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Results for “PERIODONTAL DISEASE”

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At least 235 records · Page 13Linked to original sources
PubMed2001

Effect of long-term intermittent periodontal care on canine periodontal disease.

The periodontal health status was assessed in two groups of dogs which had received different levels of periodontal care over a two-year period. The dental group received regular dental scaling and polishing, and intermittent daily tooth brushing, while the control group received no periodontal care. All dogs developed gingivitis, and two (one from each group) showed evidence of incipient periodontitis. The dental group had a reduced gingivitis index (GI) compared with the control group only when they had received daily tooth brushing before the GI assessment. When the dogs had not had their teeth brushed for four weeks before the assessment, the GI was not significantly different to that in the control dogs. This suggests that continual periodontal care throughout life is of great importance and questions the benefits of intermittent oral care. The GI of the palatal and lingual surfaces in all dogs was significantly higher than the GI of the buccal surfaces. Thus, all tooth surfaces may need to be cleaned to achieve optimal periodontal health.

Animals↗
PubMed2003

Periodontal disease in HIV-positive individuals: association of periodontal indices with stages of HIV disease.

BACKGROUND: Periodontal disease has been previously associated with human immunodeficiency virus (HIV) infection, and HIV infection has been considered a modifier of periodontal disease. The aim of this study was to report the prevalence and severity of periodontal disease in a population of HIV-positive individuals and to investigate the association between clinical periodontal indices and the stage of HIV disease, as expressed by CD4 cell counts. METHODS: Thirty-nine male HIV-positive patients were recruited and a medical history was taken. To evaluate periodontal disease, probing depth (PD), attachment level loss (AL), bleeding index (BI), and modified gingival index (MGI) were recorded. Associations between the above indices and CD4 counts were examined. RESULTS: Immunocompromised patients (with CD4 cell counts < 200 cells/microl) showed significantly lower BI and fewer sites with PD and AL > 4 mm compared to patients with CD4 cell counts > 200 cells/microl. When patients with CD4 counts < 500 cells/microl were considered alone, a correlation was observed between CD4 cell counts and BI (r2 = 0.1617, P = 0.0463), MGI (r2 = 0.2123, P = 0.0204), and number of sites with AL > 4 mm (r2 = 0.1469, P = 0.056). CONCLUSIONS: Severely immunocompromised HIV-positive patients showed less severe gingival inflammation than expected. Patients with CD4 cell counts > 500 cells/microl showed no association between CD4 cell count and periodontal indices.

Adult↗
PubMed1994

Bacteriological diagnosis of periodontal disease.

Dental plaque bacteria cause virtually all the forms of inflammatory periodontal disease. Periodontitis is caused by the specific periodontopathic bacteria, which induce destruction of connective tissue attachment and adjacent alveolar bone. Examinations to identify the infections by Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Campylobacter rectus, Bacteroides forsythus, Fusobacterium nucleatum, Eikenella corrodens and Treponema denticola have recently become essential in diagnosis of periodontal disease. Bacterial examination permits (1) identification of the causative bacteria, (2) assessment of disease activity and (3) monitoring of the effective of periodontal treatments. The author describes details of accurate and rapid methods for detecting periodontopathogens. Transmission of periodontopathic bacteria as clarified by bacterial examination is also discussed in this review. The pathogenic potential of specific bacteria varies among patients and periodontally healthy individuals and can be controlled by host defense mechanisms such as immune responses. The roles of immune responses against periodontopathic bacteria in balance shifts of periodontal disease processes are therefore also discussed in this review.

Antibodies, Bacterial↗
PubMed1997

Epidemiology and diagnosis of HIV-associated periodontal diseases.

A review of periodontal disease as a manifestation of HIV infection suggests a shift in emphasis over the past 5 years. Initially the focus was on newly described forms of periodontal disease (i.e., HIV-associated gingivitis or linear gingival erythema (LGE); HIV-associated periodontitis or necrotizing ulcerative periodontitis (NUP). While the clinical definition of LGE varies from study to study, an association between LGE and Candida infection has been described. Furthermore, the prevalence of NUP is quite low and this disorder is associated with severe immunosuppression. In contrast, the focus today is on the accelerated rate of chronic adult periodontitis occurring in seropositive patients. While the organisms that characterize adult periodontitis in seronegative individuals are present in subgingival plaque from seropositive individuals, reports suggest that atypical pathogens are also present (i.e., Mycoplasma salivarium, Enterobacter cloacae). Recent studies from our laboratory have identified a novel strain of Clostridium isolated from the subgingival plaque of injecting drug users that has pathologic potential. This organism, however, was found in both seropositive and seronegative individuals in this cohort, suggesting an association with lifestyle rather than serostatus. In addition, data has been published examining the local host response in periodontitis in seropositive individuals. Distinctly elevated levels of IgG in gingival crevicular fluid (GCF) have been observed in seropositive patients. Furthermore, data from our laboratory examining inflammatory mediators in GCF (polymorphonuclear leukocyte lysosomal enzyme beta-glucuronidase and the pro-inflammatory cytokine interleukin-1 beta) suggests an altered response in patients with HIV infection. The alteration manifests as the absence of the expected strong correlation between polymorphonuclear leukocyte activity in the gingival crevice and clinical measures of existing periodontal disease, as well as elevated levels of interleukin-1 beta in sites with deeper probing depths. Therefore, it can be concluded that the progression of periodontal disease in the presence of HIV infection is dependent upon the immunologic competency of the host as well as the local inflammatory response to typical and atypical subgingival microorganisms.

Adult↗
PubMed2001

General health risk of periodontal disease.

The possibility that periodontal disease might influence the morbidity and mortality of systemic diseases constitutes a research topic of great current interest. Human periodontal disease is associated with a complex microbiota containing approximately 500 microbial taxa and various human viruses, many of which possess significant virulence potential. Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and other periodontopathic bacteria that are unique to the oral cavity and may disseminate to other body sites comprise the best-documented form of dental focal infection. However, systemically healthy individuals seem to be at low risk of acquiring acute non-oral diseases from direct infections by periodontal pathogens. Research data from various laboratories point to periodontal infections as a risk factor for chronic medical disorders, including cardiovascular disease, cerebrovascular accidents and low-birth-weight infants. However, recent epidemiological studies have failed to show a significant relationship between periodontal disease and cardiovascular disease. This review paper evaluates the current status of knowledge on dental focal infection and suggests avenues for further research into the topic of general health risks of periodontal disease.

Aggregatibacter actinomycetemcomitans↗
PubMed1990

Identification of polymorphonuclear leukocyte collagenase and gelatinase activities in mouthrinse samples: correlation with periodontal disease activity in adult and juvenile periodontitis.

In previous studies, elevations in the levels of active and latent collagenase in gingival crevicular fluid (GCF) have been correlated positively with periodontal disease activity. To provide a simple diagnostic approach for testing collagenolytic activity, the feasibility of using a 3.0 ml water mouthrinse to collect GCF simultaneously from all sites in the mouth was assessed. Patients with adult periodontitis (AP, n = 23) and local juvenile periodontitis (LJP, n = 7) were sampled before periodontal therapy and some (12 AP, 4 LJP) were also assessed longitudinally after scaling and root planing, administration of antibiotics, and following periodontal surgery. Healthy patients (n = 19) were used as controls. The levels of active collagenase, procollagenase, and collagenase inhibitor activity were determined by functional assays and quantitated after SDS-PAGE and fluorography. Gelatinase and progelatinase were assayed by enzymography on gelatin-substrate gels. Active collagenase levels were found to be significantly higher (14- to 20-fold) in AP and LJP patients compared to controls, whereas matrix metalloproteinase activity was not detected in mouthrinses from edentulous patients. Collagenase inhibitor levels were generally low in all groups of subjects tested. Following clinical treatment the levels of active collagenase and gelatinase were reduced; the reduction was significant for active collagenase after tetracycline treatment and scaling in LJP patients. Of the clinical indices recorded (gingival index, plaque index, and pocket depth) there were no significant correlations with enzyme activity but similar trends were observed between the changes in active collagenase and gingival index. In patients with untreated periodontal disease, collagenase occurred predominantly in the active form. N-ethylmaleimide (NEM) and p-aminophenylmercuric acetate (AMPA) were equally effective as activators of the latent collagenase, indicating that the collagenase was derived from PMNs, which were also the source of gelatinase. The results of these studies indicate that measurement of active collagenase and gelatinase in mouthrinse samples is potentially useful in the diagnosis and assessment of periodontal disease activity.

Adolescent↗
PubMed2004

Relationship of periodontal disease and tooth loss to prevalence of coronary heart disease.

BACKGROUND: Studies relating periodontal disease to coronary heart disease (CHD) have provided equivocal results using tooth loss and/or clinical signs of periodontal disease as measures of periodontal exposure. METHODS: The purpose of this cross-sectional study was to evaluate the relationship of tooth loss and periodontitis to prevalent CHD at the Atherosclerosis Risk in Communities (ARIC) visit 4 using both tooth loss and clinical signs of disease in a population-based sample of 8,363 men and women aged 52 to 75 years from four U.S. communities. Each subject participated in a complete periodontal examination, assessment of missing teeth, assessment of prevalent CHD, and a number of laboratory tests and questionnaires. High attachment loss was defined as > or = 10% of sites with attachment loss > 3 mm and high tooth loss was defined as fewer than 17 remaining teeth. RESULTS: Individuals with both high attachment loss and high tooth loss (odds ratio [OR] 1.5, 95% confidence interval [CI] 1.1 to 2.0) and edentulous individuals (OR 1.8, CI 1.4 to 2.4) had elevated odds of prevalent CHD compared to individuals with low attachment loss and low tooth loss, while controlling for a number of traditional risk factors for CHD. CONCLUSIONS: These results suggest that tooth loss and periodontal disease are associated with prevalent CHD, but only when both are present. The weaker relationships between periodontal disease and CHD that have been found among older adults may be due to older adults having fewer teeth. Future longitudinal studies should be designed to ascertain the cause of tooth loss during follow-up.

Black or African American↗
PubMed2006

Salivary enzymes and periodontal disease.

BACKGROUND: Host responses to periodontal disease include the production of different enzymes that are released by stromal, epithelial or inflammatory cells. There are important enzymes associated with cell injury and cell death like: aspartate and alanine aminotransferase (AST, ALT), lactate dehydrogenase (LDH), creatine kinase (CK), alkaline and acidic phosphatase (ALP, ACP), gama glutamyl transferase (GGT). Changes in enzymatic activity reflect metabolic changes in the gingiva and periodontium in inflammation. DESIGN OF STUDY: In this paper we have examined the activity of CK, LDH, AST, ALT, GGT, ALP and ACP in saliva from patients with periodontal disease before and after periodontal treatment (experimental group, 30 samples) and in saliva from healthy patients (control group--20 samples). Periodontal disease was determined based on clinical parameters (gingival index (GI), bleeding on probing (BOP), probing depth (PD)). Patients with periodontal disease were under conventional periodontal treatment. RESULTS: Obtained results were shown statistically significant increases of activity of CK, LDH, AST, ALT, GGT, ALP, ACP in saliva from patients with periodontal disease in relation to control group. There is positive correlation between the activity of examined salivary enzymes and value of the gingival index. After conventional periodontal therapy the activity of all salivary enzymes was significantly decreased. CONCLUSIONS: Based on these results, it can be assume that activity of these enzymes in saliva, as biochemical markers for periodontal tissue damage, may be useful in diagnosis, prognosis and evaluation of therapy effects in periodontal disease.

Adult↗
PubMedDate not supplied

[Osteoclasts activation by bacterial endotoxins during periodontal diseases].

During periodontal infections, bacterial lipopolysaccharides (LPS) from Gram negative bacteria, along with other bacterial products, drive alveolar bone destruction. Tissue destruction occurs through both direct and indirect pathways. In the indirect pathway, LPS induce the secretion of proinflammatory cytokines, which in turn provokes a cascade of reactions leading to osteoclasts activation. In the direct pathway, LPS stimulate osteoblasts, osteoclasts precursors and osteoclasts, with an inflammatory cytokines independent manner. In this paper, the mechanisms involved in these two pathways are reviewed.

Endotoxins↗
PubMed1993

The current status and future prospects of altering the pathogenic microflora of periodontal disease.

Modern periodontal therapy aims to suppress or eradicate periodontal pathogens and to maintain a posttreatment flora that is compatible with health. Systemic and local antimicrobial therapies have demonstrated effectiveness against several periodontal pathogens. Sustained-release devices, or irrigators, for local application of antimicrobial agents to periodontal pockets show great promise. Replacement therapy and periodontal vaccines, although still in the early research phase, represent very interesting approaches for preventing periodontitis. Using modern molecular genetic methods, it is theoretically possible to clone virulence determinants of periodontal pathogens into a nonpathogenic organism. The carrier organism with the expressed foreign antigens may be implanted in the oral cavity or the intestinal tract to induce long-lasting immunity against the targeted periodontal pathogens.

Anti-Bacterial Agents↗
PubMed1991

[Importance of periodic follow up of periodontal diseases for the maintenance of periodontal health and the longevity of dental restoration].

The major objective of the author's investigation was to determine if the progression of attachment loss, the recurrence of active phase of periodontitis and development of new carious lesions can be controlled and prevented in individuals with prior history of aggressive periodontitis provided full mouth reconstruction and maintained at a proper level of oral hygiene. The results of a group on regular periodontal recall program were compared with the five years dental and periodontal findings on a matched group of patients having not been on regular maintenance program. The well maintained group of patients' annual recall data did not vary markedly. In five years basically the same amount of attachment apparatus was maintained. The reexamination of the non recall group at the end of the fifth year shoved a total deterioration of dentition due to the progression of periodontal disease and attachment loss. Especially those of rapidly progressing periodontitis cases shoved 70 to 100% attachment loss. This comparative study attempted to outline the insufficiency of our former dental philosophy of patient management and follow up. Authors emphasize the importance of the follow up, and maintenance of a very high level.

Adult↗