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At least 199 records · Page 11Linked to original sources
PubMed1984

Vitamin C, oral scurvy and periodontal disease.

Scurvy and periodontitis both manifest gingival bleeding but constitute separate entities. Defective collagen in scurvy reflects many symptoms emanating from deficient vitamin C physiology. The various periodontal diseases are caused by oral plaque micro-organisms, the body's reaction to which is strongly influenced by inadequate functioning of leucocytes and monocytes. Although certain infections and systemic diseases cause gingival bleeding, avitaminosis C does not cause commonly encountered periodontal disease, but will aggravate established periodontitis. Vitamin C should not be used for prophylaxis or cure of periodontitis in healthy well-nourished individuals. A patient with bleeding gingivae warrants referral to oral medicine and periodontics specialists for examination and treatment.

Adult↗
PubMedDate not supplied

The influence of smoking and non-insulin-dependent diabetes mellitus on periodontal disease.

The periodontal health of smokers and non-smokers with non-insulin-dependent diabetes mellitus (NIDDM) and non-smokers with periodontitis who were not suffering from a systemic disease was assessed. The investigation was carried out on 60 adult subjects. Levels of blood glucose, glycosylated haemoglobin and immunoglobulins G, A and M were determined, together with the plaque index, gingival index, probing pocket depths and clinical attachment level. Periodontitis was more severe in smokers and non-smokers with NIDDM than non-smokers without NIDDM, and the periodontal condition (clinical attachment level, probing pocket depth and gingival bleeding) was better in non-smokers with NIDDM than smokers with NIDDM. The results suggest that diabetes and smoking are high-risk factors for periodontal disease.

Adult↗
PubMed2006

Gingival crevicular fluid matrix metalloproteinase (MMP)-7, extracellular MMP inducer, and tissue inhibitor of MMP-1 levels in periodontal disease.

BACKGROUND: During periodontal inflammation, matrix metalloproteinases (MMPs) are under the control of several regulatory mechanisms including the upregulation of expression by inducers and downregulation by inhibitors. Our study aimed to examine the levels and molecular forms of MMP-7, tissue inhibitor of MMP (TIMP)-1, and extracellular matrix metalloproteinase inducer (EMMPRIN) in gingival crevicular fluid (GCF) from patients with different periodontal diseases. METHODS: A total of 80 subjects (20 patients with generalized aggressive periodontitis [GAgP], 20 with chronic periodontitis [CP], 20 with gingivitis, and 20 periodontally healthy subjects) were included in this study. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing, and plaque. GCF MMP-7, TIMP-1, and EMMPRIN levels and molecular forms were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western immunoblot techniques using specific antibodies. RESULTS: Total amounts of GCF MMP-7 were found to be similar between the study groups. GAgP, CP, and gingivitis groups had significantly higher total amounts of GCF EMMPRIN compared to healthy subjects (P <0.008). Among the patient groups, the GAgP group had the highest total amount of GCF EMMPRIN relative to the gingivitis group (P = 0.0004). Soluble EMMPRIN existed in GCF in multiple molecular-weight species especially in periodontitis-affected GCF under non-reducing conditions, i.e., 30-, 55-, 100-, 180-, and 200-kDa species. All patient groups had significantly elevated total amounts of GCF TIMP-1 relative to the healthy group (P <0.0001). GAgP and CP groups also had a higher total amount of GCF TIMP-1 compared to the gingivitis group (P <0.0001 and P <0.0001, respectively). The GAgP group had higher GCF TIMP-1 and EMMPRIN levels compared to the CP group, but this elevation did not reach statistical significance. CONCLUSIONS: Our data indicate that MMP-7 is associated with the innate host defense in periodontal tissues. Increased EMMPRIN and TIMP-1 levels in GCF are associated with the enhanced severity of periodontal inflammation, indicating that these molecules can participate in the regulation of progression of periodontal diseases. To our knowledge, the present study demonstrated the presence of soluble forms of EMMPRIN in GCF of patients with different periodontal diseases for the first time.

Adolescent↗
PubMed1990

[Diagnosis of plaque related periodontal diseases].

Plaque related periodontal diseases include the area of slight gingivitis and advanced destructive periodontitis featuring loss of periodontal attachment and alveolar bone destruction. The progression of periodontitis may vary from rapid progressive disease, to stable condition but also remission of the disease. Not all patients are equally susceptible to destructive periodontal disease. Therefore, the 'risk concept' was introduced. The diagnosis of periodontal diseases is based on the assessment of periodontal inflammation and loss of attachment. The diagnostic parameters are described as well as their prognostic value.

Alveolar Bone Loss↗
PubMed1991

Periodontal diseases: a review.

Periodontal diseases are a collection of disorders that may affect patients throughout life. The most common form of periodontal disease, gingivitis, which affects only the soft tissues, is seen in children, adolescents, and adults. Periodontitis, which destroys the bone supporting a tooth, is found more commonly in adults over the age of thirty-five but may be present in a variety of forms in children after three years of age. These diseases are caused by bacterial plaque but may be modulated by systemic diseases, immunologic compromise, heredity, and other contributing factors. Periodontal pathoses may be an indication of an underlying systemic condition such as leukemia or human immunodeficiency virus infection. The standard treatment of periodontal diseases is the control of intraoral plaque. This may be accomplished using mechanical, chemotherapeutic, and surgical means.

Humans↗
PubMed2005

Evaluation of a monovalent companion animal periodontal disease vaccine in an experimental mouse periodontitis model.

Periodontal disease in companion animals is clinically similar to that of human periodontal disease. Despite the usage of veterinary procedures and antibiotic therapy, the disease still remains as one of the most highly prevalent disorders seen by veterinarians. The goal of this study was to evaluate the immunogenic properties and vaccine performance of a monovalent canine periodontal disease vaccine in the mouse oral challenge model of periodontitis. Mice vaccinated subcutaneously with inactivated, whole-cell bacterin preparations of Porphyromonas gulae displayed both high titers of anti-P. gulae specific antibodies and significantly reduced alveolar bone loss in response to homologous, heterologous, and cross-species challenge. Based on the results of these studies, a periodontal disease vaccine may be a useful tool in preventing the progression of periodontitis in animals.

Alveolar Bone Loss↗
PubMed2003

Neutrophil-mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis.

Neutrophils play a major role in the host response against invading periodontopathogenic microorganisms. Localized aggressive periodontitis (LAgP) is associated with various functional abnormalities of neutrophils. Based on the recent findings, LAgP neutrophils are not "hypofunctional" or "deficient." They are "hyperfunctional," and their amplified activity is responsible for the tissue destruction in periodontal disease. Several signal transduction abnormalities are associated with elevated neutrophil function in LAgP. There is a strong correlation between defective chemotaxis and decreased intracellular Ca2+ levels; total calcium-dependent protein Kinase C (PKC) activity of neutrophils is significantly lower than healthy subjects; and there is a marked increase in diacylglycerol (DAG) accompanied by a pronounced decrease in DAG kinase activity. In a separate set of experiments on the involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators in the pathogenesis of periodontal disease, crevicular fluid samples from LAgP patients were found to contain prostaglandin E2 (PGE2) and 5-LO-derived products, leukotriene B4 (LTB4), and the biosynthesis interaction product, lipoxin LXA4. Neutrophils from peripheral blood of LAgP patients, but not from healthy volunteers, also generated LXA4, suggesting that this immunomodulatory molecule may have a role in periodontal disease. Lipoxin generation and its relationship to PGE2 and LTB4 can be visualized as an important marker for the pathogenesis of periodontal disease. Thus, major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of LAgP. LAgP is used as an example of a severe periodontal disease that is related to abnormal neutrophil function. In this model, it appears that a hyperresponsiveness of the neutrophil, due to cell priming/predisposition, results in enhanced tissue damage.

Adjuvants, Immunologic↗
PubMed1993

Classification and diagnosis of periodontal diseases.

The classic periodontal diseases are gingivitis and periodontitis; there are, however, numerous and distinct types of both of these diseases. These types of diseases are distinguished by age of onset, clinical appearance, rate of disease progression, pathogenic microbial flora and systemic influences. Determining the type of periodontal disease a patient has requires a proper medical and dental history, a thorough periodontal examination and recording, and possible additional tests such as identification of subgingival flora and medical laboratory tests. Specific periodontal diagnosis will lead to more rational and efficient patient management.

Gingivitis↗
PubMed1995

The immunopathology of chronic inflammatory periodontal disease.

Chronic inflammatory periodontal disease is known to be under the control of the immune response. However, the precise mechanism of the immunopathogenesis of this lesion has not yet been fully elucidated. In this review, the regulatory role of both lymphoid and non-lymphoid cells as well as cytokines and accessory molecules in the course of chronic inflammatory periodontal disease is discussed. Finally, based upon previous evidences, an attempt to establish a model of chronic inflammatory periodontal disease is made herein.

Animals↗
PubMedDate not supplied

Evaluation of selected peripheral blood leukocyte functions in patients with various forms of periodontal disease.

INTRODUCTION: Periodontitis (P) is an infectious disease that develops in the supporting tissues of the tooth. One of the risk factors leading to it may be dysfunction of some immune system cells. Therefore, the object of the study was to assess selected functions of peripheral blood leukocytes in patients with various forms of P. As leukocytes are able to secrete interleukin (IL)-4 and IL-6, concentrations of their soluble receptors and the expression of their membrane receptors were investigated. MATERIAL AND METHODS: Twenty generally healthy subjects with aggressive (AP)and chronic periodontitis (CP)were enrolled in the study. The control group consisted of 8 healthy subjects,with no changes in periodontium. Peripheral blood mononuclear cells (PBMCs) were isolated and cultured. Levels of IL-4,IL-6,and their soluble receptors sIL-4R and sIL-6R were determined in the supernatant by ELISA. The expressions of cell surface IL-4R and IL-6R were assayed on PBMC using flow cytometry. RESULTS: No statistically significant differences were found in the selected parameters between people with periodontal disease and healthy controls. However, in subjects with AP, there was an increasing tendency in IL-6 concentration and IL-4R expression on PBMCs. CONCLUSIONS: Our results show that leukocytes play a significant part in P and their activity is probably lesion-dependent. Estimation of the cytokines secreted by leukocytes may facilitate differentiation and prognosis of the disease progression.

Adult↗
PubMedDate not supplied

Inappropriateness of the term "periodontal disease".

Traditionally, diseases that affect the periodontium have over the years been referred to as periodontal disease. This implies that these diseases are a single disease entity or only one disease, "periodontal disease," affects the periodontium. To date, dental literature is replete with several diseases that affect the periodontium. Most of these diseases exhibit unique bacteriological, immunological, biochemical and clinical features. It is these characteristics that qualify them to be regarded as individual or different disease entities. Biased by these recent reports on distinct diseases that affect the periodontium, several dental authors have written articles where they have preferred the term "periodontal diseases" to "periodontal disease," when discussing and reporting on the diseases that affect the periodontium. This paper suggests and discusses the reasons why scientists have continued to use the term periodontal disease and presents arguments why this terminology is inappropriate. It is suggested that the term "periodontal disease" be replaced by the term "periodontal diseases".

Disease Progression↗
PubMed1983

Policy implications of the epidemiology of dental diseases for the prevention and control of periodontal disease: the North Carolina studies.

The North Carolina Dental Manpower Study indicated that periodontal disease was widespread and little was being done to control the disease. We have continued to address issues identified by the Dental Manpower Study in order to better understand the high prevalence of periodontal disease. Drawing from the theoretical basis of behavioral science and the clinical and epidemiological knowledge of periodontal disease, we have planned a strategy for testing the feasibility for controlling periodontal disease through dental health services. Only when attention to periodontal disease pervades the thinking and behavior of all segments of the dental care system--professional education, professional certification and regulation, financing mechanisms, consumers, and dental research--will factors be totally conducive to controlling this problem.

Adolescent↗
PubMed2006

Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease.

BACKGROUND: Diabetes mellitus and periodontal disease have high incidence in the general population and are associated with various degrees of dysfunction in the immune system. It has been shown that diabetic patients with severe periodontal disease have more complications of diabetes and less effective metabolic control compared with diabetic patients with healthy gingiva. Patients with diabetes and severe periodontal disease present higher levels of serous immunoglobulin A (IgA). Elevation of the IgA1 isotype is thought to contribute to this phenomenon. Another important event in the diabetes-periodontitis association is the disturbance in local and systemic production of inflammatory cytokines. OBJECTIVE: In this study we tested the hypothesis that type 2 diabetic patients with chronic moderate periodontal disease have differences in salivary IgA1 titers and cytokine expression when compared with the chronic severe periodontal disease cases. METHODS: We utilized a jacalin-IgA capture assay to determine the IgA1 titers in total saliva and reverse transcriptase-polymerase chain reaction to detect mRNA for interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in total saliva samples of 13 patients with chronic moderate periodontal disease and 10 with chronic severe periodontal disease. RESULTS AND CONCLUSIONS: We observed a predominance of IgA1 titers of 64 (45.5%) in saliva samples from chronic severe periodontal disease patients and titers averaging 512 (30.8%) in chronic moderate periodontal disease patients. We detected mRNA for IFN-gamma in six out of 10 chronic severe periodontal disease subjects and in two out of 13 chronic moderate periodontal disease patients. TNF-alpha expression was similar in both groups. Our data suggest that higher levels of IgA1 may exert partial protection of the periodontal tissue in chronic moderate periodontal disease diabetic patients when compared to severe periodontal disease. Despite the small number of patients, IFN-gamma expression had a trend association with severity of periodontitis and TNF-alpha gene expression did not correlate with severity of periodontal disease.

Artocarpus↗