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Progressive Bone Loss (progressive + bone_loss)
Selected AbstractsThyroid-Stimulating Hormone Restores Bone Volume, Microarchitecture, and Strength in Aged Ovariectomized Rats*,,§JOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2007T Kuber Sampath PhD Abstract We show the systemic administration of low levels of TSH increases bone volume and improves bone microarchitecture and strength in aged OVX rats. TSH's actions are mediated by its inhibitory effects on RANKL-induced osteoclast formation and bone resorption coupled with stimulatory effects on osteoblast differentiation and bone formation, suggesting TSH directly affects bone remodeling in vivo. Introduction: Thyroid-stimulating hormone (TSH) receptor haploinsufficient mice with normal circulating thyroid hormone levels have reduced bone mass, suggesting that TSH directly affects bone remodeling. We examined whether systemic TSH administration restored bone volume in aged ovariectomized (OVX) rats and influenced osteoclast formation and osteoblast differentiation in vitro. Materials and Methods: Sprague-Dawley rats were OVX at 6 months, and TSH therapy was started immediately after surgery (prevention mode; n = 80) or 7 mo later (restoration mode; n = 152). Hind limbs and lumbar spine BMD was measured at 2- or 4-wk intervals in vivo and ex vivo on termination at 8,16 wk. Long bones were subjected to ,CT, histomorphometric, and biomechanical analyses. The direct effect of TSH was examined in osteoclast and osteoblast progenitor cultures and established rat osteosarcoma-derived osteoblastic cells. Data were analyzed by ANOVA Dunnett test. Results: In the prevention mode, low doses (0.1 and 0.3 ,g) of native rat TSH prevented the progressive bone loss, and importantly, did not increase serum triiodothyroxine (T3) and thyroxine (T4) levels in aged OVX rats. In restoration mode, animals receiving 0.1 and 0.3 ,g TSH had increased BMD (10,11%), trabecular bone volume (100,130%), trabecular number (25,40%), trabecular thickness (45,60%), cortical thickness (5,16%), mineral apposition and bone formation rate (200,300%), and enhanced mechanical strength of the femur (51,60%) compared with control OVX rats. In vitro studies suggest that TSH's action is mediated by its inhibitory effects on RANKL-induced osteoclast formation, as shown in hematopoietic stem cells cultivated from TSH-treated OVX rats. TSH also stimulates osteoblast differentiation, as shown by effects on alkaline phosphatase activity, osteocalcin expression, and mineralization rate. Conclusions: These results show for the first time that systemically administered TSH prevents bone loss and restores bone mass in aged OVX rats through both antiresorptive and anabolic effects on bone remodeling. [source] Marginal Bone Loss at Implants: A Retrospective, Long-Term Follow-Up of Turned Brånemark System® ImplantsCLINICAL IMPLANT DENTISTRY AND RELATED RESEARCH, Issue 1 2009Odont Lic, Solweig Sundén Pikner DDS ABSTRACT Background: Lately, presence of progressive bone loss around oral implants has been discussed. Purpose: The aim of this study was to report in a large patient group with different prosthetic restorations marginal bone level and its change as measured in radiographs obtained from prosthesis insertion up to a maximum 20 years in service. Further, it also aimed to study the impact of gender, age, jaw, prosthetic restoration, and calendar year of surgery. Materials and Methods: Out of 1,716 patients recorded for clinical examination during 1999, 1,346 patients (78.4%) could be identified. A total of 640 patients (3,462 originally installed Brånemark System® implants, Nobel Biocare, Göteborg, Sweden) with a follow-up of ,5 years were included in the study, while patients with continuous overdentures and augmentation procedures were not. Distance between the fixture/abutment junction (FAJ) and the marginal bone level was recorded. Results: The number of implants with a mean bone level of ,3 mm below FAJ increased from 2.8% at prosthesis insertion to 5.6% at year 1, and 10.8% after 5 years. Corresponding values after 10, 15, and 20 years were 15.2, 17.2, and 23.5%, respectively. Implant-based bone loss was as a mean 0.8 mm (SD 0.8) after 5 years, followed by only minor average changes. Mean bone loss on patient level followed a similar pattern. Disregarding follow-up time, altogether 183 implants (107 patients) showed a bone loss ,3 mm from prosthesis insertion to last examination. Significantly larger bone loss was found the older the patient was at surgery and for lower jaw implants. Conclusions: Marginal bone support at Brånemark implants was with few exceptions stable over years. [source] Clinical characteristics at implants with a history of progressive bone lossCLINICAL ORAL IMPLANTS RESEARCH, Issue 2 2008Christer Fransson Abstract Objective: The aim of the present study was to describe the clinical characteristics at implants with a history of progressive bone loss. Material and methods: Eighty-two out of 184 previously identified subjects with a history of progressive bone loss volunteered for the study. Clinical assessments of plaque, bleeding on probing (BoP), probing pocket depth (PPD), suppuration following probing (Pus), presence of calculus on implants surfaces (Calc) and ,recession' i.e. the mucosal margin in level with or apical of the fixture/abutment junction were performed at the mesial, distal, buccal and lingual aspects of each implant and without removing the bridge constructions. Results: It was demonstrated that the frequencies of BoP, Pus, ,recession' and PPD,6 mm were higher at implants with than without ,progressive' bone loss. In addition, smokers had larger numbers of affected implants than non-smokers, and the proportion of affected implants that exhibited Pus and PPD,6 mm was higher in smokers than in non-smokers. The logistic regression analysis revealed that the findings of Pus, ,recession' and PPD,6 mm at an implant in a smoking subject had a 69% accuracy in identifying the history of progressive bone loss. Conclusion: The results from this study demonstrate an association between clinical signs of pathology and bone loss at implants. It is recommended to include clinical assessments in the evaluation of implant therapy. [source] | ||||||||||