Pathobiology of the Periodontal Tissues Mark C. Herzberg Department of Oral Sciences
Dec 21, 2015
A classification of periodontal diseases
Diagnosis• gingivitis• periodontitis
– juvenile• localized• generalized
– adult
CharacteristicsInfection -> inflammation
Loss of alveolar bone
Clinical considerationsage of onset
rate of progressionseverity
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
• 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
43-yr old woman Microscopic appearance
beagle dog
Transition from health to periodontitis
• recession• exudate
• gingival inflammation varies
bony craterexposed
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
Frequency of sites with 2mm or greater attachment loss
Younger than 25 yrs
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 infectionCompromised host
Opportunistic
CommensalPrevotella intermediaFusobacterium spp.
Peptostreptococcus microsEubacterium spp.
SpirochetesCampylobacter rectusBacteroides forsythus
Exogenous infectionHealthy carrier
Superinfection‘True’ infection
enteric rods ActinobacillusPseudomonads
actinomycetemcomitansStaphylococci PorphyromonasCandida spp. 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
genotypeFor 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
Modified from Teng. CROBM 14:237, 2003
Direct invasion of host cellsMatrix-degrading enzymesT-cell responsePro-inflammatory cytokines
Plaque
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, …