Osteoporosis, jawbones and periodontal disease

The association between osteoporosis and jawbones remains an argument of debate. Both osteoporosis and periodontal diseases are bone resorptive diseases; it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease and vice versa. Hypothetical models linking the two conditions exist: in particular, it is supposed that the osteoporosis-related bone mass density reduction may accelerate alveolar bone resorption caused by periodontitis, resulting in a facilitated periodontal bacteria invasion. Invading bacteria, in turn, may alter the normal homeostasis of bone tissue, increasing osteoclastic activity and reducing local and systemic bone density by both direct effects (release of toxins) and/or indirect mechanisms (release of inflammatory mediators). Current evidence provides conflicting results due to potential biases related to study design, samples size and endpoints. The aim of this article is to review and summarize the published literature on the associations between osteoporosis and different oral conditions such as bone loss in the jaws, periodontal diseases, and tooth loss. Further well-controlled studies are needed to better elucidate the inter-relationship between systemic and oral bone loss and to clarify whether dentists could usefully provide early warning for osteoporosis risk

Impact of chronic diuretic treatment on glucose homeostasis

Background The use of diuretics for hypertension has been associated with unfavorable changes in cardiovascular risk factors, such as uric acid and glucose tolerance, though the findings in the literature are contradictory. Methods This study investigated whether diuretic use is associated with markers of metabolic and cardiovascular risk, such as insulin-resistance and uric acid, in a cohort of adults without known diabetes and/or atherosclerotic cardiovascular disease. Nine hundred sixty-nine randomly selected participants answered a questionnaire on clinical history and dietary habits. Laboratory blood measurements were obtained in 507 participants. Results Previously undiagnosed type 2 diabetes was recognized in 4.2% of participants who were on diuretics (n = 71), and in 2% of those who were not (n = 890; P = 0.53). Pre-diabetes was diagnosed in 38% of patients who were on diuretics, and in 17.4% (P < 0.001) of those who were not. Multivariate analysis showed that insulin-resistance (HOMA-IR) was associated with the use of diuretics (P = 0.002) independent of other well-known predisposing factors, such as diet, physical activity, body mass index, and waist circumference. The use of diuretics was also independently associated with fasting plasma glucose concentrations (P = 0.001) and uric acid concentrations (P = 0.01). Conclusions The use of diuretics is associated with insulin-resistance and serum uric acid levels and may contribute to abnormal glucose toleranc

Osteonecrosis of the jaws in patients assuming oral bisphosphonates for osteoporosis: A retrospective multi-hospital-based study of 87 Italian cases

BACKGROUND: Bisphosphonates (BPs) are currently the chief drugs for the prevention/treatment of osteoporosis; one of their adverse effects is the osteonecrosis of the jaw (BRONJ). The primary endpoints of this multi-center cross-sectional study are: i) an observation of the clinical features of BRONJ in 87 osteoporotic, non-cancer patients; and ii) an evaluation of their demographic variables and comorbidities. METHODS: 87 BRONJ patients in therapy for osteoporosis with BPs from 8 participating clinical Italian centers were consecutively identified and studied. After BRONJ diagnosis and staging, comorbidities and data relating to local and drug-related risk factors for BRONJ were collected. RESULTS: 77/87 (88.5%) patients in our sample used alendronate as a BP type; the duration of bisphosphonate therapy ranged from 2 to 200 months, and 51.7% of patients were in treatment for ≤ 38 months (median value). No comorbidities or local risk factors were observed in 17 (19.5%) patients, indicating the absence of cases belonging to BRONJ forms triggered by surgery. BRONJ localization was significantly associated with age: an increased risk of mandible localization (p=0.002; OR=6.36, 95%CI=[1.89; 21.54]) was observed for those over 72 yrs. At multivariate analysis, the increased risk of BRONJ in the mandible for people over 72 yrs (OR'=6.87, 95%CI=[2.13; 2.21]) was confirmed for a BP administration &gt;56 months (OR'=4.82, 95%CI=[2.13; 22.21]). CONCLUSION: Our study confirms the fundamental necessity of applying protocols of prevention in order to reduce the incidence of BRONJ in osteoporotic, non-cancer patients in the presence of comorbidities and/or local risk factor as well as, less frequently, in their absence

MALIGNANT TUMOR-LIKE GAASTRIC LESION DUE TO CANDIDA ALBICANS IN A DIABETIC PATIENT TREATED WITH CYCLOSPORIN: A CASE REPORT AND REVIEW OF THE LITERATURE

The gastrointestinal tract of healthy individuals is colonized by hundreds of saprophytes and mycetes, especially in the candida species, are habitual ones. Under certain conditions, the fungal flora may overgrow, resulting in lesion of the digestive mucosa which rarely, can have a local diffusion and/or spread to the lympho-hematogenous system. Mycotic infections of the stomach can sometimes look like benign gastric ulcers. here, we present the case report of a woman, aged 64, who presented with type II diabetes mellitus and psoriasis, on chronic treatment with cyclosporin A and with endoscopic evidence of an ulcerated, vegetating gastric lesion secondary to Candida Albicans infection. Although strongly sugestive of malignancy, it completely healed after cyclosporin withdrawal and the administration of oral antifungal drugs

Portal vein thrombosis and Budd-Chiari syndrome as onset of Polycythaemia Vera.

Budd-Chiari syndrome may be defined as a heterogeneous group of vascular disorders characterized by obstruction of hepatic venous return to the level of hepatic venules, supra-hepatic veins, inferior vena cava or right atrium. The main cause of this syndrome is represented by myeloproliferative diseases and, in particular, by polycythemia vera. The latter may cause multiple splanchnic thrombosis, including portal vein thrombosis, particularly important for its clinical outcomes (ascites, collateral vessels genesis, etc.). We report 2 cases of a Budd-Chiari syndrome induced by polycythemia vera characterized by an abnormal clinical onset, both as regards subjects’ age (29 and 39 years old, respectively) and set of symptoms, signs and laboratory data. After a complete clinical, instrumental and genetic diagnosis, the patients were treated with combined therapy, using acetylsalicylic acid and hydroxyurea. The therapy proved successful and patients are still in follow up in our institution. Polycythemia vera should be suspected in patients affected with portal vein thrombosis and Budd-Chiari syndrome even if its clinical onset might be unusual. Every effort should be made to make a correct and early diagnosis in order to start appropriate therapy as soon as possible and to prevent patients from useless diagnostic and therapeutic treatments