摘要:

Striking remodeling activity occursadjacent to the site of injury in orthopedic surgery. This reaction has been described as regional accelerated phenomenon (RAP), as it speeds up the healing stage. The phenomenon is a transient burst of localized remodeling process following surgical wounding of cortical bone. We explored whether RAP occurs following mucoperiosteal flap surgery in the jaw bone. Mucoperiosteal flaps were performed on 60 Wistar rats, either only on the buccal aspect or both on buccal and lingual aspects of the mandible. The surgical procedure lasted an average of 30 seconds and the flap was readapted without sutures. The rats were sacrificed at 3, 7, 10, 14, 21, and 120 days. High resolution x‐ray microradiography of 1 to 1.5 mm thick ground sections between premolar and molar regions of the mandible were analyzed and revealed large areas of radiolucency which correlated to massive resorption of the alveolar bone, as well as areas in the bone proper. The RAP was observed as early as 10 days in the treated side group. Striking resorption of the cortical bone, both on the surface and the bone proper, occurred on the periodontal aspect of the crestal bone leading to widening of the periodontal ligament space, where a mucoperiosteal flap was performed on the buccal aspect. The resorption was more prominent when a mucoperiosteal flap was performed both on the lingual and buccal aspect. The alveolar bone recovered almost to control levels 120 days after surgery. Both the histology sections and the microradiographs in the mesio‐distal direction demonstrated a typical RAP mechanism to potentiate tissue healing, a phenomenon observed by orthopedists in long bone. It is this phenomenon that might be responsible for the increasing mobility immediately following periodontal surgery. Also, bone dehiscences following periodontal surgery and open flap curettage may occur when the bone in the area is thin.J Periodontol 1994;65:79–83.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.1.79

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

The dynamics of bone turnoverin the furcations of teeth treated with expanded polytetrafluoroethylene (ePTFE) membranes were evaluated using multiple fluorochrome labels in 6 male beagle dogs. Loss of attachment involving the furcation area was induced in the second, third, and fourth premolar teeth using silk ligatures. The resulting defects were treated with the use of mucoperiosteal flaps for access, debridement of the defects, and placement of ePTFE membranes covering the furcations of the second and fourth premolare (experimental teeth) while the third premolar received only debridement without membrane placement (control tooth). Five fluorochrome labels were administered intravenously at timed intervals to act as markers of the osseous response. Membranes were removed at 4 weeks and all animals were terminated at 12 weeks post‐membrane placement. One side of the mandible was decalcified, sectioned at 7 μm, and stained with either hematoxylin and eosin or Gomori's tri‐chrome. The opposite side provided non‐decalcified tissue processed as 100μm ground sections. Using fluorescent light and point‐hit evaluation, tissue in the coronal half of each specimen was classified as either labelled bone, unlabelled bone, or resorption space. In addition, microradiographs were prepared of each ground section and specimens classified as either woven bone, old lamellar bone, or new lamellar bone. No significant differences in attachment levels, or level of junctional epithelium, were observed in decalified sections although greater remodeling activity was noted in the experimental specimens. Comparison of ground sections revealed significant differences (P<0.05) in all categories with both methods of evaluation. Experimental specimens exhibited greater remodeling activity, bone apposition, and percentage of woven bone formation. These results suggest that light microscopy may underestimate the overall osseous response and that membrane placement significantly alters bone turnover in treated furcation sites.J Periodontol 1994;65:84–92.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.1.84

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

We report an unusual case of maxillaryosteosarcoma presenting as supracrestal bone formation in a 41‐year‐old woman. This case is of interest from the point of view of radiographic appearance of supracrestal bone formation with widened periodontal ligaments and the buccal and palatal swelling of the tissues. Moreover, to the best of our knowledge, the histopathologic evidence of cementai resorption has not been reported earlier.J Periodontol 1994;65:93–96.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.1.93

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.463

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.464

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

In assessing risk for disease, periodontitis can be thought to be more like some of our common medical conditions: certain people are at higher risk than others, and efforts at prevention and intervention involve a combination of personal behaviors and professional practices. This paper presents some principles of designing risk assessment studies. In addition, the choices that must be made in deciding what is high risk and the type of model to be constructed are presented along with implications of each alternative. Terms such as risk indicators, risk factors, risk predictors, risk models, and prediction models are presented and discussed. To illustrate some of the issues, findings from the Piedmont 65+ Dental Study (a longitudinal study of oral health in older adults) indicate that: 1) indicators of risk developed from cross‐sectional studies quite often are not confirmed as risk factors in longitudinal studies and longitudinal data implicate additional factors; 2) oral risk factors were important in explaining disease progression, but other categories of risk factors also played an explanatory role; 3) the risk models were able to predict who would experience attachment loss at some time during the 3‐year period with a high degree of accuracy, but there was only moderate success at predicting who would not experience attachment loss; 4) including risk predictors in the models did improve the ability of one model to predict attachment loss, but the risk predictor masked the presence of an important risk factor; and 5) it is highly likely that adding measures of host defense mechanism to the study could result in improved models.J Periodontol 1994;65:468–478.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.468

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

The purpose of this paper is to review current knowledgeof genetic risk factors for the periodontal diseases and to present updated and additional data from the Minnesota Twin Periodontal Study. Family studies suggest that susceptibility to the early onset forms of disease, particularly prepubertal and juvenile periodontitis, is, at least in part, influenced by host genotype. Inherited phagocytic cell deficiencies appear to confer risk for prepubertal periodontitis. The prevalence and distribution of juvenile periodontitis in affected families are most consistent with an autosomal recessive mode of inheritance. However, considerable etiologic as well as genetic heterogeneity within these clinically‐defined diseases is evident. Whether or not genetic factors influence the more common adult chronic periodontitis is less clear. Although results from family studies suggest that environmental factors appear to be the major determinants of variance in adult periodontitis, data from our twin studies indicate that both genetic and environmental factors influence disease. Furthermore, comparisons between reared‐together and reared‐apart adult monozygous twins indicate that early family environment has no appreciable influence on probing depth and attachment loss measures in adults.J Periodontol 1994;65:479–488.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.479

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Apatient's decision to accept treatmentrecommended by his dental health care provider will be strongly influenced by the quality of the information he is given. Estimates of prognosis and treatment predictability must be based on the evidence available from the literature and the practitioners' own experience. Thorough, accurate, and relevant clinical and adjunctive diagnostic data will be a major influence in the development of the patient's individualized treatment strategy. Some clinical findings such as severity of disease for age, deepening pockets accompanied by loss of clinical attachment, frequent bleeding on probing, and bone loss can be considered as risk and prognosis factors. “Hard” data implicating specific clinical or diagnostic findings as risk factors or markers are difficult to find because there are few randomized longitudinal trials available. A new approach which attempts to focus on reducing the risk of undesirable outcomes while improving the probability of successful outcomes following treatment has been referred to as the Treatment Predictability Model. A key feature of this approach is the focus on individual patient circumstances and preferences through the use of decision analysis techniques. A large scale, long‐term project utilizing a practice‐based research network (PBRN) provided some descriptive information about factors that could distinguish between responders and nonresponder patients undergoing treatment for advanced periodontitis. Bacterial colonization, level of post‐treatment plaque control, and smoking were major predictive variables in this group of periodontitis patients. The predictive treatment approach may be one way to develop evidence that will improve the predictability of outcomes for individual patients.J Periodontol 1994; 65:489–497.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.489

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Specific microbial specieshave been closely associated with periodontitis. Through longitudinal studies, some of these microbial species have been implicated in the etiology of progressive periodontal disease. Although putative periodontal pathogens are often isolated from individuals with severe periodontitis, they also frequently inhabit the subgingival environment and are not always associated with advanced disease. In this respect, it is becoming increasingly apparent that there is no single etiology of the various periodontal diseases. Destructive periodontal diseases are the result of environmental, host, and bacterial factors. Microorganisms, however, are essential components of any model for progressive periodontitis. This paper selectively reviews bacteria as risk markers for periodontitis. Attention focuses on bacteria in conjunction with behavioral patterns (oral hygiene habits and smoking) and host response (gingival crevicular fluid substances) as risk markers for periodontitis. Prospective studies implicating specific bacteria in progressive periodontitis are addressed and a bacterial risk assessment model for progressive periodontitis is discussed with respect to the interplay between bacterial, environmental, and host markers.J Periodontol 1994; 64:498–510.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.498

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Advances in our understandingof the relationship between the microbial challenge and the host response in periodontal disease have led to the search for pathogenesisbased risk indicators or risk factors for disease progression. This evaluation is based on analysis of non‐invasive or minimally invasive samples that allow measurement of the subgingival plaque microflora or the host response in gingival crevicular fluid (GCF), serum, or saliva. Studies conducted by us have indicated that in GCF, persistently elevated levels of β‐glucuronidase (βG, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodontitis. This finding has been confirmed in a multicenter trial. We have also observed that a statistically significant positive correlation exists between βG in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variations in the host response to the challenge. Furthermore, βG levels in GCF were inversely correlated with the IgG serum antibody titer to a panel of periodontal pathogens, suggesting the essentially protective function of the systemic humoral response in periodontal disease. Data in the literature support this concept. In addition, recent studies of the relationship of antibody isotypes in GCF to progression of clinical attachment loss have suggested that IgA in GCF has a protective function. This may relate to the lack of complement activation by IgA. Alternately, the development of IgA antigen‐specific responses are T‐cell dependent, and reductions in local levels of IgA may indicate a decrease in T‐helper cell function. These data have allowed development of strategies for identifying individual risk profiles for patients with periodontal disease based on the host response to the microbial challenge. With identification of these risk indicators/risk factors for active periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this approach to periodontal diagnosis. Improved patient management should result from the incorporation of these tests into clinical practice.J Periodontol 1994;65:511–520.

ISSN:1049-8885    

DOI:10.1902/jop.1994.65.5s.511

出版商:Wiley    

年代:1994

数据来源: WILEY