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Expression and splicing of the fibronectin gene in healthy and diseased periodontal tissue.

Fibronectin is a major component of the extracellular matrix and is considered to have an important role in chronic inflammatory periodontal disease. The fibronectin gene product has been shown to be subject to alternative splicing in 3 regions, each generating different mRNA transcripts associated specifically with normal adult tissue, embryogenesis, tissue regeneration, and wound healing. In the present study, using the reverse-transcribed polymerase chain reaction to examine splicing profiles of the primary transcript, we found that healthy periodontal tissue expressed all alternatively spliced embryonic isoforms, indicative of the extensive and ongoing rebuilding processes which occur in these tissues. In marked contrast, only the exon-skipped transcripts were generated in tissue from chronic inflammatory periodontal disease patients. The loss of the high molecular weight isoforms in lesional tissues may be due to the excess production of inflammatory mediators in this disease, since we observed that high concentrations of the cytokine IL-1beta caused down-regulation of these transcripts in normal periodontal cells in tissue culture. Moreover, we also demonstrated that growth factors likely to be involved in periodontal regeneration and repair, such as PDGF, IGF-1 and TGF-beta, elicited pronounced upregulation of the embryonic isoforms of fibronectin in these cells. Although the functional activities of the antigens corresponding to the alternatively spliced variants of fibronectin are not yet known, our finding that they are selectively expressed suggests that they have highly specific roles in both periodontal breakdown and repair.

Adult↗

An association between periodontal disease and peripheral vascular disease.

BACKGROUND: Periodontal disease has been shown to be associated with increased risk of coronary heart disease. Because coronary heart disease and peripheral vascular disease (PVD) have similar pathophysiologies, we hypothesized that periodontal disease might be a risk factor for PVD. METHODS: Using the combined data from the Normative Aging Study and Dental Longitudinal Study of the US Department of Veterans Affairs, we examined the relationship between PVD and periodontal disease. Multivariate logistic regression analysis was used. RESULTS: Over the 25 to 30 years of follow-up, 80 of these initially healthy subjects developed PVD. Compared with controls (n = 1,030), subjects with clinically significant periodontal disease at baseline had a 2.27 increment in the risk of developing PVD (95% confidence interval 1.32 to 3.9, P value = 0.003). CONCLUSIONS: Periodontal disease emerged as a significant independent risk factor for PVD in a multivariate analysis that adjusted for other established risk factors.

Adult↗

Periodontal disease treatment by local drug delivery.

The subgingival microbiologic composition of diseased periodontal sites was evaluated by darkfield microscopy before and after scaling or local delivery of tetracycline. A standardized sampling and counting method using a crevicular washing technique was developed to determine both numbers and proportions of morphotypes using darkfield microscopy. Tetracycline-loaded hollow fibers established an initial intrasulcular concentration of 200,000 micrograms/ml, which decreased exponentially to 15 micrograms/ml in 24 hours. Repetitive intrasulcular placement of these fibers at periodontitis sites produced an incremental reduction in bacterial counts over a 10-day period. Monolithic fibers made of ethylene vinyl acetate loaded with 25% tetracycline hydrochloride provided sustained release for 10 days under in vitro test conditions. Ten patients were treated in a study comparing the effects of these fibers with scaling. Fibers were placed subgingivally to fill pockets to their probable depth and covered with a periodontal dressing which was maintained for 10 days. The average intrasulcular tetracycline concentration measured at the end of the 10-day period was 643 micrograms/ml. At these sites, total counts, spirochetes, motile rods and nonmotile rods were significantly reduced immediately following treatment. Total counts were depressed to levels near the detection limit of darkfield microscopy. In comparison, scaling produced much smaller alterations of darkfield counts which were not statistically significant.

Adult↗

Periodontal disease activity.

Periodontal disease activity is defined clinically by progressive loss of probing attachment and radiographically by progressive loss of alveolar bone. The natural history of periodontal disease was originally considered to be nearly continuous and slowly progressive. Clinical research conducted in the last decade suggests that periodontal disease demonstrates periods of exacerbation and remission. Using sensitive automated probes, studies published during the past year have demonstrated that different patterns of disease activity can exist, and that these patterns may be dependent on the disease threshold. Subtraction radiography continues to be refined, but cost and methodology prevent this diagnostic tool from having widespread clinical application. A variety of clinical, microbiologic, and host-response parameters have been studied for their relationship to periodontal disease activity. Many research groups are attempting to develop a diagnostic test that identifies the risk for development of active disease. A relatively simple test based on the presence of a microbial virulence factor, or the host inflammatory or immune response to the subgingival microflora, may be a practical means for clinicians to detect the active phases of periodontal disease.

Alveolar Bone Loss↗

Assessment of risk of periodontal disease.

The Periodontal Disease Research Center at the State University of New York at Buffalo has studied two sets of subjects--those with a high prevalence of diabetes (the Pima Indians) and an urban population in Erie County, New York--to determine factors that put a patient at risk for periodontal disease. These and other studies have established that smoking and diabetes are important risk indicators for periodontal disease. Local etiologic factors associated with periodontal disease in adults include the presence of the putative periodontal pathogens Porphyromonas gingivalis and Bacteroides forsythus. Longitudinal studies and intervention studies are needed to fully establish the role of risk indicators. However, information already available from present studies suggests that modulation of risk factors, such as smoking and diabetes mellitus, as well as suppression of the pathogenic flora, will be effective in the management of periodontal disease.

Adult↗

Some risk factors for the progression of periodontal disease.

Inflammatory periodontal disease is one of the most common diseases of mankind. Gingival inflammation is widespread, but advanced periodontitis is limited to relatively small subgroups of the population. Gingivitis is initiated by microbial plaque deposits on the dento-gingival interface but progression to periodontitis is modified by several environmental, behavioural, biological and health care variables. This paper reviews the reports dealing with some risk factors for periodontal disease published in recent years and compares the data with findings in a Ljubljana population. It is concluded that male smokers with lower education and low frequency of tooth brushing represent a risk population for progression of periodontal disease. Marital status and body mass need further study to be proved as risk factors for periodontitis. A socioecological model proposed by Hansen et al. (1993) should be used for understanding the interplay of different risk factors for progression of periodontal disease.

Adult↗

Role of Treponema denticola in periodontal diseases.

Among periodontal anaerobic pathogens, the oral spirochetes, and especially Treponema denticola, have been associated with periodontal diseases such as early-onset periodontitis, necrotizing ulcerative gingivitis, and acute pericoronitis. Basic research as well as clinical evidence suggest that the prevalence of T denticola, together with other proteolytic gram-negative bacteria in high numbers in periodontal pockets, may play an important role in the progression of periodontal disease. The accumulation of these bacteria and their products in the pocket may render the surface lining periodontal cells highly susceptible to lysis and damage. T. denticola has been shown to adhere to fibroblasts and epithelial cells, as well as to extracellular matrix components present in periodontal tissues, and to produce several deleterious factors that may contribute to the virulence of the bacteria. These bacterial components include outer-sheath-associated peptidases, chymotrypsin-like and trypsin-like proteinases, hemolytic and hemagglutinating activities, adhesins that bind to matrix proteins and cells, and an outer-sheath protein with pore-forming properties. The effects of T. denticola whole cells and their products on a variety of host mucosal and immunological cells has been studied extensively (Fig. 1). The clinical data regarding the presence of T. denticola in periodontal health and disease, together with the basic research results involving the role of T. denticola factors and products in relation to periodontal diseases, are reviewed and discussed in this article.

Acute Disease↗

Salivary antioxidants and periodontal disease status.

Periodontal disease is a common chronic adult condition. The bacterium Porphyromonas gingivalis has been implicated in the aetiology of this disease, which causes destruction of the connective tissue and bone around the root area of the tooth. It has been observed that invading P. gingivalis bacteria trigger the release of cytokines such as interleukin 8 and tumour necrosis factor a, leading to elevated numbers and activity of polymorphonucleocytes (PMN). As a result of stimulation by bacterial antigens, PMN produce the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. Patients with periodontal disease display increased PMN number and activity. It has been suggested that this proliferation results in a high degree of ROS release, culminating in heightened oxidative damage to gingival tissue, periodontal ligament and alveolar bone. Antioxidant constituents in plasma have been well-documented, being chiefly ascorbate, albumin and urate, and these are known to display sensitivity to dietary antioxidant intakes. The concentration of antioxidants in saliva does not appear to mirror those of plasma. The extent of dietary influence upon salivary antioxidant status is unclear. Urate is the predominant salivary antioxidant, with albumin and ascorbate providing minor contributions. Previous research has found reduced salivary antioxidant activity in patients suffering from periodontal disease. An improved understanding of the role antioxidants play in periodontitis, and the influence of nutrition on antioxidant status, may lead to a possible nutritional strategy for the treatment of periodontal disease.

Antioxidants↗

Principles of aetiology and pathogenesis governing the treatment of periodontal disease.

Modern periodontal therapy is based on the fundamental realization that accumulation of bacterial plaque at the gingival margin causes the incipient lesion in periodontal disease. Without interference, most lesions will progress to involve deeper parts of the periodontium. Recent research has revealed that dental plaque comprises a multitude of bacteria in various combinations with a variety of pathogenic potentials, that supragingival plaque is significantly different from the subgingival variety and that particular bacterial species are associated with different periodontal disease states. However, studies have not yet clearly defined a group of bacteria, much less one species, that is responsible for the different forms of periodontal disease. Therefore, the concept of specific pathogenesis is still not ready for clinical application in the prevention and treatment of these diseases, and dental plaque must be dealt with as an entity. Investigators have failed to demonstrate local or systemic factors, other than local aggregates of micro-organisms, that cause gingivitis and periodontitis. As in any other infections, the pathological events and final outcome are determined by the relationship between the microflora and host resistance. Presently, there are no known means by which the host factors can be manipulated to enhance the defense of the periodontium. Therefore, the only rationale for the clinical management of periodontal diseases is to interfere with the microbiological events. Since it is known that gingivitis precedes periodontitis, the only useful approach to preventing the development of periodontitis is to control gingivitis. The treatment of moderate and severe periodontitis also focuses on the elimination of subgingival bacteria and inhibition of recolonization. The target for this is the root surface, which must be detoxified. Surgical elimination of periodontal pockets is still a valid approach to the treatment of the advanced periodontal lesion but only in so far as it provides access to the subgingival accumulations of plaque. The key to success in periodontal therapy is to prepare the tooth surfaces in such a way as to make them biologically acceptable to the gingival tissues. This may be achieved with or without gaining surgical access.

Dental Plaque↗

Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases.

The periodontal diseases are infectious diseases caused by predominantly Gram-negative bacteria. However, as our understanding of the pathogenesis of the periodontal diseases grows, it is becoming clear that most of the tissue damage that characterizes periodontal disease is caused by the host response to infection, not by the infectious agent directly. Investigation into the mechanism of action of host-mediated tissue injury has revealed that the neutrophil plays an important role in destruction of host tissues. In this paper, we review the biochemical pathways and molecular mediators that are responsible for regulation of the inflammatory response in diseases such as periodontitis, with a focus on lipid mediators of inflammation. Pro-inflammatory mediators, such as prostaglandins and leukotrienes, are balanced by counter-regulatory signals provided by a class of molecules called lipoxins. The role of lipoxins in the control and resolution of inflammation is discussed, as is the possibility of the development of new therapeutic strategies for the control and prevention of neutrophil-mediated tissue injury in inflammatory diseases like periodontitis.

Animals↗

[Morphological study of periodontal tissues in the initial stage of periodontal disease. Part 2. Analysis of morphological measurement and status of periodontal disease].

The morphological characteristics of periodontal tissue in periodontal disease have been interpreted differently by a number of clinical observers. Many have reported that the malposition and functional malocclusion of teeth is injurious to the periodontium. We reported in Part I that a system for evaluating periodontal status was developed for the diagnosis and management of the interproximal area at the initial stage of bone resorption. The patient group consisted of 36 adults, from 21 to 55 years of age. The severity score represented the calculated loss of periodontal support tissues: loss of alveolar bone, evaluated roentgenologically, bone level and pattern in vertical and horizontal form, periodontal pocket and gingival inflammation. Because poor oral hygiene and other factors caused swelling by gingival inflammation, we obtained study specimens from patients with chronic periodontal disease after a few tooth brushing instructions, and scalings during initial therapy in order to detect initial and established pathological changes in periodontal tissue. The purpose of this study was to clarify the relationship between periodontal disease status and morphological diagnostic indicators and different degrees of harmony and disharmony in the lower jaw. In all age groups the average percentage of bone loss and intraosseous defects tended to be higher in the groups categorized as Type III and Type F, and in the area that showed a very deep concave Spee curve to the occlusal plane in Pattern D. We considered that these morphological characteristics might be of secondary importance for diagnosis. Oral local factors were the primary extrinsic factor in the pathogenesis of horizontal and vertical interproximal bone absorption in the area of the premolars and molars.

Alveolar Process↗

Survey of periodontal disease among workers in Tianjin using Ramfjord's Periodontal Disease Index (PDI).

An epidemiologic study of periodontal disease according to Ramfjord's PDI among 2284 workers was performed in Tianjin in 1982. This study included 1066 men and 1218 women, aged 18-50. The prevalence of gingivitis and periodontitis was 89.5% and 44.4%, respectively. Only 28 workers were free from periodontal disease. Gingivitis and periodontitis were highly prevalent in both sexes, but men had more severe gingivitis and periodontitis than women. The better oral hygiene of the women may account for this difference.

Adolescent↗

An educational model for preparing dental hygiene students in the treatment of periodontal diseases.

Inflammatory periodontal disease is the leading cause of tooth loss. Experts agree that prevention is crucial, with frequent and through plaque removal being the simplest and most effective method for preventing inflammatory periodontal disease. Since it is often the dental hygienist who plays the major role in providing such care, it is imperative that dental hygiene programs educate students in the prevention and treatment of periodontal diseases and provide necessary breadth and depth in theory and clinical experience in the curriculum. The purpose of this paper is to describe an educational model designed to enhance the treatment phase of the periodontal component of the curriculum for dental hygiene students. Both the didactic and clinical components of the periodontics courses are built upon a program-planning model: students assess, plan, implement, and evaluate the periodontal needs of all patients. Case presentations permit students to assimilate and analyze clinical data while internalizing the importance of comprehensive care and adequate follow-up. In general, the program-planning model in periodontics incorporates the application of theory to practice and enhances clinical decision-making skills needed for graduates to meet the complexity of periodontal health needs.

Dental Hygienists↗