Notes: Abstract. This study was undertaken to test the hypothesis that gingival inflammation and dental calculus are important determinants of the development and progression of early-onset periodontitis. The study sample included 156 individuals who were 13–20 years old at baseline and who were examined 2× during 6 years to assess the attachment loss, gingival state and the presence of dental calculus. 33 (21%), 62 (40%), and 61 (39%) individuals were classified as having localized, generalized, or incidental EOP, respectively. The results showed an increase in the % of teeth with overt gingivitis and subgingival calculus, and also an increase in the % of teeth showing attachment loss during the 6-year period in ail classification groups. Of teeth with 0–2 mm attachment loss at the beginning of the study and which developed ≥3 mm attachment loss during the following 6 years, there were 2× as many teeth with overt gingival inflammation, and 4× more teeth with subgingival calculus at baseline than teeth without. Gingivitis and subgingival calculus when present at both examinations resulted in a stronger association with the development of new lesions than presence of these variables at baseline. Teeth with gingivitis at baseline had a significantly higher mean attachment loss during 6 years than teeth without gingivitis (p〈0.0001), and teeth with subgingival calculus at baseline had a significantly higher mean attachment loss than teeth without subgingival calculus (p〈0.0001), The presence of gingivitis and subgingival calculus at baseline and 6 years later was associated with the occurrence of even higher disease progression during this period. The association between gingival inflammation and subgingival calculus and the development and progression of attachment loss during the study period in the generalized and the localized EOP groups was significantly higher than the association in the incidental EOP group. In an appreciable % of the sites in all 3 groups, however, the presence of the 2 factors was not associated with attachment loss during 6 years. The results suggest a significant association between gingival inflammation and subgingival calculus and the development and progression of early-onset periodontitis.

Notes: The effects of local applications of a 2.2 mM (0.2 per cent) chlorhexidine gluconate solution on the oral mucous membranes have been evaluated by vital microscopy and histological and enzyme histochemical methods. Chlorhexidine gluconate applied onto intact or dekeratinized hamster cheek-pouch did not induce microvascular disturbances in the underlying connective tissue. On a defective cheek-pouch surface, however, the test solution caused hemolysis, intravascular granulo-cytosis and thrombus formation. These observations indicate that chlorhexidine gluconate does not penetrate the undamaged oral epithelium. Daily application of 2.2 mM chlorhexidine gluconate on the palatal or sublingual mucosa did not induce reactions in the underlying connective tissue. The application of the test solution onto the oral epithelium, however, induced an increase in non-enzymic formazan deposition in the surface layers. These staining reactions, which developed rapidly, did not appear to increase during prolonged administration.

Notes: The purpose of the present study was to examine the effect of chlorhexidine mouthrinses on the oral flora. Four students rinsed, twice daily, with 10 ml of a 0.2 per cent solution of chlorhexidine gluconate, and four students served as controls on a no oral hygiene programme. The number of bacteria in saliva was estimated by a cultural technique and impression preparations were used for the study of the bacteria on the gingiva and tooth surface. The controls showed a 300 per cent increase in bacterial counts during the experiment. In the chlorhexidine group the number of bacteria per ml saliva was reduced by 85 per cent, after 24 hours, reaching a 95 per cent reduction on day 5. An 85–90 per cent reduction was maintained throughout the experimental period. Impression preparations of the gingival area in the controls showed a heavier accummulation of bacteria than in the chlorhexidine group. In addition an increasing bacterial colonization of the tooth surfaces occurred in the controls throughout the experiment, but was never observed in the chlorhexidine group. Although the number of bacteria in saliva was markedly reduced, large numbers still persisted. It, therefore, appears unlikely that the inhibition of plaque formation is primarily the result of a reduction of the salivary flora.

Notes: This study indicates that chlorhexidine gluconate adsorbs to hydroxyapatite, tooth surfaces and salivary mucins and that the adsorbed chlorhexidine is released when the concentration in the environment is low. The possible formation of reservoirs of chlorhexidine on the tooth surface in vivo from which chlorhexidine is slowly released could, therefore, prevent bacterial colonization and the development of dental plaque.

Notes: The purpose of the present study was to determine the number and origin of leukocytes in saliva. Leukocytes were collected from saliva by a modification of the method of Klinkhamer. The-number of leukocytes was found to vary from person to person, and for a given person during the day. There was also a slight individual variation from day to day. Starting with clean teeth and normal gingiva 18 students ceased all oral hygiene measures for a period of 3 weeks. During this time although gingivitis developed and there was a three-fold increase of leukocytes, the number of salivary leukocytes did not reflect the gingival condition in a given subject. To prevent emanation of leukocytes through the gingival crevices, acrylic splints which covered the teeth and 5 mm of the marginal gingiva of the maxilla and mandible were made for 7 persons. The number of leukocytes accumulating under the splints indicated that the majority of salivary leukocytes enter the oral cavity via the crevices.

Notes: A cross sectional study was done in seventy-four beagle dogs from one to twelve years of age. Gingivitis, calculus, plaque, loss of attachment, pocket depth and width of keratinized gingiva were scored and descriptive statistics calculated.Gingivitis differed very little in the maxillary and mandibular incisor and canine regions at differing ages, while it was more severe on the buccal gingiva of premolars and first molars. Calculus scores were highest on the buccal surface of the maxillary P4 followed by the buccal surfaces of the maxillary Ml and mandibular P4. Plaque scores were high for the very young dogs and showed only slightly to moderately higher values with increasing age. The buccal surface of the maxillary P4 had the highest plaque score, followed closely by the buccal surfaces of the maxillary M1 and mandibular P4. Plaque scores were low in the incisor regions and on the lingual surfaces. On the buccal surfaces plaque scores increased from the C to P4, and then decreased in the molar regions.Loss of attachment was minimal for anterior teeth and was greater in the premolar and maxillary M1 regions with older age. The greatest loss occurred on the distal surface of the maxillary P4, the mesial surface of maxillary M1, and distal surface of mandibular P4. The greatest difference existed between younger dogs and those older than six to seven years. Greater pocket depths were not generally proportionate to the greater loss of attachment, since recession accompanied loss of attachment. Pocket formation was found most often at the distal surface of the mandibular P4 in dogs six to seven years of age. The width of keratinized gingiva varied only slightly and inconsistantly with age, except that slightly narrower widths were found at six to seven years of age.Periodontal disease in the beagle dog occurred in specific areas with a high plaque accumulation in young dogs and more gingivitis, calculus formation, and loss of attachment in older animals.

Notes: The present investigation was carried out in order to study some aspects of the clinical, roentgenographical and histopathological alterations of periodontal tissues in dogs which during a 4-year period were allowed freely to accumulate plaque.Twenty inbred Beagle dogs, at the start of the study 10 months of age, were used. During a preparatory period of eight weeks the animals were once weekly subjected to a careful prophylaxis and had their teeth brushed twice daily. At the end of this period the dogs were divided into two groups of ten (test and control). From day zero of experimentation and onwards the teeth of the control dogs were twice daily subjected to meticulous toothbrushing, whereas the teeth of the test dogs were not cleaned. Examinations of the periodontal tissues were performed at days 0, 7, 14, 21, 28 and after 2, 4, 6, 8, 12, 18, 24, 36 and 48 months. Biopsies of different tooth regions were made on day zero and after 6, 12, 18, 24, 36 and 48 months of experiment. In the sections were measured (i) the distance from the cemento-enamel junction (CEJ) to the most apical cells of the dento-gingival epithelium, and (ii) the distance from CEJ to the level of the marginal alveolar bone.The study demonstrated that it is possible in dogs to establish and maintain a normal gingiva simply by eliminating calculus and then subjecting the animals to daily repeated and carefully performed tooth cleanings. Dogs allowed freely to accumulate plaque rapidly developed signs of gingivitis and eventually also clinical, radiographical and histopathological signs of periodontal tissue breakdown. The observations show that at least one type of periodontal disease is induced by factors within the dental plaque.

Notes: The purpose of the present study was to examine if streptococci, isolated from human dental plaque in experimental subjects having practiced 2 years daily oral chlorhexidine hygiene, showed any difference in susceptibility to chlorhexidine compared to plaque streptococci isolated from a control group. The minimal inhibitory concentrations (MIC) of chlorhexidine were determined using the broth dilution test tube method. From an 18 h culture of each strain in brain heart infusion, 0.2 ml were inoculated into 5 ml brain heart infusion with added chlorhexidine to final concentrations of 0, 0.5, 1, 2, 4, 8, 16, 32, and 64 μg per ml. Three months later identical tests were performed. In both tests strains of Streptococcus mutans, Streptococcus milleri and Streptococcus salivarius were found to be the most susceptible to chlorhexidine, showing MIC around 4 μg chlorhexidine per ml. Strains resembling S. milleri appeared slightly less susceptible than strains identified as S. milleri. The majority of the S. sanguis strains had MIC ranging from 8 to 16 μg per ml. This species was slightly more susceptible than a group of streptococci intermediary to S. sanguis and S. mitior, while the susceptibility of the S. mitior strains ranged from 4 to more than 64 μg per ml. A difference in susceptibility to chlorhexidine between strains isolated from the chlorhexidine group and the control group was only observed for S. sanguis. Strains of this species isolated from the chlorhexidine group showed higher MIC than did strains isolated from the control group.

Notes: The purpose of the present study was to examine the influence of two years daily oral use of chlorhexidine (Löe et al. 1976) on the distribution of different streptococcal types in dental plaque. Plaque samples were collected from the molars in 16 persons in the chlorhexi dine group and from 17 control persons having used placebo solution. The samples were homogenized in yeast extract, and dilutions plated on mitis salivarius agar incubated micro aerophilically for 24 hours followed by aerobic storage at room temperature for 24 hours.Colonies of each morphological type present were counted on plates having 30–300 colonies and their number related to the total number. One colony of each type was isolated and identified by biochemical tests. The study showed that 84.8 % of the strains could be classified as S. mutans, S. sanguis, S. mitior, S. milleri, S. salivarius, a group intermediary to S. sanguis and S. mitior, and a group resembling S. milleri, using only five biochemical tests: production of extracellular polysaccharide from sucrose, fermentation of mannitol, raffinose and inulin, and hydrolysis of esculin. In the chlorhexidine group the prevalences of S. sanguis and the group of streptococci intermediary to S. sanguis and S. mitior were higher, and the prevalence of S. milleri plus streptococci resembling S. milleri lower, among the streptococcal flora in dental plaque than those observed in the control group.