All new patients commencing supportive periodontal therapy (periodontal maintenance) after treatment in a specialist periodontal practice from 1983 to 1986 were identified from practice records. Based on their compliance with the recommended schedule of visits, the patients were classified as either compliant or non-compliant. The results indicated that there were no significant differences between compliant and non-compliant patients with regards to age, sex, number of missing teeth, plaque score, or periodontal disease severity. More non-compliant patients than compliant patients were smokers (P less than 0.05). By contrast, more compliant patients were covered by private dental insurance (P less than 0.01) and more had periodontal surgery during treatment (P less than 0.001). Only 36% of the initial patient sample was found to be compliant at the end of 1989, with the greatest patient loss in the first year of supportive periodontal therapy of about 42%. The annual attrition rate decreased in subsequent years to average about 10% of those remaining in each year, indicating that a patient is more likely to remain compliant if he or she attends for at least 1 year of supportive periodontal treatment. Non-compliant patients were sent a questionnaire seeking reasons for their non-compliance. Forty percent of the questionnaires were returned. The most common reason given for non-compliance was that a general dental practitioner was attending to the patient's periodontal treatment needs. Many considered supportive periodontal therapy to be too expensive, while a significant proportion considered that they no longer required treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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The antimicrobial effects of subgingival chlorhexidine (CH) irrigations on the pathogenic flora in advanced periodontal lesions were assessed. Changes in the patterns of colonization within the subgingival sites were monitored by differential dark-field microscopy, in 16 patients, over a period of 10 weeks. In addition, changes in the clinical parameters of the diseased sites were also monitored. Initial base-line evaluations were made for both the clinical and microbiological parameters. 4 sites of moderate to advanced periodontal disease were selected in each patient. These were randomly irrigated with a single dose of either 0.2% CH gel, 0.2% CH solution, or physiological saline, while 1 site was left as a control. The patients were seen weekly, until the 5th week, then at the 7th and 10th weeks. At each appointment, a microbiological sample was taken from the subgingival region of each site, together with an assessment of the clinical indices. Results indicated that a single irrigation of an 0.2% solution of CH or 0.2% CH gel had a marked effect in decreasing the % of spirochaetes and, to some extent, motile bacteria. There was a concomitant shift in colonization to cocci, fusiform and filamentous organisms in pockets that were irrigated; this coincided with a reduction in the % of bleeding sites. Various patterns of colonization were observed which have been described and may assist in differential dark field (DDF) monitoring of lesions. Bleeding on blunt probing was found to be correlated with a flora dominated by spirochaetes. No other correlations were found over the 10-week period between the other parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

After gingival health had been achieved in four subjects they were instructed to cease all oral hygiene measures. At 0, 8 and 21 days Plaque and Gingival Indices were recorded and gingival biopsies were removed from the buccal aspect of a first molar. Frozen sections of the gingival oral epithelium were stained for ATPase and 5'-nucleotidase to determine the number of Langerhans cells in a defined cross-sectional area. It was found that, as plaque accumulated, there was a statistically significant increase in the number of Langerhans cells in oral epithelium, particularly in the stratum spinosum. These results indicate that dental plaque can elicit a response in Langerhans cells located in the oral epithelium of the gingiva.

The relationship between the gingival inflammation and plaque scores of patients who had received kidney transplants and were taking immunosuppressive drugs to combat rejection pheomena was compared with data from a control group. Equivalent plaque scores were associated with less gingival inflammation in the patients taking the immunosuppressive drugs. While there was no signficant difference between the plaque scores of the two groups the control group displayed signficantly more gingival inflammation. The implications of these results with respect to possible etiological mechanisms operating in periodontal disease are discussed.

Epithelial Langerhans cells in samples of healthy and diseased gingival tissue were studied using ATPase histochemistry and the monoclonal antibodies OKT6 and anti HLA‐DR. In healthy gingiva Langerhans cells were seen in both oral and sulcular epithelium; they were generally positioned in the basal layers. No Langerhans cells were seen in junctional epithelium. In diseased tissue there was a large increase in the number of Langerhans cells in both oral and sulcular epithelium with many more being situated in the stratum spinosum. There was an increase in the expression of the Class 2 antigen, HLA‐DR, and morphological polarization occurred with dendrites preferentially orientated towards the surface. No Langerhans cells were seen in the pocket lining epithelium of periodontally diseased gingiva.

Changes occurring in a population of Langerhans cells (LC) were investigated using human gingival epithelium maintained in organ culture. The enzyme adenosine 5′‐triphosphatase together with the surface antigens HLA‐DR and T6 were used to identify and quqntitate these cells. An exponential fall in the expression of each of these markers was seen to occur with increasing incubation lime, suggesting that a true loss of these cells is in fact occurring. HLA‐DR antigen is shed from LC at a rate significantly greater than thai al which LC are lost. A mathematical model which simulates the behaviour of LC within organ culture is presented, and several implications and possible explanations proposed.

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