[Impact of tobacco use on the periodontium--an update (I)--Part 1: Epidemiologic und pathogenetic aspects of tobacco-related periodontal diseases]

This literature review represents the second in a series of articles from the Swiss task force "Smoking--Intervention in the private dental office" on the topic "tobacco use and dental medicine". In this article, the epidemiological background as well as some pathogenetic processes are described and discussed critically for tobacco-related periodontal diseases. Earlier publications confirmed tobacco consumption as a risk factor for periodontal diseases. Over the last few years, oral health research has significantly contributed to the understanding of the mechanisms leading to the deterioration of the hard and soft tissues supporting the teeth. With the recording of the number of cigarettes smoked per day and the amount of years tobacco was used, a dose response relationship was established. Various, potentially significant pathogenic effects of tobacco-related substances may exist on the periodontal tissues, the immune response system or the composition of the oral flora. Moreover, there is reference that tobacco consumption may change the genetically determined susceptibility for periodontal diseases.

Platelet receptors and their role in diseases

The absence or deficiency of specific platelet glycoprotein receptors has a well-defined role in causing several rare bleeding disorders such as Bernard-Soulier syndrome or Glanzmann's thrombasthenia. Several new rare disorders caused by defects in other receptors or their signalling pathways have recently been described. Platelet receptors are also often targets for antibodies in pathological conditions. The roles of platelet receptors or their polymorphism variants in diseases such as cardiovascular disorders have started to be intensively investigated over the last 5 years. Many of these findings still remain controversial. Recent evidence points to a fundamental role for platelets and their receptors in the origins of atherosclerosis. Studies on the role of platelet receptors in diseases such as asthma, diabetes and HIV are still at an early stage.

Platelet receptors for adhesion and activation. Variability as a factor in susceptibility to cardiovascular diseases

Polymorphisms in coagulation factors leading to altered susceptibility to cardiovascular diseases have been known for some time and some are now well-established risk factors. More recently, an increasing number of polymorphisms have been identified in platelet receptors and a series of studies indicate that these too may play a role as individual risk factors for stroke and myocardial infarction. The effect of these platelet polymorphisms appears less clear-cut than some of the coagulation factor effects and other, associated, risk factors may be important in defining their role. In this review platelet receptor polymorphisms and their role as risk factors are surveyed and their possible relevance discussed.

Platelet glycoproteins and their role in diseases

The role of platelet glycoprotein receptors in disorders caused by their absence or defects such as in Bernard-Soulier syndrome or Glanzmann's thrombasthenia has been known for many decades now. Their function as targets for pathological antibodies is also well established. The possible roles of platelet receptors or their polymorphism variants in the origins of diseases such as cardiovascular disorders are less well studied. Investigation of this area began about five years ago and many findings still remain controversial. The involvement of platelet receptors in other diseases like asthma, diabetes and HIV are only starting to be studied.

Detection of latent tuberculosis in immunosuppressed patients with autoimmune diseases: performance of a Mycobacterium tuberculosis antigen-specific interferon gamma assay

OBJECTIVE: To analyse the performance of a new M. tuberculosis-specific interferon gamma (IFNgamma) assay in patients with chronic inflammatory diseases who receive immunosuppressive drugs, including tumour necrosis factor alpha (TNFalpha) inhibitors. METHODS: Cellular immune responses to the M. tuberculosis-specific antigens ESAT-6, CFP-10, TB7.7 were prospectively studied in 142 consecutive patients treated for inflammatory rheumatic conditions. Results were compared with tuberculin skin tests (TSTs). Association of both tests with risk factors for latent M. tuberculosis infection (LTBI) and BCG vaccination were determined and the influence of TNFalpha inhibitors, corticosteroids, and disease modifying antirheumatic drugs (DMARDs) on antigen-specific and mitogen-induced IFNgamma secretion was analysed. RESULTS: 126/142 (89%) patients received immunosuppressive therapy. The IFNgamma assay was more closely associated with the presence of risk factors (odds ratio (OR) = 23.8 (95% CI 5.14 to 110) vs OR = 2.77 (1.22 to 6.27), respectively; p = 0.009), but less associated with BCG vaccination than the TST (OR = 0.47 (95% CI 0.15 to 1.47) vs OR = 2.44 (0.74 to (8.01), respectively; p = 0.025). Agreement between the IFNgamma assay and TST results was low (kappa = 0.17; 95% CI 0.02 to 0.32). The odds for a positive IFNgamma assay strongly increased with increasing prognostic relevance of LTBI risk factors. Neither corticosteroids nor conventional DMARDs significantly affected IFNgamma responses, but the odds for a positive IFNgamma assay were decreased in patients treated with TNFalpha inhibitors (OR = 0.21 (95% CI 0.07 to 0.63), respectively; p = 0.006). CONCLUSIONS: These results demonstrate that the performance of the M. tuberculosis antigen-specific IFNgamma ELISA is better than the classic TST for detection of LTBI in patients receiving immunosuppressive therapy for treatment of systemic autoimmune disorders.

Surveillance systems for sexually transmitted diseases in Switzerland

BACKGROUND: In Switzerland (population 7.4 million), 3 different systems contribute to surveillance for sexually transmitted infections. GOAL: The goal of this study was to compare time trends from surveillance systems for chlamydia, gonorrhea, and syphilis. STUDY DESIGN: We studied surveillance data (1997-2003) from laboratory reports in women and men, men attending dermatology clinics, and women attending gynecologists. RESULTS: Laboratory reports of episodes of Chlamydia trachomatis and Neisseria gonorrhoeae increased by 31% (from 2573 to 3449 cases) and 104% (from 259 to 528 cases), respectively. Over the same period, chlamydia reports from men attending dermatology clinics and women attending gynecologists did not change and dermatology clinic-based reports of gonorrhea in men increased only slightly. Syphilis reports from dermatology clinics increased by 127% (from 22 to 50 cases). CONCLUSIONS: Increases in laboratory reports of chlamydia and gonorrhea were not consistently detected in sentinel populations. Numbers of cases reported to all 3 systems were low. The performance of surveillance systems for sexually transmitted infections should be evaluated regularly.

Pollakisuria in a dwarf goat due to pathologic enlargement of the uterus

Pollakisuria in adult goats can be caused by diseases of the urinary tract and by distension of parts of the genital tract leading to irritation of the bladder. Hydrometra is the most common cause of uterine distension in goats and usually can be resolved by prostaglandin injections. But other pathologies of the uterus can generate a similar syndrome. A dwarf goat was presented at the clinic with a history of chronic pollakisuria and tenesm. An initial ultrasonographic examination of the abdomen led to the suspicion of hydrometra, but treatment with injections of prostaglandin were not successful. Blood samples revealed low progesterone and high oestrogen values. A laparotomy was performed and an enlarged uterus with 1.5 L of mucous content and cystic ovaries were found and partially removed. A single solid leiomyoma was diagnosed histologically in the uterine wall. Two months later the goat's condition had deteriorated and therefore she was euthanized. Necropsy and pathohistological examination revealed the presence of a metastasized adenocarcinoma of the uterus. In this case, the pollakisuria provoqued by distension of the uterus was not caused by hydrometra, but by neoplasia. The syndrome and the pathogenesis of the adenocarcinoma in consideration of the hormonal status of the patient is discussed.

TREM-1--expressing intestinal macrophages crucially amplify chronic inflammation in experimental colitis and inflammatory bowel diseases

Triggering receptor expressed on myeloid cells-1 (TREM-1) potently amplifies acute inflammatory responses by enhancing degranulation and secretion of proinflammatory mediators. Here we demonstrate that TREM-1 is also crucially involved in chronic inflammatory bowel diseases (IBD). Myeloid cells of the normal intestine generally lack TREM-1 expression. In experimental mouse models of colitis and in patients with IBD, however, TREM-1 expression in the intestine was upregulated and correlated with disease activity. TREM-1 significantly enhanced the secretion of relevant proinflammatory mediators in intestinal macrophages from IBD patients. Blocking TREM-1 by the administration of an antagonistic peptide substantially attenuated clinical course and histopathological alterations in experimental mouse models of colitis. This effect was also seen when the antagonistic peptide was administered only after the first appearance of clinical signs of colitis. Hence, TREM-1-mediated amplification of inflammation contributes not only to the exacerbation of acute inflammatory disorders but also to the perpetuation of chronic inflammatory disorders. Furthermore, interfering with TREM-1 engagement leads to the simultaneous reduction of production and secretion of a variety of pro-inflammatory mediators such as TNF, IL-6, IL-8 (CXCL8), MCP-1 (CCL2), and IL-1beta. Therefore, TREM-1 may also represent an attractive target for the treatment of chronic inflammatory disorders.