As with most infections, the inflammatory reaction within the gingival tissue serves to contain or stop a local microbial attack, and prevents the spread of attacking organism. However, a robust inflammatory reaction may also result in the destruction of surrounding cells, connective tissue matrix and eventually bone. The progression from relative health to advanced disease is best explained by reviewing the mechanisms of plaque induced inflammation and the immune components involved in initiating and propagating the inflammatory process.
Early visible inflammatory changes in the gingival margin occur within a few days if plaque growth is undisturbed. Within 10 to 20 days the plaque mass changes composition from mostly gram-positive coccoid and filamentous bacteria to gram-negative rods and spirochetes. A gram-positive plaque is usually associated with periodontal health, while a gram-negative is associated with disease. This complex community of microorganisms is referred to as a biofilm.
Gram-negative and gram-positive microorganisms within the biofilm produce and release a variety of metabolic by-products that are toxic to host tissues. These include exotoxins, endotoxins, odor-producing metabolites (e.g., hydrogen sulfide) and many different tissue-degrading enzymes, including bacterial collagenase and various proteases.
Several of the more common periodontal pathogenic bacteria are grouped into complexes based on their association with the periodontal lesion. The most virulent of organisms form the Red Complex and consists of Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola. The Orange complex is composed of Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus micros, Eubacterium nodatum, Streptococcus constellatus, three Campylobacter species including Campylobacter rectus, and 4 species of Fusobacterium. These two complexes of periodontal pathogens become more prevalent in numbers and occurrence as the periodontal pocket deepens. Aggregatibacter actinomycetemcomitans serotype b, which is strongly associated with aggressive forms of periodontitis, appears to be an “outlier” (i.e., not placed into any grouping or complex, but very virulent just the same).
Other groups of periodontal biofilm bacteria that form the Blue, Yellow, Green and Purple Complexes primarily consist of tooth surface colonizers including Streptococcus, Actinomyces and Capnocytophaga species. The Red and Orange Complex bacteria, on the other hand, mostly colonize nearer to epithelial surfaces of the pocket wall. Certain strains (subtype of a microorganism) of the most virulent organisms, Porphyromonas gingivalis, Tannerella forsythis, Aggregatibacter actinomycetemcomitans Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, and Eikenella corrodens have also been shown to invade epithelial cells. This is a characteristic that allows the microorganism to evade the immune system.
Not all plaque-induced inflammatory lesions progress from gingivitis to periodontitis. A healthy immune response will protect the host by eliminating the noxious stimuli through coordinated response of the innate and acquired immune system. Lesions that do progress are the result of a heightened inflammatory response in a susceptible host. This response may be related to a variety of factors including: 1) the type and virulence of the bacteria in the plaque biofilm; 2) host immune defects that are genetically determined or acquired, such as in the Acquired Immune Deficiency Syndrome (AIDS); 3) decreased immune function resulting from medically related conditions (e.g., diabetes, leukemia and autoimmune diseases); 4) social habits such as drug and alcohol abuse and smoking; and 5) environmental factors such as stress and exposure to toxins.
In order to better understand the complex role of the innate and acquired immune system in the initiation and progression of periodontal disease, models of disease will be presented which utilize the four stages in the pathogenesis of inflammatory periodontal disease originally described by Page and Schroeder, Laboratory Investigation, 1976.