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In this study we evaluated the traditional view that the severity of periodontal disease varies between populations in that African and Asian populations are more severely affected than other populations. Our data on periodontal destruction in two random samples of a Kenyan and a Chinese adult population were recalculated to conform with the methods of examination and data presentation utilized in each of 6 other studies of attachment loss levels in different populations. The adult Kenyan and the adult Chinese group, who had very poor oral hygiene conditions and massive gingival inflammation, had attachment loss levels which were quite similar to those in a Japanese population (31), in a Norwegian population (27) and in a New Mexico group of adults (30). Attachment losses were similar in a population of young US adults (26) aged between 35 and 60 years relative to the corresponding Kenyan and Chinese groups while young US citizens had higher and elderly US citizens had lower mean attachment levels than either Kenyans and Chinese. Higher attachment loss levels beyond the age of 27 years were reported for a population of Sri Lankan Tamil tea workers (27) and across all ages in two South Pacific island populations (29). Overall, the analysis indicates that the periodontal attachment loss profiles may differ between populations, but that these differences do not conform with the traditional generalization that African and Asian populations suffer more severe periodontal breakdown than other populations.

This study investigates the relationship between CPITN findings and the prevalence and severity of periodontal attachment loss in a rural Kenyan population comprising 1131 persons aged 15-65 years. All persons were examined for calculus, gingival bleeding, pocket depths and attachment loss levels on 4 sites of each tooth present. Recordings of bleeding, calculus and pocket depths were used to compute CPITN scores based on the 10 index teeth originally proposed, and these CPITN scores were subsequently related to the attachment loss findings derived from the full-mouth assessment. In most cases, persons with a CPITN score < or = 1 did not have attachment loss > or = 4 mm. However, among 40+ year-old persons with CPITN score 2 over 90% had attachment loss > or = 4 mm and over 50% of the 50+ year-olds with CPITN score 3 had attachment loss > or = 6 mm. Less than 20% of the 15-29 year-olds with CPITN score 3 had attachment loss > or = 6 mm, and usually the attachment loss levels ranged between 0 and 3 mm. Beyond the age of 35 years over 10% of the sextants with CPITN score 0 had attachment loss > or = 4 mm. Below the age of 35 years more than one third of all sextants with CPITN score 3 had attachment loss levels < or = 3 mm. Thus, the CPITN findings overestimate both prevalence and severity of periodontal attachment loss among the younger age groups and underestimate these parameters among elderly subject.

Aqueous extracts from 5 plants used widely in Kenya as chewing sticks (mswaki) for the control of oral hygiene were tested for their ability to inhibit extracellular peptidase and glycosidase enzyme activities produced by the periodontopathic bacteria Porphyromonas gingivalis (formerly Bacteroides gingivalis), Bacteroides intermedius and Treponema denticola. The plants studied were Rhus natalensis, Cupressus hisitanica, Sida cordifolia, Olea africana and Euclea divinorum. Protease activities, including glycylprolyl dipeptidase and trypsin-like activities of P. gingivalis, chymotrypsin-like and glycylprolyl dipeptidase activities of B. intermedius and the trypsin-like activity of T. denticola, were particularly affected by extracts from Rhus natalensis and Euclea divinorum. Glycosidase activities were generally less affected with the notable exceptions of the inhibition of beta-mannosidase activity of P. gingivalis by all extracts and the inhibition of neuraminidase activity of T. denticola by Rhus natalensis and Euclea divinorum. Generally, these same proteolytic and glycosidic activities were inhibited by tannic acid and to lesser extents by gallic acid and gallic acid methyl ester. An inhibitory component, present in all extracts, exhibited physical and chemical properties identical to those of tannic acid. The inhibition of these enzyme activities is likely to reduce the virulence of these periodontophathic bacteria and to reduce the rate of dental plaque formation.

The aim of the study was to assess the occurrence of some putative periodonto-pathogens in "test" and "control" sites in "diseased" and "non-diseased" persons, respectively, from an adult rural Kenyan population exhibiting poor oral hygiene and widespread loss of attachment (LA). 14 persons (less than 35 years) were assigned to a "diseased" category on the basis of at least 4 sites with LA greater than or equal to 4 mm; at least 5 mm LA and a pocket greater than or equal to 4 mm interproximally in a lower incisor ("test" site): and less than 2 mm LA and no pocket greater than or equal to 4 mm distal to a lower canine or mesial to a lower first premolar ("control" site). Age-matched "non-diseased" persons were identified on the basis of no sites with LA greater than 2 mm and no pockets greater than or equal to 4 mm associated with LA. Paperpoint samples from test and control sites as well as a scraping sample from the dorsum of tongue were examined for presence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides intermedius, B. melaninogenicus group, Capnocytophaga, Selenomonas spp., and Wolinella recta. P. gingivalis was found in 79% of test sites and 36% of control sites in "diseased" persons, and in 18% and 35% of test and control sites, respectively, in "non-diseased" persons. "No other bacterial group discriminated significantly between test and control sites or between diseased and non-diseased subjects. The surprisingly high occurrence of P. gingivalis in non-diseased subjects, both subgingivally and on tongue, indicates that deep periodontal pockets are not prerequisite ecological environments for P. gingivalis establishment.

This paper reports the findings of an experimental gingivitis study conducted in smokers and non-smokers. 33 volunteers were examined and underwent prophylaxis during a period of 4 weeks. 28 subjects who showed a plaque index less than 0.20 on all prophylaxis occasions were permitted to continue in the study. Subjects then had their gingival status recorded, had their teeth polished and were requested to abstain from all oral hygiene measures for the following 21 days. After 5 days, 10 days and 21 days, plaque and gingival status were recorded using the criteria of the plaque index and gingival index. After the examination on day 21, the teeth were polished and oral hygiene was re-instituted. Following 2 weeks of supervised oral hygiene, recordings of plaque and gingival status were performed. At the initial examination, there was no difference between the clinical assessment of plaque and gingival status in smokers and non-smokers. Similar amounts of plaque accumulated in the 2 groups during the period of no oral hygiene, but smokers exhibited less gingival inflammation assessed clinically than non-smokers. This difference occurred as a result of an apparently lowered incidence rate and a markedly higher recovery rate in smokers compared to non-smokers. These findings may indicate that smokers for reasons yet unknown have a reduced capacity to mount and maintain an effective defense reaction to a given plaque challenge.

This study comprised 1131 persons who constitute a stratified random sample of the entire population aged 15-65 years in Machakos District, Kenya. Each person was examined for tooth mobility, plaque, calculus, gingival bleeding, loss of attachment and pocket depth on the mesial, buccal, distal and lingual surface of each tooth. The oral hygiene was poor with plaque on 75-95% and calculus on 10-85% of the surfaces depending on age. Irrespective of age, pockets greater than or equal to 4 mm was seen on less than 20% of the surfaces, whereas 10-85% of the surfaces had loss of attachment greater than or equal to 1 mm. The proportion of surfaces per individual with loss of attachment greater than or equal to 4 mm or greater than or equal to 7 mm, and pocket depths greater than or equal to 4 mm or greater than or equal to 7 mm, respectively, showed a pronounced skewed distribution, indicating that in each age group, a subfraction of individuals is responsible for a substantial proportion of the total periodontal breakdown. The individual teeth within the dentition also showed a marked variation in the severity of periodontal breakdown. Our findings provide additional evidence that destructive periodontal disease should not be perceived as an inevitable consequence of gingivitis which ultimately leads to considerable tooth loss. A more specific characterization of the features of periodontal breakdown in those individuals who seem particularly susceptible is therefore warranted.

In Nairobi (Kenya) 334 women prostitutes of whom 80.5% were HIV-1 positive, were examined for oral mucosal lesions; 15.6% of seropositive, and 4.6% of seronegative, women had oral mucosal lesions, predominantly oral candidiasis. In the seropositives, 8.6% had erythematous, 1.1% had hyperplastic candidiasis, and 0.4% had hairly leukoplakia as the only oral lesions; 0.4% had a combination of erythematous and hyperplastic candidiasis, and 1.5% had combinations of pseudomembranous and erythematous candidiasis in the presence of hairly leukoplakia. Of the 211 seropositive women for whom we knew the first date on which a positive serologic test was obtained, the likelihood of developing an oral mucosal lesion was found to be dependent on the duration of seropositivity. The low incidence of oral mucosal lesions in this population may be due to the relatively recent acquisition of HIV-1 infection.

A microbiological study was performed of the subgingival plaque on 2 sites in each of 20 adults originating from a rural area 40 km outside Nairobi, Kenya. The recovery rate of B. gingivalis was 70%, of B. intermedius 100% and of A. actinomycetemcomitans 40% of the subjects, and 50%, 90% and 28%, respectively, of the sites. The isolated strains exhibited similar biochemical characteristics and antibiotic susceptibility pattern as type strains of these species. The high recovery rate of these 3 bacterial species in adult Kenyans was a rather surprising finding, since pathological pocketing was found only sporadically. Furthermore, the results of 2 methodological approaches tested demonstrated that such microbiological studies can be carried out in countries with limited laboratory facilities.

This paper considers a possible explanation for the occurrence of periodontal breakdown in bursts and remissions. We show that such bursts and remissions, apart from being the result of major biological events, can also be generated by a stationary process of Brownian motion.

This study was conducted in order to investigate the dynamics of the gingival inflammatory status during periods of plaque accumulation and thorough oral hygiene. After a period of prophylaxis, 42 volunteers were asked to abstain from all oral hygiene measures for 2 weeks, whereafter oral hygiene was reinstituted. In the absence of oral hygiene, plaque was found at virtually all sites after 7 days and the number of sites with gingivitis increased simultaneously. A reduction in gingival inflammation occurred subsequent to plaque removal. During phases of both plaque accumulation and thorough oral hygiene, sites were found to convert from non-inflamed to inflamed status concurrently, as in the reverse direction. No association between plaque and gingivitis was revealed. The gingival status of a single site was a poor predictor of its status on the subsequent occasion. The proportion of inflamed sites converting to non-inflamed status was greater than the proportion of non-inflamed sites converting to inflamed status at any time. The estimated incidence rate remained fairly constant during both the plaque accumulation phase and the oral hygiene phase, whereas the estimated recovery rate was considerable lower during the plaque accumulation phase compared to oral hygiene phase. The clinical appearance is the outcome of the dynamics between these rates. The steady-state prevalences derived from the estimated "incidence" and "recovery" rates were quite similar to the actual findings after 14 d of plaque accumulation and the subsequent 10 d of thorough oral hygiene.