Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0031099 (periodontitis)
12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant antigens of outer surface proteins (Osps) OspA, OspB, OspC, OspE, and OspF of Borrelia burgdorferi sensu stricto and of p41-G, an antigenic region of flagellin of this spirochete, were tested with human sera in class-specific and polyvalent enzyme-linked immunosorbent assays (ELISAs). In analyses for immunoglobulin M (IgM) antibodies, 18 (85.7%) of 21 serum samples from persons who had been diagnosed as having Lyme borreliosis on the basis of the presence of erythema migrans reacted positively in ELISAs with one or more Osp antigens or the p41-G antigen. Eleven serum samples contained antibodies to OspC antigen, and of these, six also reacted to the p41-G antigen and to one or more of the other recombinant antigens. The remaining five serum samples reacted solely to OspC (n = 4) or to OspC plus OspA and OspE without reactivity to p41-G (n = 1). In analyses for IgG antibodies, seropositivity was comparable to that of IgM analyses and was marked by predominant reactivity to p41-G, OspC, and OspF. Similarly, all 21 serum samples were positive in polyvalent and class-specific ELISAs with whole-cell B. burgdorferi. Minor cross-reactivity was noted when sera from persons who had syphilis, periodontitis or other oral infections, or rheumatoid arthritis were tested with OspC, OspE, OspF, and p41-G. With relatively high degrees of specificity, ELISAs with recombinant antigens, particularly OspC and p41-G, can help to confirm B. burgdorferi infections.
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PMID:Use of recombinant antigens of Borrelia burgdorferi in serologic tests for diagnosis of lyme borreliosis. 878 93

Comprehensive studies of 92 commercial sex workers in Senegal, Africa included an oral examination in which we obtained measurements of decayed, missing, and filled (DMF) teeth; plaque index; gingival index; recession; probing depth (PD); clinical attachment loss (CAL); and the presence of HIV-associated periodontal lesions, under conditions wherein the examiner was unaware of the subject's HIV status. Twenty-seven subjects (29%) were HIV seropositive, 19 of whom were positive for HIV-1, 7 positive for HIV-2, and 1 positive for both. Most subjects were not taking any medications and previous dental care was limited. HIV-seronegative and HIV-seropositive subjects were similar in mean age, number of DMF teeth, percentage of sites with visible plaque, and number of sites with recession. However, the frequency of sites with gingival bleeding, with PD > or = 6 mm, and with CAL > or = 6 mm was significantly greater in seropositive than seronegative subjects. No differences were observed between HIV-1 and HIV-2 positive subjects. About 26% of HIV-seropositive subjects and about 5% of the seronegative subjects exhibited at least one site with concurrent PD > or = 6 mm and CAL > or = 6 mm. HIV-associated periodontal lesions were seen in 3 HIV-seropositive subjects (2 linear gingival erythema, 1 necrotizing periodontitis). One HIV-seronegative subject exhibited necrotizing gingivitis. In this population with multiple risks to oral health, both HIV-1 and HIV-2 infections were associated with a significantly increased prevalence of periodontal disease.
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PMID:Periodontal status of HIV-1 and HIV-2 seropositive and HIV seronegative female commercial sex workers in Senegal. 937 25

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.
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PMID:Epidemiology and diagnosis of HIV-associated periodontal diseases. 945 78

Oral health care has been an integral part of the care of patients with HIV infection and AIDS since the disease was first identified in the early eighties. The spectrum of HIV-associated opportunistic diseases occurring in the oral cavity propelled dental health care providers to the forefront of patient care. Infection control issues soon became important in oral health care for patients infected with HIV, and for the first decade these two issues overshadowed the concerns about appropriate management of the dental needs of HIV-infected patients. Several concerns need to be considered in the management of dental care for patients infected with HIV. These include decreased salivary flow and increased sugar intake, prevention and management of routine inflammatory gingival and periodontal disease as well as the atypical forms of gingival and periodontal disease associated with HIV infection (linear gingival erythema [LGE], necrotizing ulcerative gingivitis [NUG] and necrotizing ulcerative periodontitis [NUP]). Finally, although reports of complications secondary to dental treatment of HIV-infected individuals are rare, it is important to consider those factors related to the medical status of HIV-infected patients which may interfere with oral health care. These include potential bleeding problems related to thrombocytopenia and disease or medication related liver abnormalities, increased risk of local infection particularly in patients with severe neutropenia and adverse effects of multiple medications taken by HIV patients. Prevention and management of dental and periodontal disease in HIV-infected individuals is important to self esteem, quality of life and maintenance of adequate nutritional intake. Oral health care continues to be an important component of overall health care for HIV-infected patients.
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PMID:Dental lesions: diagnosis and treatment. 945 96

Periodontal manifestations of human immunodeficiency virus (HIV) infection were first described in 1987. Initially, the lesions receiving attention were HIV-associated gingivitis (now known as linear gingival erythema [LGE]) and HIV-associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (< or = 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV- patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV- injecting drug users (IDU), levels of the proinflammatory cytokine interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (> or = 4 mm), total IL-1 beta in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase beta-glucuronidase (beta G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total beta G in GCF and probing depth in the HIV-IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total beta G was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute total periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss.
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PMID:New concepts regarding the pathogenesis of periodontal disease in HIV infection. 972 91

To understand the characteristic clinical features of human immunodeficiency virus (HIV)-related oral lesions and determine the prevalence of various oral lesions in HIV-infected patients in Taiwan, we conducted a cross-sectional study of 207 HIV-infected patients at the Taipei Municipal Institute for Venereal Disease Control. Overall, 108 (52.2%) patients had at least one oral lesion. The most common oral manifestation of HIV infection among these 207 patients was oral hairy leukoplakia (OHL, 29.5%), followed by candidiasis (12.1%), xerostomia (10.6%), aphthous ulcers (8.7%), and linear gingival erythema (5.8%). Less frequently encountered oral lesions included leukoplakia (1.9%), papilloma (1.4%), necrotizing ulcerative periodontitis (1.0%), Kaposi's sarcoma (1.0%), herpes simplex (0.5%), Burkitt's lymphoma (0.5%), and parotid gland enlargement (0.5%). Thirty-one (15%) patients had multiple oral lesions. Patients with oral candidiasis or multiple oral lesions had significantly lower mean CD4 lymphocyte counts and CD4/CD8 lymphocyte ratios than those without any oral lesions (p < 0.05). Chi-square analysis revealed that patients with CD4 lymphocyte counts below 200 cells/mm3 were more prone to have OHL (p < 0.002), oral candidiasis (p < 0.001) and multiple oral lesions (p < 0.001). Those with CD4/CD8 lymphocyte ratios below 0.4 were more likely to have OHL (p < 0.02), oral candidiasis (p < 0.01) and multiple oral lesions (p < 0.02) than those with higher counts. In conclusion, the occurrence of oral lesions, especially OHL and oral candidiasis, is fairly common in Taiwanese HIV-infected patients.
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PMID:Oral manifestations of human immunodeficiency virus-infected patients in Taiwan. 979 27

In the course of infection by the Human Immunodeficiency Virus (HIV) typical changes of inflammatory periodontal diseases can arise. The prevalence of these illnesses may be up to 5%. The HIV-associated periodontal diseases include linear gingival erythema (LGE), necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). The necrotizing forms appear particularly in severe or advanced immunosuppression. It can be safely assumed that the HIV infection and the resulting immunological defects are responsible for these severe forms of destruction of the periodontal tissue. Periodontal therapy consists in the removal of necrotic tissues and removal of soft and hard plaque-deposits. This is supported by a chlorhexidine digluconate mouthrinse and antibiotics. In the interest of further prophylactics a strict system of recall appointments is recommended.
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PMID:Cases of HIV-associated characteristic periodontal diseases. 1008 80

The results gained with the treatment of benzylalcohol and amyl-m-cresol tablets in oral inflammatic diseases (153 cases) and in the prophylaxis of possible infections (119 cases) accompanied with surgical interventions has been summarised. It was concluded that, the average healing process shortened by 30% in time, and the quality parameters (pain, function etc.) showed 30% better results in 78.4% of the cases treated with Strepsils. 88.3/ of patients preferred to get the tablets, the tolerability was excellent. The two third of the patients suffering from inflammatory diseases reported reduction of the pain within the first 60 minutes after the very first tablet application. The experience gained with 272 patients showed very good effectivity especially in the cases aphtha, gingivostomatitis herpetica, stomatitis mycotica, gingivitis, denture stomatitis, erythema exsudativum multiforme, stomatopharyngitis, periodontitis. The drug has showed of remarkable result in the prophylaxis of periodontal, dentoalveolar, implant, soft tissue, maxillofacial surgical interventions.
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PMID:[Clinical experience with the use of benzylalcohol and amyl-m-cresol (Strepsils) in stomatological diseases]. 1076 92

All physical examinations of HIV-infected individuals should include a detailed examination of the mouth, since oral lesions are common. There are about 40 oral manifestations of HIV infections that may be the first clinical features of the disease. HIV-related cancers, such as Kaposi's sarcoma or lymphoma, may present as oral lesions. A variety of bacterial infections may be found in the mouth, including linear gingival erythema, necrotizing ulcerative periodontitis, tuberculosis, Mycobacterium avium complex, and bacillary angiomatosis. Viral infections include herpes infections, cytomegalovirus ulcers, hairy leukoplakia, and warts. Among fungal infections, various types of candidiasis are common, and histoplasmosis or cryptococcosis may also cause lesions. Other manifestations include recurrent aphthous ulcers, immune thrombocytopenic purpura, HIV-salivary gland disease, and pigmentation disorders. Treatments are available for many of these disorders.
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PMID:Oral manifestations of HIV infection. 1136 17

Human Immunodeficiency Virus (HIV) has profoundly affected the clinical practice of dentistry since the early 1980s. Acute lesions such as linear gingival erythema (LGE) and necrotizing ulcerative periodontitis (NUP) were described as HIV-related oral lesions. The behaviour of chronic gingivitis and periodontitis as well as other practice-related issues are discussed in this paper.
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PMID:HIV infection and periodontal disease. 1170 67


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