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Results for “PERIODONTAL DISEASE”

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PubMed1991

Chemotherapeutic agents as adjuncts in the treatment of periodontal disease.

Periodontal disease is a broad term designating a number of infectious disease entities involving the supportive tooth structures. It has become clear that the various forms of periodontal disease are associated with specific groups of microorganisms. This evidence has led to treatment strategies that are primarily aimed at the suppression or elimination of specific periodontal pathogens. Until recently, surgical and mechanical intervention remained the principal methods for control of the multifactorial disease process. Recent advances in the development of chemotherapeutic agents have led to the increasing use of antimicrobials to suppress pathogenic flora. The use of antimetabolic agents to modulate host inflammatory response to the accumulation of bacterial plaque has also increased. Both types of chemotherapeutic agents can be used alone or in conjunction with traditional periodontal therapy to provide effective and predictable clinical improvement.

Anti-Bacterial Agents↗

PubMed1994

Antibiotic gels for periodontal disease.

Periodontal disease is a major cause of tooth loss. The underlying pathology is inflammation caused by bacterial plaque affecting the supporting structures of the teeth. Conventional treatment involves mechanical debridement of calcified plaque (calculus) by the dentist combined with meticulous oral hygiene by the patient. A more recent approach is to apply antimicrobial drugs locally to the diseased gingival tissue after debridement. Two antibiotic preparations, minocycline 2% gel (Dentomycin-Lederle) and metronidazole 25% gel (Elyzol-Dumex), are now licensed for the treatment of patients with periodontal disease. Are these treatments an advance on conventional therapy?

Gels↗

PubMed1999

The microbiology of periodontal disease.

Periodontal disease result from mixed bacterial infections, in which both host resistance barriers and bacterial interactions are important. Approximately ten bacterial species are strongly implicated with various forms of periodontal disease, although species that cannot yet be cultivated are likely also to be relevant. New technologies have shown that pathogenic bacterial species are present in defined complexes within subgingival plaque, thus identifying specific targets for therapeutic intervention. In light of increasing antibiotic resistance amongst oral bacteria, new strategies for control of periodontal bacterial complexes must be developed that inhibit the bacterial factors necessary for colonization and destruction of host tissues.

Aggregatibacter actinomycetemcomitans↗

PubMed2001

[Pathology of periodontal disease].

Periodontal diseases are usually divided into two categories, periapical and marginal periodontal diseases, according to the sites. The marginal periodontitis is common and causes loss of teeth in the adult. This begins as a marginal gingivitis, which usually progresses to destructive chronic periodontitis. The authors describe here the classification, pathology and various related factors of human adult periodontitis.

English Abstract↗

PubMedDate not supplied

Using host response modifiers in the treatment of periodontal disease.

Periodontal disease is the result of a complex interaction between microbial plaque, the host's inflammatory response to the plaque, and host modifying factors (e.g., smoking, diabetes, genetics) that may have an impact on the disease process. It is known that plaque initiates periodontal disease but that the host response is responsible for the destruction of periodontal tissues. This article describes why host response modifiers may be used to help control inflammation and tissue destruction as part of the initial phase of periodontal therapy in selected patient groups.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2004

Cardiovascular disease and periodontal diseases: commonality and causation.

Periodontal diseases have long been recognized as a public health problem. Awareness of the destructive nature of periodontal diseases and the importance of a tight control of bacterial plaque are basic concepts of periodontal treatment. In the past decade, there has been a conceptual shift from periodontal diseases as an oral problem to periodontitis having an impact on systemic health. Recent evidence suggests a strong relationship between periodontal inflammatory disease and systemic diseases, such as cardiovascular disease. It is now generally accepted that inflammation plays an important role in atherosclerosis, and factors that systemically amplify inflammation are under close investigation. This article reviews some of the emerging concepts for the inflammatory mechanisms of periodontal diseases and atherosclerosis and examines the potential role of local inflammation in systemic inflammatory disease.

Animals↗

PubMed1991

Etiology of periodontal diseases.

Periodontal diseases are a series of complex, distinct, pathologic entities caused by the interaction of bacterial plaque and the host. This interaction results in destruction of the supporting alveolar bone and connective tissue. Although bacterial plaque has been implicated as the primary etiologic agent in most forms of periodontal disease, there are local and systemic factors which may modify both microbial and host components. Local factors may favor plaque accumulation and maturation, while systemic factors may modulate and decrease the host's protective response.

Dental Occlusion, Traumatic↗

PubMed1994

[Bacteriological aspects of periodontal disease].

Periodontal diseases are caused by specific bacteria in the periodontal pocket. Despite the vast complexity of the flora on the teeth and the more than 300 types of bacteria that may be found in the mouth, studies have been able to narrow the list of pathogens to a small group of suspected bacteria. It is not clear, however, how much of the destruction of periodontal tissue is caused by the direct effects of the bacteria and how much by indirect effects mediated by the host's reaction to the bacteria.

Adolescent↗

PubMedDate not supplied

Coronary artery disease and periodontal disease: is there a link?

BACKGROUND: Cardiovascular disease is the number one killer worldwide. The so-called classic risk factors of coronary heart disease do not account for all of its clinical and epidemiological features. Recent evidence suggests that certain infections, among them dental infections and in particular periodontal disease, are involved in the pathogenesis of coronary artery disease. AIM: To evaluate the association between periodontal disease and coronary artery disease. PATIENTS AND METHODS: Fifty patients referred for diagnostic coronary angiography were assessed for periodontal disease. All patients underwent a thorough physical examination, routine laboratory testing, cardiac evaluation and dental examination which included pantomography x-ray evaluation. RESULTS: Pantomography x-rays and coronary angiograms of the participants were scored blindly by a dentist and cardiologists respectively. The association between periodontal disease and coronary atheromatosis remained significant after adjustment for age, smoking, blood lipids, body mass index, hypertension and the presence of diabetes. IMPLICATIONS: Periodontal disease was still significantly associated after all the known risk factors were accounted for. The implication here is that periodontal disease could be a potential risk factor for heart disease by predisposing the individual to chronic low-grade infections. If so, then dental health becomes an important parameter for medical health.

Aged↗

PubMed2001

[Periodontal disease and systemic disease].

Periodontal diseases are now recognized as bacterial infections among the chronic diseases of humans. The influence of the oral environment on systemic health, especially the periodontium, has long been supported by scientific evidence. However, an evidence base for the influence of periodontal disease on vital organs such as heart, lung has only recently begun to be established. We are hopeful that this information will stimulate new collaborations between physicians and dentist and serve as basis for studies to help improve the total health.

English Abstract↗

PubMed1985

The therapeutic use of antimicrobial agents in patients with periodontal disease.

Periodontal disease is the collective term given to a variety of inflammatory conditions in the tissue that supports and secures the teeth to the jawbone. The inflammatory response is to bacterial products and/or bacteria that enter the tissue from the dental plaque. The dental plaque is a complex microbial community containing over 190 different taxa that exist on the tooth surfaces. In periodontitis the majority of the plaque bacteria are anaerobes including the black pigmented bacteroides species and motile forms such as spirochetes. This suggested that a systemic antimicrobial specific for anaerobes might be of value in the treatment of periodontitis. Two double blind studies are reviewed which indicate that metronidazole plus mechanical debridement of the root surfaces is significantly better than placebo plus mechanical debridement in the treatment of advanced cases of periodontitis especially when the periodontal pockets are 6 mm or more in depth.

Bacteria, Anaerobic↗

PubMed1993

Specific antibodies and their potential role in periodontal diseases.

Periodontal diseases are thought to result from inflammatory responses to bacterial challenges in the gingival crevicular area. Antibodies are a major host-protective mechanism in many bacterial infections. Consequently, the antibody responses to suspected periodontal pathogenic bacteria have been extensively measured as to their relationship to diseases and specificity for suspected pathogens associated with progressing disease sites. Recently, studies on the bacterial immunogen characterization, antibody-subclass identification, and antibody biological capabilities have been reported. Although increased antibody levels to certain suspected periodontal pathogens were associated with periodontal diseases in humans, little evidence exists as to the role of these antibodies in the infectious process. In vivo experiments in animals indicated that specific antibodies against certain suspected periodontal pathogens were associated with suppression of bacterial colonization, limiting the spread of infection, and a decrease in alveolar bone loss. However, in vitro as well as in vivo experiments suggested that phagocytic cells are required for efficient bactericidal activity of antibodies and that the presence of other sensitized immune cells may either have inhibited or enhanced the infectivity of certain periodontal pathogens. Possible explanations for the observed inconsistencies are presented and the potential for utilization of specific anti-periodontal pathogen responses in the understanding and prevention of diseases is discussed.

Animals↗

PubMed1994

Pathogenic mechanisms in periodontal disease.

Periodontal diseases have been considered as "infections" in which micro-organisms initiate and maintain the destructive inflammatory response. Host-mediated tissue destruction occurs via complement activation and the release of lysosomal enzymes, and connective tissue matrix metalloproteinases. Microbial enzymes may damage connective tissues directly, and, together with toxic metabolites and structural materials, are thought to disrupt the reparative activities of fibroblasts and cells of the immune defenses. The significance and relative contributions of host and microbial factors to the disease process remain unresolved. Environmental changes in the gingival sulcus and periodontal pocket and tissues, the degree of the host response and nutrient availability, concomitant with disease progression, compromise tissue metabolism and repair, and allow for enhanced or de novo expression of microbial virulence factors, such as proteases, which alter microbial pathogenicity. Proteolytic destruction of specific antibodies and complement by both viable and non-viable bacterial cells may retard phagocytic killing and removal of pathogens, thus prolonging the inflammatory response. Bacterial products may indirectly mediate tissue destruction by stimulating release of matrix metalloproteinases or by proteolytically inactivating the specific inhibitors of these enzymes.

Endotoxins↗

PubMed2005

Systemic inflammatory markers, periodontal diseases, and periodontal infections in an elderly population.

OBJECTIVES: To study the levels of systemic markers for inflammation with parameters of periodontal diseases in older people. DESIGN: A cross-sectional study was conducted in a cohort that is being followed prospectively on the effects of aging and body composition on morbidity. SETTING: University of Pittsburgh, Pittsburgh, and University of Tennessee, Memphis. PARTICIPANTS: One thousand one hundred thirty-one participants (mean age+/-standard deviation 72.7+/-2.8); 66% white and 50% male. MEASUREMENTS: Periodontal examination, including probing depth and attachment loss, was performed. Periodontal disease extent was divided into 0% of sites with probing depth of 6 mm or more, 1% to 10% of sites with probing depth of 6 mm or more and more than 10% of sites with probing depth of 6 mm or more. Subgingival plaque samples were collected from four molar teeth, and the levels of periodontal pathogens were determined using the benzoyl-DL-arginine-naphthylamide (BANA) test. Plasma interleukin-6 (IL-6), C-reactive protein (CRP), plasminogen activator inhibitor type-1 (PAI-1), and tumor necrosis factor alpha (TNF-alpha) levels were measured in all participants. Assessments of risk factors associated with elevated levels of markers of systemic inflammation were also determined. Multiple regression analysis was employed to analyze the data. RESULTS: IL-6 levels were significantly higher in participants with more-extensive periodontal disease than in other participants. Periodontal disease extent was significantly associated with higher TNF-alpha plasma levels, controlling for established risk factors for elevated TNF-alpha levels. Participants with BANA-positive species had significantly higher CRP plasma levels when controlling for risk factors for elevated CRP levels. CONCLUSION: Periodontal disease and infection may be modifiable risk indicators for elevated levels of systemic inflammatory markers in older people.

Aged↗

PubMed1998

Prevention of periodontal disease.

Periodontal disease is the most common disease affecting adult dogs and cats. It is also a very preventable disease. The insidious nature of the disease and requirement for the pet owner to be actively involved make client and public education absolutely vital. Although clients are commonly aware of their pets' bad breath, they rarely notice gingivitis, fractured teeth, and traumatic malocclusions. The annual National Pet Dental Health Month program has resulted in a tremendous increase in public awareness. Veterinarians must carry this further in their everyday practices, convincing our clients of the need for preventive dental care. It is only through clients' ongoing desire and persistence that a long-term preventive program can be successful. This requires a coordinated effort by the entire hospital staff. When successful, clients' pets will live healthier and longer lives.

Animals↗

PubMed2000

Predisposing factors and gross examination findings in periodontal disease.

Periodontal disease is the most frequently encountered condition by small animal practitioners. A complete oral examination including visual examination, periodontal probing, and intraoral radiographs are necessary to determine the grades of disease present, and the predisposing factors contributing to it.

Animals↗

PubMed2000

Local antimicrobial therapies in periodontal disease.

Periodontal therapy has the primary aim of halting periodontal disease progression. Clinical trials over the years have indicated that meticulous scaling and root planing in conjunction with a patient's proper plaque control can arrest periodontitis, but this therapy is not always completely effective and thus adjunctive therapies need to be considered. Local delivery of antibacterial agents into periodontal pockets has been extensively developed and investigated since the late 1970s and many systems have been designed to maintain high levels of antimicrobial agents in the crevicular fluid with minimal systemic uptake. More recently subgingival antimicrobial delivery systems have become available to the practising periodontist for clinical use. These systems, employ different antimicrobial agents but also different delivery systems which influence the concentration of available drug over time. The dental profession is confused by the wide variety of available slow release subgingival antimicrobial devices on the market and clearly comparative independent assessment of these therapies is needed. This review will summarise the findings of a comparative study on three commonly available periodontal local delivery antimicrobial systems on sites with previously unsuccessful mechanical therapy. The slow release devices studied adjunctively with root planing were: Actisite, Dentomycin and Elyzol, compared to root planing alone. Substantivity of an antimicrobial system is the ability of the system to maintain an effective concentration of drug over time which may be the most significant difference between the three delivery systems rather than the type of antimicrobial drug used. Although all three locally applied antimicrobial systems seem to offer some benefit over scaling and root planing alone, a treatment regime of scaling and root planing plus tetracycline fibre placement gave the greatest reduction in probing pocket depth over the six months after treatment.

Administration, Topical↗

PubMed2006

[The mechanism of bone resorption in chronic inflammation of periodontal disease].

Periodontal disease is caused by infections with oral periodontitis-associated microorganisms. Virulence factors like lipopolysaccharide (LPS) from those microorganisms initiate host immune response and gingival chronic inflammation. As a result, elevated receptor activator of NF-kappaB ligand (RANKL) expression stimulates alveolar bone resorption followed by loss of teeth.

Animals↗