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Results for “PERIODONTAL DISEASES”

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At least 19 recordsLinked to original sources
PubMed2001

[The prevalence of periodontal disease. Periodontal disease in black Africa. The impact of socioeconomic factors and cultural customs].

The lack of reliable and recent information about the oral and dental health conditions of many African countries is a serious object of concern. There is an urgent need of up-to-date information about the oral and dental diseases existing among the various African populations and about their deciding factors. This study takes stock of the periodontal diseases in black Africa and mention the influence of the socio-economic advancing and the cultural habits.

Adult↗
PubMedDate not supplied

Bacteriocin production by Actinobacillus actinomycetemcomitans isolated from the oral cavity of humans with periodontal disease, periodontally healthy subjects and marmosets.

The ability of Actinobacillus actinomycetemcomitans to produce bacteriocin has rarely been reported. Antagonistic substance production may confer an important ecological advantage for the producer microorganisms, especially in a competitive ecosystem such as the oral cavity. In the present study, 75 A. actinomycetemcomitans strains isolated from the oral cavity of human patients with periodontal disease, periodontally healthy subjects and marmosets, as well as two reference strains (A. actinomycetemcomitans ATCC 29523 and FDC Y4) were evaluated for auto-, iso-, and heteroantagonistic activity. Fifty-one (68.00%) strains exhibited antagonistic activity; heteroantagonism was observed more often than isoantagonism. Isolated strains antagonized 17 different species of gram-positive and gram-negative bacteria from the oral and nonoral microbiota. Sensitivity to heat and to proteolytic enzymes constituted strong evidence that the antagonistic substance has a proteic nature. Taken together, our data enabled us to confirm that the antagonistic substance detected was a bacteriocin. The wide spectrum of activity indicates the possibility that more than one antagonistic substance is produced and that these substances play an important role in the ecological balance of the oral ecosystem.

Actinobacillus Infections↗
PubMed2006

Studies on periodontitis and analyses of individuals at risk for periodontal diseases.

Periodontal disease is an infectious disease initiated by microbial plaque, which accumulates on the tooth surface at the gingival margin and induces an inflammatory reaction. The function of the inflammatory process is to protect the host, however the process may also contribute to tissue destruction. Most individuals show gingival inflammation, but only a limited number suffer from periodontitis i.e. loss of attachment. Without treatment, periodontitis will result in tooth mobility and subsequent tooth mortality. Independent of ethnicity, 10%-15% of an adult population will develop severe periodontitis The aim of this thesis has been to analyse individuals at risk for periodontal disease. Four studies have been conducted in 2 different groups of individuals with: Recurrent periodontitis kept in a maintenance care program--studies I-III. Type 2 diabetes (T2D)--study IV. In study I, the clinicaleffect of local periodontitis treatment with an antibiotic gel was investigated. In study II, the microbiologicaleffect of periodontitis treatment with the same antibiotic gel as in study I was investigated. In study III, it was investigated whether the interleukin-l (IL-1alpha and beta) and interleukin-6 (IL-6) gene polymorphisms were associated with the susceptibility of chronic periodontitis. In study IV, the prevalence of periodontitis in individuals with T2D was investigated, together with the prevalence of diabetic complications in relation to periodontal disease. We also studied whether there was a difference in dental care habits and knowledge of oral health between T2D subjects with and without periodontal disease. In conclusion, this thesis did not find any significant clinical and microbiological differences between subjects with recurrent periodontal disease treated with a locally delivered metronidazole gel compared to a placebo gel. Neither could we find an association between genetic variants in the IL-lalpha, IL-beta and IL-6 genes in individuals with or without periodontal disease. The prevalence of severe periodontitis, according to radiographic criteria, was almost 20% in subjects with T2D. This was further confirmed by clinical parameters. T2D individuals with periodontal disease demonstrated a higher HbAlc level, a higher prevalence of cardiovascular complications and a higher proportion of smokers compared to periodontally healthy T2D subjects. Finally, T2D individuals seem to lack sufficient knowledge about oral health.

Adult↗
PubMed2005

Immune response: the key to bone resorption in periodontal disease.

Periodontal disease infection with oral biofilm microorganisms initiates host immune response and signs of periodontitis, including bone resorption. This review delineates some mechanisms underlying the host immune response in periodontal infection and alveolar bone resorption. Activated T lymphocytes have been historically implicated in experimental periodontal bone resorption. An experimental rat adoptive transfer/gingival challenge periodontal disease model has been demonstrated to require antigen-specific T lymphocytes and gingival instillation of antigen and LPS for bone resorption. Interference with costimulatory interactions between T cells and antigen-presenting cells abrogated bone resorption, further emphasizing the significance of immune response in periodontal disease. Receptor activator of nuclear factor kappaB ligand (RANKL), a critical osteoclast differentiation factor, is expressed on T lymphocytes in human periodontal disease as determined by immunohistochemical and confocal microscopic analyses. Interference with RANKL by systemic administration of osteoprotegerin (OPG), the decoy receptor for (and inhibitor of) RANKL, resulted in abrogation of periodontal bone resorption in the rat model. This finding indicated that T cell-mediated bone resorption is RANKL-dependent. In additional experiments, treatment of T cell-transferred rats with kaliotoxin (a scorpion venom potassium channel inhibitor) resulted in decreases in T-cell RANKL expression, diminished induction of RANKL-dependent osteoclastogenesis, and abrogation of bone resorption, implicating an important role of immune response/RANKL expression in osteoclastogenesis/bone resorption. In other experiments, adoptive transfer of antigen-specific, RANKL-expressing B cells, and infection with the antigen-bearing Actinobaccillus actinomycetemcomitans gave rise to periodontal bone resorption, indicating that B cells also have the capacity to mediate bone resorption, probably via RANKL expression. In humans, prominent T lymphocytes have been identified in periodontal disease, and diseased tissues showed elevated RANKL mRNA expression, as well as decreased OPG mRNA expression. Mononuclear cells from periodontal lesions involving T cells and B cells of patients induced osteoclastogenesis in vitro. In summary, a biofilm interface initiates immune cell infiltration, stimulating osteoclastogenesis/bone resorption in periodontal disease. This resorption can be ameliorated by inhibition of RANKL activity or by diminishing immune cell stimulation. These two procedures, if localized, have the potential to lead to the prevention or therapeutic management of periodontal disease and therefore require further study.

Aggregatibacter actinomycetemcomitans↗
PubMed2001

Clinical usefulness of microbiological diagnostic tools in the management of periodontal disease.

Periodontal diseases comprises a group of chronic inflammatory conditions affecting tooth supporting structures. It has been known for a long time that pathogenic oral bacteria colonizing the tooth surface are associated with the initiation of the disease process. However, to date, a dozen or so bacterial species have been implicated in the pathogenesis of periodontal disease and no one species by itself is synonymous with disease onset. This multibacterial etiology renders the diagnosis of active periodontal disease based on microbiological data difficult. Numerous studies have attempted to relate the usefulness of microbiological diagnostic aids such as microscopy, bacterial culture, immunological and enzymatic assays. Furthermore, recent technical advances have resulted in the use of nucleic acid probes and amplification techniques for the identification of genetic material belonging to potential periodontal pathogens. Despite the availability of a large number of microbiological testing protocols, identification of the microbial etiological agents remains hampered by the complexity of the microbial challenge during periodontal disease. This review discusses the clinical usefulness of these tests in detection and management of periodontal disease.

Bacteria↗
PubMed2000

Polymorphism of the N-acetyltransferase (NAT2), smoking and the potential risk of periodontal disease.

Periodontal disease is a common multifactorial process that leads to bone destruction and tooth loss. Interactions of environmental and genetic factors determine the extent and severity of periodontal disease. Smoking is one of the risk factors for periodontal disease, and the risk may be influenced by the polymorphism of N-acetyltransferase (NAT2) via metabolism of smoke-derived xenobiotics. We therefore hypothesized that a NAT2 genotype would be a risk factor for periodontal disease. A total of 154 Caucasian subjects were assigned to one of two groups (1) no or mild and (2) severe periodontal disease based on radiographic (bone destruction) and clinical criteria (probing depth, attachment loss) and the number of teeth. In all subjects genotyping for mutations on NAT2 was performed by means of PCR and RFLP analysis. In the less-affected group genotyping showed a fraction of predicted slow and rapid acetylators (53.6% and 46.4%, respectively) corresponding to the normal distribution in Caucasians. Severely affected patients were predominantly slow acetylators, the odds ratios being between 2.38 and 5.02 for the NAT2-related risk depending on the outcome parameters chosen. Adjustment for age had no influence on these findings. Our data indicate that the slow acetylator phenotype is associated with a higher risk of periodontitis, especially with respect to the severity of the disease. Possible implications with respect to the risk associated with smoking are discussed.

Acetylation↗
PubMed2003

The effect of oral hygiene instructions on diabetic type 2 male patients with periodontal diseases.

Periodontal disease and diabetes are two common chronic diseases affecting humans. The aim of this study was to assess the effect of oral hygiene instructions on periodontal disease among type 2 male diabetic Saudi subjects. Sixty subjects completed the study and were divided into three groups of 20: healthy (non-diabetic) with periodontal disease, type 2 diabetic with early or moderate periodontal disease, and type 2 diabetic with advanced periodontitis. The age ranged from 24-64 (42 +/- 13.60) years. The subjects were examined at King Saud University, College of Dentistry, Riyadh, Saudi Arabia. Oral hygiene practices and smoking habits were recorded. Oral hygiene instructions given to patients were to use an Oral B medium toothbrush and brush three times daily for 7 days using the by Bass technique for 2 minutes. Fasting blood glucose level (FBGL), gingival crevicular fluid (GCF), community periodontal index of treatment needs (CPITN), and plaque index (Pll) were used to assess patients' profiles at baseline and at recall visit after 7 days. The results showed there was a significant overall decrease in FBGL, baseline 172.67 mg/dl (+/-64.69) to recall visit 162.20 (+/-58.78) P = 0.000, and GCF volume decreased from.4041 micro l (+/-.1260) to .3698 micro l (+/-.1164) P = 0.000. There was a significant reduction in subjects' CPITN mean scores (from 13.98 (+/-8.24) to 13.32 (+/-8.97) P = 0.000), but there was no significant difference in Group 3 with advanced periodontitis, i.e., 22.25 (+/-1.37) to 22.30 (+/-1.38). There was more than a 47% reduction in the overall percentage of plaque scores. The decrease ranged from 82.27 (+/-19.34) to 34.45 (+/-17.04) at baseline and recall visit respectively. It is concluded oral hygiene instructions (a standardized regimen) has an effect on FBGL, GCF, CPITN, and PlI. It is also concluded CPITN is not very sensitive to assess change in periodontal status over a 7 days period. Further studies are needed among diabetic and healthy subjects with a larger sample size and over a longer period of time.

Adult↗
PubMed2001

[The pathological entirety of periodontal diseases].

Periodontal disease is a major cause in the lost of human teeth. The pathological entirety of periodontal disease is a diverse and obscure. However, a large amount of outcomes concerning the pathogenesis of periodontal diseases due to the recent development of bacteriology and molecular biology have been obtained. Among these, the evidence of formation of biofilm by periodontopathic bacteria, which disturbs periodontal therapy, and the concept of risk factors on the pathogenesis of periodontal disease are novel. It is currently suggested the possibility of genetic diagnosis of the susceptibility to periodontal diseases.

English Abstract↗
PubMed1985

Current concepts in periodontal diseases.

Periodontal diseases are common oral diseases that afflict all humans to some degree. The major aetiological agent is dental plaque--the complex microflora which forms on teeth in the absence of effective oral hygiene. The interaction of the microbial flora and the periodontal tissues produces an inflammatory response and tissue breakdown. Recent information has categorized periodontal diseases on the basis of increased knowledge about the particular microorganisms associated with the different clinical conditions. In addition, the important role of host defences, in particular the phagocytic cellular elements, has allowed for a better understanding of the pathological processes. This knowledge is contributing towards the development of rational and effective therapy for all forms of periodontal diseases. Because of the widespread occurrence of periodontal diseases and their potential relationships to systemic conditions, it is important that medical practitioners should be able to recognize, and be conversant with methods of treatment of, these diseases.

Acute Disease↗
PubMed2004

Periodontal disease and biomarkers related to cardiovascular disease.

Periodontal disease is a chronic infection of the gums characterized by a loss of attachment between the tooth and bone, and by bone loss. We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. The final sample consisted of 468 men (ages 47-80 yrs), participating in the Health Professional Follow-up Study, who provided blood and were free of CVD, diabetes, and cancer. In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). Based on our data, periodontal disease showed significant associations with biomarkers of endothelial dysfunction and dyslipidemia, which may potentially mediate the association between periodontal and cardiovascular disease.

Age Factors↗
PubMed2002

Inhibition of alveolar bone loss by matrix metalloproteinase inhibitors in experimental periodontal disease.

Periodontal disease is characterized by excessive host collagenase resulting in loss of gingival and periodontal ligament collagen and adjacent alveolar bone. Intragingival endotoxin injection induces a model of periodontal disease characterized by rapid bone loss with biochemical features similar to that of naturally occurring adult periodontitis. CH1766, a peptide with a zinc binding moeity which fits into the active site of the enzyme, and CH6631, a hydroxamic acid derivative with aryl-substituted sulphonamide residues, are inhibitors of matrix metalloproteinases (MMPIs) with differing inhibitory profiles as characterized by in vitro assays. In this study, endotoxin was injected into the gingivae of rats which were then treated orally with either 3 mg/kg or 30 mg/kg of one of the two inhibitory compounds. The gingival tissues were assessed for collagenase and gelatinase activity, plus three different pro-inflammatory cytokines. In addition, alveolar bone height in defleshed jaws was studied by computerized morphometric analysis and scanning electron microscopy. Both drugs reduced active and/or total MMP activity, in many cases to normal, and also partially normalized cytokine levels as well. A dose-response effect was seen with regard to amelioration of lipopolysaccharide-induced alveolar bone loss with both drugs. Other than studies with tetracyclines, this is the first report of beneficial effects of MMPIs in a model of periodontal disease, strongly suggesting that this class of agents could bring therapeutic benefit to patients with this disorder, and that periodontal disease can be used as a model to demonstrate in vivo efficacy of this class of drugs.

ADAM Proteins↗
PubMedDate not supplied

The role of salivary cytokines in the etiology and progression of periodontal disease.

Periodontal disease is a common oral disease in all segments of the population, regardless of their systemic health status. The disease is generalized or localized and the severity of lesions can vary at different sites. It is possible to recognize a number of different types of periodontal disease on the basis of clinical and pathological criteria, which include the extent of periodontal destruction, the age of onset and severity of disease, the distribution of lesions, the microflora involved, and the variation in host responses. The ultimate outcome of periodontal disease in adults, whether treated or untreated, depends on patient susceptibility. While periodontopathic bacteria are recognized as the etiologic agents in periodontal disease, their interaction with and modulation of the host immune response is of fundamental importance. An interplay of protection and pathology active in periodontal disease is that of T-lymphocyte cells and the subsequent production of cytokines within the periodontal tissues.

B-Lymphocytes↗
PubMed1996

Peripheral blood leukocyte populations in the elderly with and without periodontal disease.

Periodontal disease in the elderly has not been characterized. Initial reports suggest that the disease is common and severe. Deficiencies in the immune response have also been reported to occur in the elderly. Consequently it was hypothesized that aging-related changes in the immune response may contribute to the severity and occurrence of periodontal disease in the elderly. To test that hypothesis, the % and number of leukocytes and leukocyte subsets in the peripheral blood of elderly (65-75 years) subjects were tested and used as indicators of the immune potential of those individuals. Age and gender effects on several of the parameters tested were identified. With the exception of increased number of leukocytes in the elderly group with severe periodontal disease, no other alteration in the leukocyte parameters tested were identified. These results suggest that periodontal disease in the elderly was not associated with obvious changes in the leukocyte and leukocyte subsets in the peripheral blood due to aging.

Adult↗