AETIOLOGY OF PERIODONTAL DISEASE Primary Factors : Bacterial irritation Specific Theory Only a single specific pathogen is the cause

of inflammatory periodontal disease Treatment directed towards elimination of the specific pathogen with appropriate narrow spectrum antibiotic Plague control not necessary since plague with non-specific pathogen is not pathogenic

Non-specific Theory Indigenous oral bacteria colonize gingival crevice to form plague in absence of effective oral hygiene Inflammatory periodontal disease develops when bacterial proliferation exceeds threshold of host resistance All plague bacteria have virulence factors causing gingival inflammation and periodontal destruction Total plague control is necessary to prevent and treat inflammatory periodontal disease

Unified Theory A number of bacteria species is responsible for destructive periodontitis and additional species is responsible for a small number of cases Supports both specific and non-specific theory, combination of both Any composition of plague in sufficient quantity in gingival crevice causes gingivitis but only in some cases leads to destructive periodontitis Different combinations of bacteria may be present in individual lesion and together produce virulence factors

Secondary Factors: Faulty restorations Carious cavities Food impaction Badly designed partial dentures Orthodontic appliances Malalignment of teeth Lack of lip-seal Development grooves on cervical enamel and root surface Tobacco smoking (systemic and local effects)

Tobacco Smoking Associated With Periodontal Disease Tooth staining from nicotine Increases the deposition of calculus and plague Credits: xandamator@live.com

Poorer oral hygiene than non-smokers Younger smokers have same or higher degree of gingivitis than non-smokers Older aged smokers have less gingival inflammation than non-smokers Less gingival bleeding of smokers due to vasoconstriction More keratinization of gingiva in smokers with increased keratinocytes Refractory periodontitis more common in smokers Pocket depth and alveolar bone loss is greater in smokers Vasoconstriction causes less blood flow and less inflammatory response Less antibodies and leukocytes are produced into periodontal tissues Nicotine inhibits function of oral neutrophils Tobacco smoke decreases motility and chemotaxis of oral leucocytes Tobacco smoke causes abnormal PMN phagocytosis in refractory periodontitis Nicotine enhances attachment of fibroblast

General Effects of Smoking Greater alveolar bone loss Increased number of deep pockets Increase rate of disease progression Increased calculus formation Less clinically apparent gingival inflammation Less gingival bleeding than non-smokers

Credits: xandamator@live.com