Eighty‐five 12–18‐yr‐old adolescents suffering from insulin‐dependent diabetes mellitus (IDDM) and their healthy age‐ and sex‐matched controls were investigated with respect to dental caries, salivary flow rate, pH and buffering capacity of saliva, counts for lactobacilli and mutans streptococci, and salivary glucose content. The diabetics had their disease well controlled according to the HbA1 levels. The results showed no statistically significant difference between diabetics and controls in DMF and DMFS indexes and the number of initial caries lesions. Mean number of initial caries lesions was 3.2 in diabetics, 2.3 in controls. Mean stimulated salivary flow rate was 1.2 ml/min in the patients, 1.4 ml/min in the controls. The pH and buffering capacity values were 7.3 and 4.8 in the patients, 7.4 and 5.1 in the controls, respectively. High counts of mutans streptococci (> 106 CFU/ml) and lactobacilli (> 105 CFU/ml) were observed more often, but not significantly so, among the patients than in the controls. The mean concentration of glucose in saliva was 10.3 μg/ml in the patients, 9.7 lμg/ml in the controls. Thus, if the patients' IDDM is well controlled, their salivary and caries data does not differ from that of healthy controls.

The clinical trial was primarily designed to determine to what extent the stiffness of toothbrush bristles and the abrasiveness of dentifrices influence the degree of gingival erosion. Further, the plaque removing effectiveness of the toothbrushes and dentifrices tested was evaluated. 24 dental hygienist students with clinically healthy gingivae volunteered for the study. A "soft" toothbrush with a bristle thickness of 0.15 mm, a "hard" toothbrush with a bristle thickness of 0.23 mm and 2 dentifrices of different abrasiveness were used for the experiment. The 2 brushes were also used without a dentifrice. Prior to each examination the teeth of the test subjects were brushed by the same dental hygienist. Evident signs of laceration or.ulceration at any 1 of 4 gingival aspects of each tooth were recorded as brushing injuries. The teeth were then stained with basic fuchsin and the amount of remaining plaque was assessed according to the PLQ Index (Bay & Ainamo 1974). The use of the hard brush resulted in lower plaque scores and, at the same time, more gingival erosions than the use of the soft brush. With both brushes a significantly greater number of lesions was recorded after use of an abrasive powder than when no dentifrice was employed. The difference in the amount of erosions occurring when utilizing either brush, without a dentifrice or with a moderately abrasive toothpaste, was not, however, found to be statistically significant. When assessed separately for the 2 brushes, the slight tendency towards lower PLQ scores with increasing abrasiveness of the dentifrice was not considered statistically significant. The study showed that the modes decrease observed in mean PLQ scores with increasing stiffness of the toothbrush bristles and with increasing abrasiveness of the dentifrice is accompanied by increased damage caused to the soft gingival tissues.

This article reviews the current knowledge of the sources, function and interactions of proteolytic enzymes and their inhibitors in chronic inflammatory periodontal disease. Proteolytic tissue degradation is a typical phenomenon in chronic inflammatory periodontal disease. The proteolytic enzymes can be both host- and bacteria-derived. The proteases of the inflammatory cells are aimed for digestion of bacteria, enhanced locomotion through connective tissue, demarcation of the site of infection and tissue remodeling. Uncontrolled release of proteases in inflammation causes self-digestion and tissue destruction. The potential of the bacterial proteases in degradation of connective tissue is not yet known. Biochemical and immunologic mediators of inflammation are released by proteolytic reactions. Immunoglobulin-cleaving proteases present a specific mechanism in perturbation of host defenses. The 2 main protease inhibitors in serum, alpha-1-antitrypsin and alpha-2-macroglobulin, are also present in the gingival tissue fluid guarding the function of proteases. It has been suggested, although not confirmed, that deficiency in serum protease inhibiting capacity could be correlated with susceptibility to periodontal disease. Mucous secretions contain local low molecular weight protease inhibitors, but their possible rôle in saliva is not known. Bacteria-derived, antiproteolytic short peptides may prove to be useful in pharmacological control of tissue destruction at inflammatory sites.

The periodontal status of 85 12-18 year-old Finnish adolescents with insulin-dependent diabetes mellitus (IDDM) and their paired, age- and sex-matched healthy controls was assessed clinically and radiographically. The clinical examination consisted of plaque index, gingival index (GI), retentive calculus index, WHO community periodontal index of treatment needs, number of pockets greater than or equal to 4 mm and number of surfaces bleeding after probing. Alveolar bone loss was measured interproximally from the first molars in bite-wing radiographs (all subjects) and from the first incisors in periapical X-rays (patients only). The results show that in spite of similar plaque scores, the patients had higher GI scores and more surfaces bleeding after probing. No differences were found in the number of greater than or equal to 4 mm pockets or radiographical bone loss in the first molars.

The concentration of salivary IgG and IgA and the levels of salivary IgG and IgA antibodies to Actinobacillus actinomycetemcomitans Y4 were measured by ELISA in 205 persons including patients with juvenile and adult periodontitis as well as healthy subjects. Compared to the concentration observed in subjects with a healthy periodontium, a significantly increased concentration of salivary IgG was found in 34% of the patients with moderate adult periodontitis and in 57% of the patients with severe adult periodontitis. The level of salivary IgA was less influenced by the periodontal condition. The level of salivary IgG antibody to A. actinomycetemcomitans was significantly elevated in 55% of the patients with untreated juvenile periodontitis and in 28% of the patients treated for JP. 28% of the patients with adult periodontitis had a significantly elevated level of IgG antibody to A. actinomycetemcomitans Y4. Significantly elevated levels of IgA antibody to this bacteria was found less frequently, 27% in untreated JP, 20% in treated JP and 17% in adult periodontitis.