Microbial etiological agents of destructive periodontal diseases

The bacteria of periodontal diseases

Question Set 1. What are the important destructive mechanisms in periodontal diseases? 2. What are the important protective mechanisms in periodontal diseases? 3. What are the important genetic factors and what is the state-of-the art relative to assessing these genetic factors in periodontal diseases? 4. What do we know about the mechanism of action of possible risk factors, such as smoking and diabetes on the host? 5. What is the evidence that host modulating agents will be effective in prevention or treatment ofperiodontal diseases?

Periodontal diseases: pathogenesis.

Regulation of the immune response by prostaglandins.

Of all the arachidonic acid metabolites, only prostaglandin E (PGE) has been shown to have a clear role in the regulation of cellular and humoral immune responses. In cellular immune responses such as T cell proliferation, lymphokine production, and cytotoxicity, PGE usually acts as a feedback inhibor of the response. This is also true of macrophage and natural killer cytotoxicity. In some instances PGE is responsible for cellular activation rather than inhibition. This is clearest in the control of humoral immunity, where PGE production is a necessary component in the generation of some type of T suppressor cells. Disturbances in immune function found in several human conditions and diseases have been linked to changes in PGE mediated immunoregulation. Either increased production of PGE or increased sensitivity to PGE results in depressed cellular immunity. Conversely drugs which inhibit PGE production act as stimulants of cellular immune functionin vitro andin vivo.

Regulation of the immune response by prostaglandins

Five cases are reported of periodontitis affecting the deciduous teeth in young children. The purpose of the report is to define prepubertal periodontitis as a clinical entity, establish diagnostic criteria, demonstrate clinical, radiographic, and historical features, document progression, and explore methods of treatment. The disease occurs in localized and generalized forms. In the localized form, either few teeth or many may be affected. The onset appears to be around the age of 4 years or before. The gingival tissue manifests only minor inflammation, if any, and microbial plaque is minimal. Alveolar bone destruction proceeds more rapidly than in adults or teenagers with periodontitis, but much slower than in individuals with generalized prepubertal periodontitis. In some cases, otitis media and upper respiratory infections are also present, although these are not life-threatening. The progress of the disease can be halted, so far as is known, by curettage coupled with antibiotic therapy and improved t...

Prepubertal periodontitis. I. Definition of a clinical disease entity.

The prevalence and quantity of mycoplasmata in the gingival sulcus area of periodontally diseased and periodontally healthy subjects was tested. Mycoplasma salivarium was the predominant sulcular species and occurred in a significantly higher percentage of diseased subjects than healthy subjects (p<.0005) (86.7 % vs 31.8 %). When mycoplasmata were present in the sulcus their concentration was usually 106–107 per gram of fluid whereas the concentration in saliva was approximately 100 to 1000 fold less. Therefore M. salivarium appears to be primarily a sulcular organism. M. salivarium may be part of the complex plaque which appears to produce gingivitis.

Mycoplasma salivarium in human gingival sulci.

Biochemical alterations in the connective tissue matrix are a common feature of many diseases, and they account in major part for their functional impairment. Such alterations are especially important in acute and chronic inflammatory diseases where they may take the form of degradation of matrix components or their excessive accumulation leading to fibrosis. Although a wealth of morphologic information is available, very little is known about these changes at the biochemical level. Using human gingival tissue as a model, we have carried out studies aimed at assessing the effects of chronic inflammation on the collagen isotypes comprising the connective tissue matrix. Tissue obtained from patients undergoing surgical treatment for periodontitis was separated on the basis of clinical features into healthy and inflamed portions. After confirming the inflammatory status of each specimen histologically, each set of tissue pairs was extracted at 4 degrees C in 0.5 M acetic acid containing 1 mg/ml of pepsin, and the extracted collagens were fractionated with NaCl. Alpha chains were separated by polyacrylamide slab gel electrophoresis, and methods devised for their quantitation. The results showed that the proportions of type I and III collagens present in normal and inflamed tissues did not differ significantly. In contrast, the type V collagen, which accounted for 0.1 to 1.3% of the total collagens present in normal tissue, was increased by 2- to 9-fold in the chronically inflamed tissue. Because of the unique binding and connecting role type V collagen is thought to play, this alteration may have major pathologic and functional significance.

The effect of chronic inflammation on the composition of collagen types in human connective tissue.

Gingivitis and periodontitis account for more than 95% of all inflammatory diseases of the tissues surrounding the teeth, comprising the principal cause of tooth loss in adults. Gingivitis is a relatively innocuous inflammation of the gums, with associated bleeding and exudation. Gingivitis may convert to periodontitis, a destructive aggressive disease with resorption of alveolar bone, destruction of collagen with fibrosis, and formation of deep pockets around the necks of the teeth. Gingivitis and periodontitis are caused by microorganisms populating the gingival sulcus and periodontal pocket. Treatment is directed toward arresting the progress of the disease through debridement and stabilization of the teeth. Toothbrushing and other measures by which the teeth are mechanically cleaned remain the most effective way to control plaque accumulation and periodontal disease.

Chronic inflammatory gingival and periodontal disease.

Twenty-eight patients diagnosed as having rapidly progressive periodontitis (RPP) were enrolled in a study in which samples of subgingival microflora were harvested from test teeth and assayed for the presence of Porphyromonas gingivalis, and GCF collected and analyzed by ELISA for specific antibody for P. gingivalis. Clinical conditions were measured and recorded, and treatment by scaling and root planing provided at baseline and at 3, 6, 9, and 12 months. Reduction in pocket depth, stabilization of attachment level, and resolution of inflammation were comparable to previously reported values. By 3 months, mean and median specific antibody concentration had decreased, and continued to decrease through 12 months. The proportion of samples in which specific antibody was not detectable increased from 27% at baseline to 73% at month 12. GCF samples from sites at which P. gingivalis was present had greater than 2-fold higher median specific antibody than samples from P. gingivalis-negative sites. At baseline, specific antibody titer of 30-second GCF samples positively correlated with pocket depth, and GCF volume significantly correlated with antibody titer and concentration, and with pocket depth. In addition, change in specific antibody titer of 30-second samples from baseline to both 6 and 12 months correlated positively with pocket depths. Thus sites infected by P. gingivalis manifested high levels of specific antibody, and levels were related to clinical status. Following treatment, antibody levels decreased significantly as pocket depths decreased, attachment levels stabilized, and inflammation resolved.

L. David Engel

Papers

Prepubertal periodontitis. I. Definition of a clinical disease entity.

Mycoplasma salivarium in human gingival sulci.

The effect of chronic inflammation on the composition of collagen types in human connective tissue.

Chronic inflammatory gingival and periodontal disease.

Effects of Treatment on Antibody Titer to Porphyromonas gingivalis in Gingival Crevicular Fluid of Patients With Rapidly Progressive Periodontitis