Characterization of treponemes isolated from human and non-human primate periodontal pockets

Treponemes were isolated from ligature induced periodontal pockets of non-human primates, and from humans with periodontitis. Approximately 39% of the microscopic count were spirochetes from humans, while 65% of the microscopic microbiota was accounted for by spirochetes from non-human primates. Metabolically, the human treponemal isolates grew on trypticase-yeast extract based media while the non-human primate isolates grew only on pectin, glucuronic or galacturonic acids. The end-products of glucose fermentation by the human treponemes were acetate and propionate, while acetate was produced by the non-human primate treponemes from pectin. All of the human isolates were indole positive, hemolyzed blood, required serum for growth, but did not require thiamine pyrophosphate (TPP). The non-human primate treponemes were indole negative, were inhibited in their growth by blood, grew in the absence of serum, and required TPP for growth. PAGE analysis of whole cell proteins revealed three categories of treponemal isolates: (i) human isolates similar to Treponema denticola ; (ii) human isolates of small size; and (iii) non-human primate isolates similar to the pectinolytic treponemes. Serologically, the human treponemal isolates were similar to T. denticola , while the non-human primate isolates were similar to the pectinolytic treponemes. Four human, 4 non-human primate, and 4 reference treponemes exhibited a Mol% G + C of their DNA of 40.0-43.1. The metabolic differences between the human and non-human primate treponemal isolates may be a reflection of ecological differences in the periodontium of the pathological entities which exist in human and non-human primates.     

IL-1 gene polymorphism and smoking as risk factors for peri-implant bone loss in a well-maintained population

The aim of the present study was (i) to investigate the relation between specific interleukin-1 (IL-1) gene polymorphisms and peri-implant bone loss at osseointegrated ITI(R) dental implants and (ii) to explore the association between these allelic variants of the IL-1 gene complex and peri-implant mucosal inflammation, in both smoking and non-smoking individuals. A sample of 90 consecutive Caucasian patients (aged 33-88 years), treated with at least one ITI-implant participated in this retrospective investigation. Standardized periapical radiographs were taken after prosthetic rehabilitation (133.6 days, SD 136.9 days) and at the time of the re-examination, on average 5.6 years (SD 2.5 years) thereafter. The radiographs were analyzed by a calibrated examiner for changes in peri-implant bone levels. The examiner was blind with respect to clinical parameters and IL-1 status. The distance between the implant shoulder and the first visible bone-implant contact (DIB) at the respective time points were measured using a computerized method. The absolute bone level difference during the years of service (ABL) and the annual bone loss (DeltaBL/year) were calculated for all the implants. Percentages of full mouth bleeding on probing (BOP), as well as of BOP calculated separately for teeth and implants, were determined for all visits and averaged for the entire observation period. Out of the total patient sample, there were 14 heavy smokers (= 20 cigarettes/day), 14 moderate smokers (5-19 cigarettes/day), 23 previous smokers (smoking cessation > 5 years) and 39 non-smokers. Twenty-eight (31.11%) patients were IL-1 genotype positive. Upon stratification for smoking status, significant differences were found for the variables ABL (P < 0.04, U-test) and DeltaBL/year (P < 0.04, U-test) between non-smokers and heavy smokers for the IL-1 genotype positive group but not for the IL-1 genotype negative group. Moreover, significant differences in ABL (P < 0.04, U-test) and DeltaBL/year (P < 0.04, U-test) were identified between former smokers and heavy smokers for the IL-1 genotype positive group. The differences in inflammatory parameters (BOP) did not reach statistical significance. This study suggests that in heavy cigarette smokers, carriage of a functionally significant IL-1 gene complex polymorphism is associated with an increased risk for peri-implant bone loss following prosthetic reconstruction and during the supportive periodontal care phase of the treatment.     

Host modulation as a therapeutic strategy in the treatment of periodontal disease.

Specific microorganisms initiate the immunoinflammatory processes that destroy tissue in periodontitis. Recent work has demonstrated, in addition to bacterial control, that modulation of the host immunoinflammatory response is also capable of controlling periodontitis. Matrix metalloproteinases (MMPs) destroy collagen and other matrix components, and the osteoclastic bone remodeling determines the periodontal bone response to a bacterial challenge. Other components of the biology, including cytokines and prostanoids, regulate MMPs and bone remodeling and are also involved in regulating the production of defensive elements, such as antibody. Agents directed at blocking MMPs or osteoclastic activity are effective in reducing periodontitis. Agents that inhibit prostaglandin E2 and selective blockage of specific cytokines have also been effective. Improved knowledge of bacterium-host interactions and of the processes leading to tissue destruction will help to identify targets for host modulation to reduce periodontitis in selected situations.     

Modulation of immunoreactivity to periodontal disease-associated microorganisms during pregnancy.

The lymphocyte blastogenic response to a panel of antigens and mitogens was assessed in a group of 20 women throughout their pregnancy. In addition, a group of five nonpregnant women was monitored simultaneously to identify variations in response to the same stimulants. The stimulants included orally associated bacterial antigens (Streptococcus sanguis, Actinomyces viscosus, Bacteroides asaccharolyticus, Bacteroides melaninogenicus subsp. intermedius, Bacteroides [Capnocytophaga] ochraceus, and Fusobacterium nucleatum) and non-orally associated-stimulants (streptokinase-streptodornase, tetanus toxoid, concanavalin A, phytohemagglutinin, and pokeweed mitogen). Intrinsic (cells cultured in male AB plasma) suppression of the lymphocyte response to these stimulants was observed to occur by the second trmester of pregnancy and was resolved after parturition. Additionally, an extrinsic (cells cultured in autologous plasma) suppression was also suggested to occur in a similar manner. There was no detectable enhancement of the blastogenic response to oral bacteria associated with elevated gingivitis, which is generally reported to occur during nonpregnancy gingivitis. We propose that concomitant immunosuppression occurs during the second trimester, which masks such enhancement.     

Diagnostic and prognostic tests for oral diseases: practical applications

Dental caries and periodontitis are initiated by specific bacteria and modified by host and environmental factors. Individuals have great differences in their rates of disease progression, but a small set of risk factors, such as smoking and diabetes, can distinguish patients at high risk for more severe disease. The application of information about factors that influence disease can be used to improve disease prevention and management. Knowledge of when specific information may be valuable should lead to the optimal management of individual patients. The use of diagnostic and prognostic tests and their application to the assessment and management of dental caries and periodontitis are the focus of this review.