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

2 intraoral lesions associated with human immunodeficiency virus (HIV) infection have recently been described: an atypical gingivitis and a rapidly progressive periodontitis. The microbiota associated with these gingival and periodontal lesions was investigated. Subgingival plaque samples were taken from 45 HIV-seropositive homosexual men and from 44 HIV-seronegative control subjects. Each sampled site was clinically and radiographically classified as HIV-associated gingivitis, HIV-associated periodontitis, healthy in an HIV-seropositive subject, or healthy, conventional gingivitis or classical periodontitis in a control subject. Plaque samples were examined by indirect immunofluorescence with polyclonal antisera to detect Bacteroides gingivalis, B. intermedius, Fusobacterium nucleatum, and Actinobacillus actinomycetemcomitans. Anaerobic culturing was used to detect black-pigmented Bacteroides species, Fusobacterium species, and A. actinomycetemcomitans to confirm the immunofluorescence findings. We detected B. gingivalis, B. intermedius, F. nucleatum, and A. actinomycetemcomitans in significantly more HIV-periodontitis sites (80, 65, 59 and 61% of sites, respectively) and HIV-gingivitis sites (61, 70, 52 and 52%, respectively) than in HIV-seropositive healthy and control sites (p less than 0.05). The results indicate that the microbiota found in HIV-periodontitis is similar to that of classical periodontitis. In contrast, however, the microbiota associated with HIV-gingivitis is strikingly different from that of conventional gingivitis. The similarity in the prevalence of periodontopathic organisms in both HIV-gingivitis and HIV-periodontitis suggests that the HIV-gingivitis lesion may be a precursor to the tissue destruction observed in HIV-periodontitis. Hence, early detection and treatment of the HIV-gingivitis lesion may prevent the rapid and extensive breakdown of periodontal tissues associated with HIV-periodontitis.
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PMID:The microbiology of HIV-associated periodontal lesions. 269 96

Skin and mucous membranes including the oral mucosa are among the preferential locations of opportunistic infections and secondary neoplasms in patients infected with the human immunodeficiency virus (HIV). Infections of the oral mucosa such as thrush occur in a high percentage of AIDS patients, patients with AIDS-related complex or HIV-seropositive individuals. The clinical appearance of the infections (herpes virus infection, periodontitis) is often marked by aggressive expansion, frequent recurrences or resistance to therapy. Oral "hairy" leukoplakia is considered to be a characteristic lesion in HIV-infected individuals. Tumors like Kaposi's sarcoma, squamous cell carcinoma and non-Hodgkin lymphoma of the oral mucosa may cause marked morbidity in AIDS patients. Such oral lesions are frequently the first indication of an HIV-infection. Dentists should be aware of the oral manifestations of HIV-infection and initiate diagnostic and therapeutic measures in the interest of the patients and for epidemiologic reasons.
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PMID:[Oral manifestations of HIV infection]. 270 Apr 12

Alterations in polymorphonuclear leucocyte (PMN) function are frequently associated with intraoral disease. The purpose of this study was to evaluate if alterations exist in three early stimulatory events of PMN function in individuals with intraoral manifestations of human immunodeficiency virus (HIV) infection. Peripheral PMNs were isolated from nine HIV-seropositive male homosexuals with HIV-associated periodontitis and intraoral candidiasis and healthy HIV-seronegative age-matched heterosexuals (controls). Phagocytosis was assessed using fluorescent microspheres, oxidative burst was assessed via hydrolysis of 2',7'-dichlorofluorescein (FCDH) to 2',7'-dichlorofluorescein (FCDA) with PMA stimulation, and F-actin formation was assessed with NBD-phallacidin stain after stimulation with f-Met-Leu-Phe. Compared to controls, seven of nine HIV-seropositive patients demonstrated a significant increase in the percentage of phagocytic cells while seven of nine HIV-seropositive patients demonstrated a 5-59% increase in number of beads per cell. In the oxidative burst assay, seven of seven HIV-seropositive patients demonstrated a significant increase over controls in FCDA stain with PMA stimulation. In the F-actin assay, four of five HIV-seropositive patients demonstrated a significant increase over controls in NBD-phallacidin staining after f-Met-Leu-Phe stimulation.
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PMID:Elevated phagocytosis, oxidative burst, and F-actin formation in PMNs from individuals with intraoral manifestations of HIV infection. 321 15

A multitude of oral lesions have been described in individuals infected with the human immunodeficiency virus (HIV). Few studies have attempted to correlate specific oral findings with immune status and HIV disease progression in the population reflecting the demographic profile of this epidemic. A prospective study was conducted among 700 ambulatory HIV-infected individuals seeking dental care between July 1, 1988 and June 30, 1992. Patients entered the study when they first applied for care and were followed at regular intervals unless death occurred before the conclusion of the study. The prevalence rate of necrotizing ulcerative periodontitis (NUP) was calculated for the entire population and specific to race, gender, and HIV transmission category. Survival analysis was used to estimate the cumulative probability of death within 24 months of a NUP diagnosis. The association between NUP diagnosis and CD4+ cell count below 200 cells/mm3 was also investigated, and it was found that HIV-infected individuals presenting with a diagnosis of NUP were 20.8 times as likely to have a CD4+ cell count below 200 cells/mm3 compared to HIV-infected individuals presenting without NUP. The prevalence of NUP was 6.3%. The lesion was significantly more common among men having sex with men (MSM), 8.4%, compared with non-MSM males, 1.8%. No racial difference was noted. The mean CD4+ cell count for patients with NUP was 51.8 cells/mm3 (SD +/- 71.2) while the median CD4+ cell count was 32.0 cells/mm3. The predictive value of a CD4+ cell count below 200 cells/mm3 in patients with this lesion was 95.1%. A cumulative probability of death within 24 months of a NUP diagnosis was 72.9%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Necrotizing ulcerative periodontitis: a marker for immune deterioration and a predictor for the diagnosis of AIDS. 791 62

A multitude of oral lesions, including unique forms of periodontal disease, have been discovered in individuals infected with the human immunodeficiency virus (HIV). Although the frequency of HIV-associated periodontal diseases appears to be less than previously thought, many researchers agree that an important factor influencing the prevalence of unique periodontal disease in the HIV population is the degree of immunodeficiency. The pathogenesis of HIV-associated periodontal diseases remains unclear, but may be the result of microbiota and/or alterations in the host. HIV-gingivitis, now called linear gingival erythema, and HIV-periodontitis, now called necrotizing ulcerative periodontitis, have microbiology profiles similar to conventional adult periodontitis, although these lesions are quite different clinically. This article reviews clinical signs and symptoms, treatments, and the pathogenesis of HIV-related periodontal findings. It specifically focuses on the immuno-incompetence of HIV disease as a risk factor for periodontal disease. Because the caseload of acquired immunodeficiency syndrome patients will increase significantly in the future, the dental practitioner must be able to recognize and manage the periodontal lesions associated with HIV infection.
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PMID:HIV disease as a risk factor for periodontal disease. 798 97

As the scope of the acquired immunodeficiency syndrome (AIDS) epidemic grows to include increasingly larger proportions of heterosexual adults and children, there has also been a change in the severity of human immunodeficiency virus (HIV)-related periodontal conditions at one San Francisco clinic. The cases of HIV-associated gingivitis, now called linear gingival erythema, HIV-associated periodontitis (or necrotizing ulcerative periodontitis), and necrotizing stomatitis have been less severe, despite an increase in overall HIV caseload. No clear basis for this trend has been established, but possible explanations include: biased population samples, increased immunosuppression as the disease matures, use of antimicrobial therapy, or a change in patient demographics. Several studies have failed to identify a single causative organism. This article presents a review of HIV-related periodontal complications and points out that the condition can be treated with local and systemic antibiotics and that dental professionals throughout the world can expect a tremendous increase over the next several years in HIV-infected patients with special clinical complications.
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PMID:Periodontal complications of HIV infection. 803 7

Gingival biopsies were taken from 27 HIV (human immunodeficiency virus)-seropositive persons with gingivitis or periodontitis and 16 HIV-seronegative persons with periodontitis. Sections were stained with hematoxylin and eosin or periodic acid-Schiff. Candidal hyphae and pseudohyphae were found in the parakeratinized oral epithelium in 7 specimens from the HIV-infected patient group such specimen. No fungal invasion was found in any of the biopsies from the HIV-seronegative persons. Candidal invasion was significantly more frequent (P < 0.05) in patients with a confirmed history of necrotizing periodontal diseases (5/9) than in patients without known episodes of such diseases (3/18). The most prominent histopathologic changes observed in connection with candidal invasion comprised polymorphonuclear leucocyte infiltration of the oral gingival epithelium and numerous mitoses, some of which were located suprabasally. It is suggested that Candida albicans may contribute to the development of necrotizing periodontal diseases in HIV-infected persons.
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PMID:Candidal infection of the gingiva in HIV-infected persons. 804 55

Apical periodontitis was simulated in 100 white rats with secondary immunodeficiency induced by a single total x-ray irradiation with the RUM [correction of PYM]-17 device. Nonspecific resistance of the rat body was assessed from the neutrophilic phagocytic activity, serum bactericidal activity, lysozyme and complement levels. These parameters were found reduced in the experimental animals; x-ray examinations revealed changes round the dental root apices. Daily injections of tactivin for 10 days in a dose 2-5 mg/kg b.m. resulted in elevation of the nonspecific resistance parameters, and the x-ray picture in this group of animals was the same as in intact controls; therefore, tactivin normalized the immunity system status and indirectly improved the clinical course of apical periodontitis.
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PMID:[The use of taktivin in experimental apical periodontitis exacerbated by a secondary immunodeficiency state]. 804 17

Periodontal diseases may be the first clinical sign of human immunodeficiency virus (HIV)-infection. Since the immunosuppression and subsequent susceptibility may alter the responses of the oral tissues as well as the microflora, both periodontal treatment and result of therapy may be modified. The periodontal diseases in HIV-seropositive patients include common as well as less conventional forms of gingivitis and periodontitis, and bacterial, mycotic and viral infections are seen. Neoplasias may also involve the periodontium; most common are Kaposi's sarcoma and non-Hodgkin's lymphoma. Recent studies of unselected groups of patients indicate that periodontal health in at least some groups of HIV-seropositive patients is better than previously reported.
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PMID:Periodontal diseases in HIV-infected patients. 819 44

Yesterday's immunodeficiencies emphasized the clinical and familial associations of the syndromes and date from the 1920s (ataxia-telangiectasia, chronic mucocutaneous candidiasis), the 1930s (Wiskott-Aldrich syndrome), skipping the 1940s, but blossoming in the 15-y period from 1950 to 1965. In this period, primary immunodeficiencies affecting all the major limbs of the immune system were first described (1950: severe combined immunodeficiency; 1952: X-linked agammaglobulinemia; 1957: chronic granulomatous disease; 1965: C2 deficiency). Today's immunodeficiencies, as detailed in Stiehm's Immunologic Disorders in Infants and Children (Edition 1, 1973; Edition 2, 1980; and Edition 3, 1989) emphasize the immunologic and genetic aspects of immunodeficiency. These increased from 43 syndromes in the 1973 edition (34 primary, nine secondary) to 94 syndromes in the 1989 edition (66 primary, 28 secondary). This means that about two primary and one secondary immunodeficiencies have been uncovered annually. Tomorrow's immunodeficiencies, to be covered in Edition 4, will include new clinical and immunologic observations and molecular and biochemical studies that characterize some unique immunodeficiencies. These include the following six groups of defects: 1) neutropenic syndromes with hypogammaglobulinemia, including the WHIM syndrome; 2) phenotypic genetic syndromes with immunodeficiency including Bloom's syndrome and Schimke's immuno-osseous dysplasia; 3) natural killer cell defects associated with a) other primary immunodeficiencies, b) other nonimmunologic illness, and c) primary natural killer defects; 4) T-cell membrane defects; 5) IL defects; and 6) miscellaneous phagocytic illnesses including periodontitis and the asplenia syndrome.
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PMID:New and old immunodeficiencies. 843 70


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