Pathobiology of the Periodontal Tissues

Mark C. HerzbergDepartment of Oral Sciences

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

Age of onset of periodontitis

Heinz-Mayfield et al. J Clin Perio 30:902, 2003

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

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, …