The role of smoking as a risk factor for Periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of Periodontitis was markedly higher among current smokers compared with never smokers (P < 0.005) in both the 19 to 30 year-old (46% vs. 12%) and 31 to 40 year-old groups (88% vs. 33%). The subject mean percent of sites with gingival pocket depth >4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the Periodontitis in the 19 to 30 year old group and 32% of the Periodontitis in the 31 to 40 year old group, is associated with smoking. These findings suggest that smokers are a high risk group for Periodontitis, and that smoking may be the single most important environmental risk factor for Periodontitis. / Periodontol 1993; 64:16-23.
This case‐control study compares the prevalence of cigarette smoking among patients in a periodontal practice (cases) with that of patients in referring general dental practices (controls). Smoking histories of patients (age ≥25 years) in a periodontal practice and five general dental practices were obtained by questionnaire. From the general practices, only patients reporting negative histories for Periodontitis were studied. Periodontal status of the periodontal practice patients was based on bone loss from full mouth radiographic surveys and gingival pocket depths. Patients were stratified by age (25 to 40, 41 to 55, and >55 years) and sex. The combined frequency of current or former cigarette smoking reported by 196 periodontal practice patients with moderate or advanced Periodontitis (M‐A perio group) was higher than that reported by 209 general dental practice patients (gen prac group) in all age and sex catagories. The age and sex adjusted summary odds ratio for a positive smoking history among M‐A perio subjects relative to gen prac subjects was 2.6 (P <0.001). Separate corresponding odds ratios (age and sex adjusted) for current smoking versus never smoking in the two groups were 3.3 (P <0.001) and for former smoking versus never smoking 2.1 (P <0.004). Among current smokers, patients in the M‐A perio group reported heavy smoking (> 10 cigarettes/day) relatively more often than control subjects (adjusted R.O. = 5.7; P <0.001). In the M‐A perio group the frequency of current smoking increased with disease severity. These associations add to the accumulating evidence suggesting that both current and former smokers are at increased risk for Periodontitis, and that cigarette smoking is a major risk factor for Periodontitis. J Periodontol 1992;63:100‐106.
A large-scale retrospective study was undertaken to determine the incidence of clinical infection after periodontal surgery and the effectiveness of prophylactic antibiotic therapy in preventing postoperative infection. All second-year postgraduate students reviewed their patient records and completed a questionnaire. Eight infections were found in 884 operations performed without antibiotics, while one infection was found in 43 operations performed with antibiotics. Of 268 operations involving osseous surgery, six infections were noted while two infections were observed following 336 operations involving flap surgery without osteoplasty or ostectomy. The data indicated that the incidence of infection after periodontal surgery is very low in patients treated with or without antibiotics. It was concluded that unless there is a medical indication, there is no justification for using prophylactic antibiotic therapy to prevent infection following periodontal surgery.
A group of poorly‐controlled insulin dependent diabetes mellitus (IDDM) patients were examined in a cross‐sectional design for total microbial levels, microbial incidence, and the percent levels of selected periodontal microorganisms. These organisms were selected on the basis of prior reports that associated them with either periodontal disease or health. One periodontally‐healthy and one periodontally‐diseased site were examined in each IDDM patient. Increased levels of the periodontal pathogens Prevotella intermedia, P. melaninogenica spp., Bacteroides gracilis, Eikenella corrodens, Fusobacterium nucleatum and Campylobacter rectus (formerly Wolinella recta) were found at the periodontal diseased sites. Increased prevalence of the organisms P. intermedia, P. melaninogenica spp., and C. rectus were found at the diseased sites. A significantly higher percentage of P. intermedia was found at the sites exhibiting deep pockets and attachment loss. J Periodontol 1992; 63:274–279.
The role of Igh-linked loci in the generation and expression of T cell help for antibody responses to sheep erythrocytes (SRBC) was investigated. The production of IgM, IgG3, IgG1, IgG2b, and IgG2a antibody to SRBC was shown to be T cell dependent. The Igh-congenic mouse pair CBA/Tufts (Ighj) and CBA.Ighb gave equivalent responses to SRBC. CBA.nude mice (Ighj) supplemented with peripheral T cells of either Ighj or Ighb genotype produced equivalent, high responses. Therefore, T cell-B cell mismatching for the Igh haplotype is not in itself a bar to the generation or expression of help. In contrast, T cells primed in an environment that lacks Ighj-linked products are inefficient helpers for Ighj B cells. These results suggest that antigen-primed B cells or their products prime a set of T cells that can help B cells that bear matching, Igh-linked gene products.
Studies have been carried out on the genetic control of the expression of individual Ig classes in the responses of A/J (A) and C57BL/6J (B6) mice to sheep red blood cells (SRBC). An isotopic anti-immunoglobulin test employing Ig class-specific reagents was used to measure levels of IgM, IgA, IgG1, IgG2a, IgG2b and IgG3 anti-SRBC antibodies in sera of hyperimmunized mice. Compared with B6 mice, A mice are low IgM and IgA responders but high responders with respect to all IgG subclasses. In (B6 X A)F1 mice low responsiveness was dominant for all Ig classes indicating that IgM and IgA responses are controlled by genes different from those which control IgG subclass responses. Analysis of the responses of [(B6 X A)F1 X A] and [(B10.A X A)F1 X A] backcross mice indicates multigenic control of IgG subclass responses. Expression of IgG2a and IgG3 responses appear to be regulated largely by single genes whose action is modified by genes at other loci; control of IgG1 and IgG2b is, clearly, polygenic with no evidence for major control by any single gene. The magnitude of all IgG subclass responses appears to be regulated by a gene(s) associated with or linked to the IgCH locus. Analysis of the responses of H-2-congenic mice shows that major histocompatibility genes do not have a strong influence on the patterns on IgM and IgG responses in A or B6 mice. The overall results indicate that while there is some common control of all IgG classes, there is also separate polygenic control of individual Ig classes.
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