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PubMed1994

The role of cytokines in the pathogenesis of periodontal disease.

Recent advances in cellular and molecular biology have allowed investigators to better understand the mechanisms of inflammatory and immune responses in many infectious diseases. Soluble mediators produced by various inflammatory and structural cells, collectively called cytokines, have been shown to play a crucial role in the pathogenesis of most of these diseases, including periodontal disease. This paper globally reviews recently reported findings implicating cytokines in periodontal pathophysiology. Inflammatory mediators, such as interleukin-1, tumor necrosis factor-alpha, and interferon-gamma, known to regulate bone resorptive activity are present in diseased periodontal tissues. Similarly, metalloproteinases, which degrade extracellular matrix, have been shown to have increased activity in diseased sites, and enhanced levels of their inhibitors correlate with absence of disease activity. Finally, certain polypeptide growth factors originally known to play a role in wound healing are now shown to have a significant effect in inflammatory responses.

Collagen↗
PubMed1995

Tetracyclines in the management of periodontal diseases. A review.

Periodontal diseases essentially comprise a group of oral infections whose primary aetiological factor is dental plaque. Removal of the cause (and its effects) is the primary aim of both non-surgical and surgical treatment regimens, although the infective nature of the diseases has led to the widespread use of antimicrobials as an adjunct to mechanical debridement. The tetracyclines are primarily bacteriostatic agents that are effective against many Gram-negative species including putative periodontopathogens such as Actinobacillus actinomycetemcomitans (A.a.). The proven efficacy of this group of drugs in the management of periodontal diseases may be related not only to their antibacterial actions, but to a number of additional properties that have been recently identified. These include collagenase inhibition, anti-inflammatory actions, inhibition of bone resorption and their ability to promote the attachment of fibroblasts to root surfaces. Consequently, tetracyclines have also been used as an adjunct to bone grafting in periodontal defects, and as agents for 'conditioning' root surfaces to enhance the regeneration of periodontal tissues. When tetracyclines are taken orally, consideration must be given both to the potential unwanted effects and to interactions with other drugs that are taken concurrently. Such problems are minimised however, when the drugs are incorporated into controlled, slow-release formulations which are currently being researched and marketed for intra-oral use.

Aggressive Periodontitis↗
PubMed2005

Gorham's disease of the mandible mimicking periodontal disease on radiograph.

BACKGROUND: Gorham's disease is a rare disorder characterized by spontaneous and progressive osteolysis of one or more skeletal bones. The radiographic findings associated with Gorham's disease are particularly dramatic, as in some cases a complete resorption of the involved bone can occur, leading to the definition of phantom bone, vanishing bone, or disappearing bone disease. MATERIAL AND METHODS: A 24-year-old female patient with a previous diagnosis of periodontal disease and progressive mandibular alveolar bone loss was referred to our Oral Medicine section. The initial radiographic picture showed infrabony defects and horizontal bone loss. RESULTS: After further extensive local and systemic evaluation, including histopathological, laboratory and imagine techniques investigations, the patient was diagnosed to be affected by Gorham's disease. Meanwhile the progression of the osteolytic process had caused the loosening of all the left mandibular teeth and a pathologic fracture. Appropriate medical therapy was successful in stabilizating the resorptive process, with no evidence of further progressive disease. CONCLUSIONS: When Gorham's disease involves the mandible, the role of the periodontologist is extremely important in diagnosing promptly the disorder and preventing the functional and aesthetic consequences of advanced and extensive bone loss. Gorham's disease should be included among the pathologic entities mimicking periodontal disease on radiograph, such as inflammatory disease (e.g. osteomyelitis), endocrine disease (e.g. hyperparathyroidism), intra-osseous malignancies or metastases, lymphoma, histiocytosis X, mainly eosinophilic granuloma, infective process (e.g. tuberculosis and actinomycosis), odontogenic tumours.

Adult↗
PubMed2004

Cigarette smoking, periodontal disease: and chronic obstructive pulmonary disease.

BACKGROUND: Cigarette smoking is a significant risk factor for both chronic obstructive pulmonary disease (COPD) and periodontal disease. The goal of this study was to better understand the role of smoking in a possible relationship between periodontal disease and COPD. METHODS: The study population consisted of 7,625 participants in the Third National Health and Nutrition Examination Survey (NHANES III) during 1988-1994 who were aged 30 years or older when examined and who received a spirometric examination. The data analysis employed logistic regression models and accounted for the complex sampling design used in NHANES III. RESULTS: After adjustment for potential confounders, there was no statistically significant association between periodontal disease and COPD among former or non-smokers. Current smokers with > or = 4 mm mean loss of attachment had an odds ratio of 3.71 (95% confidence interval: 1.74, 7.89). CONCLUSIONS: These results suggest that cigarette smoking may be a cofactor in the relationship between periodontal disease and chronic obstructive pulmonary disease. The key role played by smoking in the etiology of both periodontal disease and chronic obstructive pulmonary disease suggests that much of the observed increase in risk may actually reflect the exposure to smoking. Additional research into smoking-related effect modification is needed to clarify the role of periodontal disease in the etiology of smoking-related systemic diseases.

Adult↗
PubMed2004

Dose-effect relation of smoking and the interleukin-1 gene polymorphism in periodontal disease.

BACKGROUND: Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, smoking, age, gender, diabetes, and socioeconomic and genetic factors. Smoking has the highest impact on the course of the disease modulated by all the other factors. Here, we report the relationship between smoking and the genetic polymorphism of interleukin-1 (IL-1). METHODS: In a randomly selected population-based study, we genotyped 1,085 test persons for the IL-1 genotype, examined their periodontal status, and assessed their smoking behavior including present and past quality and quantity of smoking. RESULTS: There was a significant dose-effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there was a gene-environmental interaction. Subjects bearing at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 (genotype positive) had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts. With genotype-negative non-smokers as a reference, logistic regression resulted in odds ratios of 0.98 (95% confidence interval: 0.83 to 1.14), 2.37 (1.96 to 2.87), and 4.50 (2.30 to 8.82) for genotype-positive non-smokers, genotype-negative smokers, and genotype-positive smokers, respectively. CONCLUSIONS: There is a gene-environmental interaction between smoking and the IL-1 genetic polymorphism. Smokers bearing the genotype-positive IL-1 allele combination have an increased risk of periodontitis. The IL-1 genotype has no influence in non-smokers.

Adult↗
PubMed1976

A periodontist's view on the assessment of periodontal disease in the community.

Periodontal treatment differs from other forms of dental treatment in that it demands long term cooperation from the patient without which the dentists' efforts are largely without value. The earliest stage of periodontal disease is gingivitis which is characterized by bleeding on gentle probing. It is a reversible condition which, depending on many poorly understood factors, may or may not progress to periodontal disease. This stage is characterized by the apical migration of junctional epithelium, pocket formation and loss of alveolar bone. Pocket depth, though not indicating the presence of active disease, is the best available measure of periodontal disease. In school children the majority of disease is gingivitis which can be largely eliminated by plaque control which they should be taught to practise from themselves. In adults a screening procedure has been developed which will rapidly identify those in need of treatment. Patients with gingivitis can be referred to hygienists. Those with moderately advanced disease are scheduled for non-surgical periodontal therapy which should be followed by re-evaluation and redefinition of the treatment plan. Those with advanced periodontal disease are usually referred for specialist treatment. It has been shown that pockets of up to 5 mm in depth can be maintained without further destruction by plaque control combined with scaling and root planing. The most important aspect of periodontal health remains the quality of long term maintenance care and the motivation of the patient to accept responsibility for it.

Adolescent↗
PubMed1992

Host responses in periodontal diseases: current concepts.

In periodontal diseases, bacteria trigger inflammatory host responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T-cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF-beta, gamma-interferon, and IL-1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms.

Antibody Formation↗
PubMed2000

Oral hygiene in the prevention of caries and periodontal disease.

While some periodontal disease may be as old as mankind itself, caries as a public health problem appeared with the development of flour and sugar mills, and the universal access to fermentable carbohydrates. As a consequence, during the last 500 years caries and periodontal disease have been the most common diseases afflicting the human mouth. Together, these two diseases have been responsible for untold pain and suffering, and for excessive destruction and loss of people's teeth. With improving social circumstances in most industrialised nations, increased availability and affordability of modern oral health care, and the promotion of conservative treatment concepts, the 20th century saw significant progress in eliminating pain and tooth loss. Moreover, during the last 50 years advances in the oral health sciences and in technology, have not only increased our understanding of the nature of these diseases and their causes, but also introduced and tested new approaches to their prevention.

Dental Caries↗
PubMed2001

Periodontal diseases and osteoporosis: association and mechanisms.

There is increasing evidence that osteoporosis, and the underlying loss of bone mass characteristic of this disease, is associated with periodontal disease and tooth loss. Periodontitis has long been defined as an infection-mediated destruction of the alveolar bone and soft tissue attachment to the tooth, responsible for most tooth loss in adult populations. Current evidence including several prospective studies supports an association of osteoporosis with the onset and progression of periodontal disease in humans. The majority of studies have shown low bone mass to be independently associated with loss of alveolar crestal height and tooth loss. However studies that focus on the relation of clinical attachment loss and osteoporosis are less consistent. To date, the majority of studies on the relationship between periodontal disease and osteoporosis have been hindered by small sample sizes, limited control of other potential confounding factors, varying definitions of both periodontal disease and osteoporosis, and few prospective studies where the temporality of the association can be established. Potential mechanisms by which host factors may influence onset and progression of periodontal disease directly or indirectly include underlying low bone density in the oral cavity, bone loss as an inflammatory response to infection, genetic susceptibility, and shared exposure to risk factors. Systemic loss of bone density in osteoporosis, including that of the oral cavity, may provide a host system that is increasingly susceptible to infectious destruction of periodontal tissue. Studies have provided evidence that hormones, heredity, and other host factors influence periodontal disease incidence and severity. Both periodontal disease and osteoporosis are serious public-health concerns in the United States. Prevalence of both osteoporosis and tooth loss increase with advancing age in both women and men. Understanding the association between these common diseases and the mechanisms underlying those associations will aid health professionals to provide improved means to prevent, diagnose, and treat these very common diseases. This paper reviews the current evidence on the association between periodontal disease and osteoporosis.

Adult↗
PubMed2001

The localization of periodontal-disease-associated bacteria in human periodontal pockets.

Some Gram-negative anaerobes are associated with the incidence and progression of periodontal disease. In periodontal pockets, however, the localization of those bacteria is unknown. We investigated the localization of 5 bacterial species in human periodontal pockets. Fifteen teeth with a part of periodontal pockets from 10 adult periodontitis patients were obtained, and the localization of bacteria was examined immunohistochemically. Positive reactions with anti-Prevotella nigrescens antibody were located at the epithelium-associated plaque area in the middle pocket zones. In the middle and deep pocket zones, Fusobacterium nucleatum and Treponema denticola were especially localized in the unattached plaque area, but Eikenella corrodens was observed in the tooth-attached plaque area. Actinobacillus actinomycetemcomitans, detected in 2 of 15 samples examined, was found in the unattached plaque area, in the middle pocket zone. The present findings indicated that the 5 bacterial species examined localized at distinct regions in human periodontal pockets.

Adult↗
PubMed2000

Negative effects of chronic inflammatory periodontal disease on diabetes mellitus.

Periodontal disease is the result of a complex interplay of bacterial infection and host responses, and is often modified by various systemic diseases such as diabetes mellitus. Such diseases are capable of affecting the periodontium and/or the treatment of periodontal disease. However, recent research has changed our concept of how periodontal disease should be treated. Here we present several concerns directed towards the periodontal therapy of patients with diabetes mellitus based on our studies. When treating periodontitis patients who have diabetes mellitus it is important to consider the type of diabetes. Patients with non-insulin dependent diabetes mellitus can be further classified according to the degree of insulin resistance, since recent epidemiological studies have suggested that successful anti-microbial therapy might result in improved insulin resistance in highly insulin resistant patients. Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored. On the other hand, diabetic patients positive for serum anti-glutamate decarboxylase auto-antibody should be examined for the source of this antibody, since 1) gingival and periodontal ligament fibroblasts were found to express glutamate decarboxylase, and 2) some otherwise healthy periodontitis patients develop anti-glutamate decarboxylase antibody. Thus, chronic periodontitis may influence the level of this antibody which is widely used as a predictive marker for slowly progressive insulin dependent diabetes mellitus. Not only is periodontal disease thereby affected by systemic diseases, but carefully managed periodontal therapy may also have a positive effect on the general health of patients with systemic diseases.

Anti-Bacterial Agents↗
PubMed2002

Treatment with SRL172 (heat-killed Mycobacterium vaccae) inhibits progression of established experimental periodontal disease in Wistar rats.

Periodontal disease is accompanied by a change in the periodontal bacterial flora, and an increase in Th2 cytokine expression. Therefore, preparations that can down-regulate Th2 responses and increase Th1 responses to bacteria may have therapeutic effects. SRL172, a preparation of heat-killed Mycobacterium vaccae (NCTC11659), has been shown to have these properties in man and animals and, in a previous study, a single subcutaneous injection of this material 13 days before application of ligatures to the right second molars of Wistar rats strikingly reduced subsequent destruction of the tooth-supporting tissues. The same material has therefore been tested in a therapeutic protocol, in rats with ongoing periodontal disease. A silk ligature was placed round the maxillary right second molar in the gingival sulcus on day 0. This was removed after two weeks, and the animals immediately received 0.1 mg SRL172 s.c. or saline. One week later (i.e. at three weeks), a boost of 1.0 mg SRL172 or saline was given. Animals were sacrificed at eight weeks (i.e. five weeks after the booster dose). Treatment of ongoing periodontal disease with SRL172 significantly reduced fibre loss (p = 0.046 by histometry) and bone loss (p = 0.0008 by radiography) on the ligatured side, and reduced fibre loss (p = 0.0086) on the control side. Thus SRL172 is an effective treatment in this model. As SRL172 has undergone extensive safety testing in man, these results justify clinical studies in periodontal disease, and such studies are now planned.

Animals↗
PubMed1996

The role of osteopenia in oral bone loss and periodontal disease.

Osteoporosis and periodontitis are diseases which affect a large number of women and men, with incidence increasing with advancing age. Osteopenia is a reduction in bone mass due to an imbalance between bone resorption and formation, favoring resorption, resulting in demineralization and leading to osteoporosis. Osteoporosis is a disease characterized by low bone mass and fragility and a consequent increase in fracture risk. Periodontitis is characterized by inflammation of the supporting tissues of the teeth, resulting in resorption of the alveolar bone as well as loss of the soft tissue attachment to the tooth and is a major cause of tooth loss and edentulousness in adults. The relationship of osteopenia to oral bone loss and periodontal disease has been addressed in a limited number of studies. A review of current knowledge regarding this relationship is presented. Interpretation of the literature is complicated by the variety of methods used to assess osteopenia, oral bone mass, and periodontitis, as well as varying definitions of outcomes of interest. Results of a previously unpublished study are presented which suggest that severity of osteopenia is related to loss of alveolar crestal height and tooth loss in post-menopausal women. The literature on the relationship among these disorders is limited and points to the need for additional studies which thoroughly evaluate the influence of potential confounding factors to further define the relationship between low bone mineral density and periodontal disease in larger populations. Clearer understanding of this relationship may aid health care providers in their efforts to detect and prevent osteoporosis and periodontal disease. Increased dialogue among medical and dental professional will be increasingly important in achieving and maintaining patients' optimal health.

Adult↗