorption of
alveolar bone
Transition from health to periodontitis
• Periodontitis and
gingivitis are
infections that cause
inflammation
• Gingivitis marked by
inflamed gingiva
without measureable
loss of alveolar bone
Transition from health to periodontitis
• Gingivitis and
periodontitis
caused by
microorganisms in
dental plaque
• Plaque can reside
on or in calculus
(‘tarter’)
Transition from health to periodontitis
• Gingivitis and periodontitis are
different infections
• Gingivitis typically does not progress
to periodontitis
• Periodontal diseases, therefore, are a
set of infections that affect the
supporting structures of the teeth
Transition from health to periodontitis:
gingivitis
beagle dog
43-yr old woman
Microscopic appearance
• Attached gingiva in caucasians is pale pink
• With inflammation, the crestal or marginal gingiva
becomes increasingly red
• Microscopically, attached epithelium attracts
large numbers of inflammatory, white blood cells
Transition from health to periodontitis
• recession
• exudate
• gingival inflammation
varies
bony crater
exposed
Post-surgical treatment
Transition from health to periodontitis
• Proliferation
of epithelial attachment
• Loss of alveolar bone
• Disruption of connective tissue attachment
• Inflammatory cell infiltrate
X-ray bone loss
Cryptic infection
Age of onset of periodontitis
Heinz-Mayfield et al. J Clin Perio 30:902, 2003
Younger than 25 yrs
Frequency of sites with
2mm or greater
attachment loss
55 yrs or older
Heinz-Mayfield et al. J Clin Perio 30:902, 2003
Subgingival dental plaque
• Dental plaque is a
complex community of
microbes - biofilm
• When attached to the
tooth (or root as
shown here), the
community can exist in
different
architectural forms
Uncovering causative microorganisms
Indigenous infection
Exogenous infection
Compromised host
Healthy carrier
Opportunistic
Superinfection
Commensal
‘True’ infection
Prevotella intermedia
Fusobacterium spp.
Peptostreptococcus micros
Eubacterium spp.
Spirochetes
Campylobacter rectus
Bacteroides forsythus
enteric rods
Pseudomonads
Staphylococci
Candida spp.
Actinobacillus
actinomycetemcomitans
Porphyromonas
gingivalis
Examples of Syndromic Forms of
Periodontitis in Which Inheritance is
Mendelian and Due to a Genetic Alteration at
a Single Gene Locus
Papillon-Lefèvre syndrome
Haim-Munk syndrome
Ehlers-Danlos syndrome type 4
Ehlers-Danlos syndrome 8
Cyclic neutropenia
Chronic familial neutropenia
Chediak-Higashi syndrome
Congenital disorder of
glycosylation type IIc
Leukocyte adhesion
deficiency
Adapted from Kinane & Hart. CROBM 14:230, 2003
The classic relationship among
phenotype, environment, and genotype
For the periodontal disease phenotype, environmental
risk factors include:
• smoking status
• plaque control
• socio-economic status
• diabetes, ...
• Phenotype = environment + genotype + genotype x
environment
• G x E is the interaction between environment and genotype
(includes gene-gene interactions).
Adapted from Kinane & Hart. CROBM 14:230, 2003
Is periodontitis in healthy adults a
genetic disease?
Yes, but genetics may be reflected in the relative
susceptibility or resistance.
• Identical twins raised together and apart were
compared for clinical expression of periodontitis.
• 50 to 70% of the variability in clinical expression
was attributable to genetics.
Michalowicz et al. J Periodontol 62:293, 1991
• The search for genetic markers, polymorphisms,
SNPs, mutations, … is in progress.
Host response to periodontal infection: bone loss
Plaque
Direct invasion of host cells
Matrix-degrading enzymes
T-cell response
Pro-inflammatory
cytokines
Modified from Teng. CROBM 14:237, 2003
Paquette et al, 1999
Paquette et al, 1999
Paquette et al, 1999
Paquette et al, 1999
Paquette et al, 1999
Pathobiology of periodontal diseases
Complex infection initiated by microorganisms in
dental plaque causing inflammatory diseases
Genetics appear to contribute to clinical expression
of disease
Risk factors such as smoking, diabetes are strongly
associated
Host response may be both protective and
destructive
‘Local’ periodontitis linked to systemic diseases:
pathogen load, cytokine signaling, …