Periodontal diseases have been recognized and treated for at least 5000 years. Clinicians have recognized for many years that there are apparent differences in the presentation of periodontal diseases and have attempted to classify these diseases. Systems of classifications of disease have arisen allowing clinicians to develop structures which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patients' diseases. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Common systems of classification also allow effective communication between health care professionals using a common language. Early attempts at classification were made on the basis of the clinical characteristics of the diseases or on theories of their aetiology. These attempts were unsupported by any evidence base. As scientific knowledge expanded, conventional pathology formed the basis of classification. More recently, this has been followed by systems of classification based upon our knowledge of the various periodontal infections and the host response to them. Classification of periodontal diseases has, however, proved problematic. Over much of the last century clinicians and researchers have grappled with the problem and have assembled periodically to review or develop the classification of the various forms of periodontal disease as research has expanded our knowledge of these diseases. This has resulted in frequent revisions and changes. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It is expected that systems of classification will change over time. This review examines the past and present classifications of the periodontal diseases.Keywords: Diagnosis, classification, periodontal diseases, gingivitis, periodontitis.Abbreviations and acronyms: AST = aspartate aminotransferase; CAL = clinical loss of attachment; GCF = gingival crevicular fluid; LJP = localized juvenile periodontitis; NUG = necrotizing ulcerative gingivitis; NUP = necrotizing ulcerative peridontitis.

Patients with untreated adult periodontitis are at greater risk of bacteremia due to periodontal probing than patients with chronic gingivitis. For individuals at risk of infective endocarditis, radiographic assessment prior to periodontal probing would be advisable to identify those with periodontitis so that appropriate antibiotic prophylaxis can be provided.

Bacteraemia of oral origin may result in infective endocarditis in susceptible individuals. The aim of this pilot study was to investigate the occurrence of bacteraemia due to periodontal probing. Thirty patients (15 male, 15 female; mean age 42.7 years) with untreated periodontitis were investigated. All were free of significant medical disorders and none had taken antibiotics in the previous month. Prior to and immediately following periodontal probing, 20 mL of venous blood were obtained from each patient and inoculated into aerobic and anaerobic blood culture bottles and incubated. Negative bottles were monitored continuously for three weeks before being discarded. Periodontal probing consisted of measuring pockets at six points around each tooth and recording the presence or absence of bleeding. A positive bacteraemia was recorded for three of the patients prior to probing. One patient exhibited Prevotella species whilst two exhibited skin commensals. Following probing, 13 patients (43 per cent) exhibited bacteraemia of oral origin. Viridans streptococci were the most common isolates (45 per cent). No significant correlations were found between bacteraemia and the severity of periodontitis or extent of bleeding on probing. The results indicate that periodontal probing can cause bacteraemia in patients with periodontitis. It would be advisable for patients considered at risk of developing infective endocarditis to receive antibiotic

Rinsing with 7.5% povidone-iodine reduced the incidence and magnitude of bacteraemia and eliminated viridans streptococci from such bacteraemia. Povidone-iodine rinsing may be helpful for ultrasonic scaling of gingivitis patients at risk of infective endocarditis.

Previous investigations have reported increased plaque formation in the presence of gingival inflammation as compared with gingival health. In these investigations, experimental gingivitis has been induced by total abolition of oral hygiene such that increased levels of salivary bacteria could contribute to the increased plaque formation. In the present study, experimental gingivitis was localized to 2 selected teeth whilst maintaining normal oral hygiene measures in the rest of the mouth. The aim of this study was to investigate whether the mass of plaque accumulating in a 3-day period is influenced by the inflammatory status of the adjacent gingival margins. Following scaling, prophylaxis and a period of optimal hygiene to establish gingival health, "plaque-guards" were worn during routine oral hygiene performance to prevent any cleaning on the buccal surfaces of teeth 14 and 15 from days 0 to 3. On day 3, accumulated plaque was removed from a 1.5 mm zone on the buccal surfaces of 14 and 15 adjacent to the gingival margins and weighed immediately. Subjects continued to wear their plaque-guards during oral hygiene until day 14 to induce experimental gingivitis around the experimental teeth. At day 14, all plaque was cleaned from the buccal surfaces of the experimental teeth and the mass of plaque accumulating over the next 3 days weighed on day 17. Comparison of plaque weights showed that the wet-weight of 3 day-old plaque was higher in the presence of experimental gingivitis than in the presence of gingival health (p = 0.02). This observation suggests that the inflammatory status of the marginal gingiva has an important effect on early, supragingival plaque accumulation.