Bone mineral density in patients with rapidly destructive or common hip osteoarthritis.

BACKGROUND: Recent findings that subchondral insufficiency fracture in the femoral head may precede rapid chondrolysis suggest a role for systemic low bone mass in the genesis of rapidly destructive hip osteoarthritis (RDHOA). OBJECTIVE: To compare bone mineral density (BMD) in females with RDHOA and those with common hip osteoarth-ritis (OA). METHODS: This prospective case-control study involved 26 females with RDHOA recruited from our institution between March 2000 and November 2006. BMD was measured at the femoral neck and lumbar spine (L1-L4) by dual-energy x-ray absorptiometry. For comparison, BMD was measured in 33 women with common hip OA who were scheduled for primary total hip arthroplasty. RESULTS: Patients with RDHOA and those with common hip OA were similar in age (74.9+/-9.9 vs. 74.7+/-8.8 years) and BMI (26.3+/-4.3 vs. 26.3+/-5 g/m2) and did not differ in mean BMD at the lumbar spine (1.0+/-0.2 vs. 1.1+/-0.2 g/cm2; mean T-score: -0.6+/-1.3 vs. -0.8+/-1.5) or at the femoral neck (0.7+/-0.1 vs. 0.8+/-0.2 g/cm2; mean T-score: -1.5+/-1.1 vs. -1.4+/-1.4). CONCLUSION: The results of this study do not suggest a role for systemic low bone mass in the pathophysiology of RDHOA.

Frailty, osteoporosis and hip fracture: causes, consequences and therapeutic perspectives.

OBJECTIVE: The aim of this review of the literature is to report the factors which both contribute to the frailty syndrome and increase hip fracture risk in the elderly. This work is the fruit of common reflection by geriatricians, endocrinologists, gynecologists and rheumatologists, and seeks to stress the importance of detection and management of the various components of frailty in elderly subjects who are followed and treated for osteoporosis. It also sets out to heighten awareness of the need for management of osteoporosis in the frail elderly. DESIGN: The current literature on frailty and its links with hip fracture was reviewed and discussed by the group. RESULTS: The factors and mechanisms which are common to both osteoporosis and frailty (falls, weight loss, sarcopenia, low physical activity, cognitive decline, depression, hormones such as testosterone, estrogens, insulin-like growth factor-I (IGF-I), growth hormone (GH), vitamin D and pro-inflammatory cytokines) were identified. The obstacles to access to diagnosis and treatment of osteoporosis in the frail elderly population and common therapeutic pathways for osteoporosis and frailty were discussed. CONCLUSION: Future research including frail subjects would improve our understanding of how management of frailty can can contribute to lower the incidence of fractures. In parallel, more systematic management of osteoporosis should reduce the risk of becoming frail in the elderly population.

Radiation-induced undifferentiated pleomorphic sarcoma after radiation therapy for a desmoid tumour.

Radiation-induced sarcoma is a long-term complication of radiation therapy. The most common secondary neoplasia is the undifferentiated pleomorphic sarcoma, which is usually described in the deep soft tissue of the trunk or extremities. Radiation-induced sarcomas have a poor prognosis. An early diagnosis and management are needed to improve the survival rate of such patients. We presently report a case of a radiation-induced undifferentiated pleomorphic sarcoma of the left gluteus maximus muscle, which developed 25 years after an initial diagnosis of aggressive fibromatosis and 21 years after a tumour recurrence. This case study illustrates the risk of developing a sarcoma in a radiation field and the need for long-term follow-up after radiation therapy. Unnecessary radiation therapy, in particular in the case of benign conditions in young patients, should be avoided.

Multiple domains interacting with Gs in the porcine calcitonin receptor.

The molecular basis for Gs activation by the calcitonin (CT) receptor was investigated. Based upon the analysis of conserved regions in G protein-coupled receptors, two nonoverlapping regions in the heptahelical porcine CT receptor (CTR) were selected as candidate Gs-interacting domains: the third intracellular loop residues 327-344 (KLKESQEAESHMYLKAVR, P3 region) and the C-tail residues 404-418 (KRQWNQYQAQRWAGR, P4 region). To assess their Gs-interacting function, we expressed these sequences in hybrid insulin-like growth factor II receptors in which the receptor native Gi-interacting domain was converted to CTR sequences. In COS cells transfected with either P3- or P4-substituted hybrid receptor, membrane adenylyl cyclase activity significantly increased. The up-regulated activity of cAMP was confirmed by measuring the transcriptional activity of the cAMP response element in cells expressing either hybrid receptor. A mutant CTR lacking the P4 region maintained positive cAMP response but with an attenuated maximal capacity to produce cAMP. In contrast, we could not assess the function of the P3 region using a conventional deletion method, as CT bound poorly to cells transfected with either of the two P3-deficient CTRs (one lacking the P3 region and the other lacking P3 but having the P3 sequence in reverse orientation). These data suggest that the third intracellular loop and the C-tail in CTR have domain-specific roles in Gs activation and that the hybrid receptor approach used here, combined with a conventional mutagenesis approach, is useful for intact cell analysis and functional dissection of G protein-coupled receptors.

Stress fractures of the lower limbs in osteoporotic patients treated with fluoride.

We report clinical and bone morphometric findings in 18 osteoporotic patients who experienced stress fractures during fluoride therapy. Patients were treated with either sodium fluoride (n = 15), or sodium monofluorophosphate (n = 3). Oral calcium supplementation was given in 11 patients, and vitamin D in 13. Stress fractures occurred after 17.1 +/- 10.3 months of therapy (range: 5-41 months). Atraumatic sudden pain in a lower limb bone extremity, normal initial roentgenogram, high 99technetium uptake on early bone scan, and a 3 to 4 week delay in linear bone condensation area at the same site were characteristics of stress fracture. The most frequent sites were the tibial metaphysis (n = 13), femoral neck (n = 10), and calcaneus (n = 4). Biochemical data showed increased plasma alkaline phosphatase levels in 11 patients, and mild renal failure in 2. Bone histomorphometry was performed on an iliac crest specimen in 10 patients at the time of the stress fracture. Trabecular bone volume was normal, and formation parameters were increased. Features of osteomalacia were encountered in only 2 patients with decreased renal function. Trabecular resorption was increased, as assessed by the osteoclastic surface (1.01 +/- 1.15% bone surface), and the number of osteoclasts (0.44 +/- 0.49 per mm2 bone section). The clinical course was favorable in all patients who stopped fluoride, although 5 patients who continued the treatment had either completion of femoral neck stress fractures to hip fractures (n = 2), or recurrent stress fractures (n = 2), or both (n = 1). Fluoride appears to be a key factor in the pathogenesis of stress fractures, and may be associated with increased trabecular resorption in some treated patients.

Cyclosporin A induces in vivo inhibition of resorption and stimulation of formation in rat bone.

We investigated a possible "in vivo" effect of cyclosporin A, an immunosuppressive agent, on normal rat bone remodeling. At an oral daily dose of 7 mg/kg for 14 days, the blood level of cyclosporin A was in the usual effective range and no change in renal function or magnesium metabolism was observed. Treated rats had decreased bone resorption: urinary hydroxyproline, plasma acid phosphatase, and the number of osteoclasts in caudal vertebrae were significantly reduced. By contrast, bone formation assessed by dynamic histomorphometry after double tetracycline labeling was increased. No modification of calciotropic hormones (vitamin D metabolites and parathyroid hormone as assessed by urinary cyclic AMP) was observed at the end of the treatment. These results suggest that in vivo cyclosporin A treatment induces bone remodeling modifications related to either a direct or a lymphokine-mediated effect on bone cells.

Short-term local injections of transforming growth factor-beta 1 decrease ovariectomy-stimulated osteoclastic resorption in vivo in rats.

Estrogen deficiency in rats is responsible for increased osteoclastic resorption and a subsequent rapid bone loss. TGF-beta, which is known to have acute effects on bone resorption in several in vitro models, has been shown to be secreted by osteoblastic cells in vitro in response to 17 beta-estradiol, but little is known about its in vivo effects on bone resorption. We therefore decided to investigate the short-term effect of TGF-beta 1 on bone resorption in ovariectomized rats. TGF-beta 1 (0.04-20 ng/injection), or vehicle, was injected daily directly into the bone marrow space, through a thin catheter implanted in the distal end of the right femur, during 4 consecutive days, starting 14 days after the ovariectomy. Bone histomorphometry was performed in the secondary spongiosa of the metaphysis of injected femurs and compared with vehicle-injected femurs of sham ovariectomized rats. Ovariectomy was associated with a marked increase in the resorption surface, a 2-fold increase in the number of osteoclasts, and no change in the number of TRAP-positive marrow cells distant from bone surfaces. Bone resorption was significantly lower in the TGF-beta 1-injected bones of ovariectomized rats, as compared with vehicle injected bones: the osteoclast surface and the number of osteoclasts were, respectively, 11.0 +/- 5.1% versus 20.8 +/- 1.3% and 287 +/- 41 versus 505 +/- 53, in bones injected with 0.2 ng of TGF-beta 1 as compared with vehicle-injected bones (mean +/- SE, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclosporin-A in vitro decreases bone resorption, osteoclast formation, and the fusion of cells of the monocyte-macrophage lineage.

We studied the in vitro effect of cyclosporin-A (CyA) on bone resorption using a fetal rat long bone-resorbing assay. CyA inhibited both PTH-stimulated and unstimulated bone resorption. The inhibitory effect of CyA on basal resorption was dose dependent, and it was more pronounced during the second period (less than or equal to 0.1 microgram/ml) of culture (days 5-7) than during the first period (days 2-4). A cytotoxic effect was ruled out by the absence of decrease in [3H]thymidine incorporation into bones up to a concentration of 5 micrograms/ml CyA. Histomorphometry performed after 4 and 7 days of culture showed that CyA (1 microgram/ml) decreased the number of osteoclasts per bone section after 7 days of culture (23.5 +/- 4.0 vs. 41.7 +/- 2.9 osteoclasts/bone section; P less than 0.05), but not after 4 days (25.6 +/- 3.3 vs. 23.0 +/- 2.5). These data suggested an effect of CyA on osteoclastic differentiation rather than on the function of mature osteoclasts. We further assessed the mechanisms of the inhibitory effect of CyA on osteoclastic differentiation in order to determine 1) the level of this action (proliferation and/or fusion of osteoclast precursors), and 2) if this action is direct or indirect. Autoradiographic studies were performed on bone sections after incubation of bones with [3H]thymidine for the last 48 h of culture. CyA decreased slightly but significantly the percentage of labeled nuclei per osteoclast and the number of osteoclasts containing at least one labeled nucleus (20.2 +/- 0.7 vs. 33.2 +/- 3.5; P less than 0.02). Moreover the number of nuclei per osteoclast was decreased after 7 days in CyA-treated bones (2.4 +/- 0.05 vs. 3.0 +/- 0.1; P less than 0.02). Taken together these results demonstrate that CyA slightly decreased the proliferation of osteoclast precursors, but markedly decreased their fusion. Similar effects were observed in cultures of rat marrow macrophages. CyA (1 microgram/ml) inhibited the fusion of macrophages into multinucleated cells elicited by 1 nM 1,25-dihydroxyvitamin D3, but had only a slight effect on the proliferation of these cells, as assessed by autoradiography. CyA also inhibited the formation of multinucleated cells and the fusion index in long term cultures of human cord blood monocytes, a cellular model for osteoclastic differentiation. By contrast, CyA had no effect on the formation of myotubes by fusion of cultured mononucleated rat myoblasts.(ABSTRACT TRUNCATED AT 400 WORDS)

Phospholipase D- and protein kinase C isoenzyme-dependent signal transduction pathways activated by the calcitonin receptor.

The calcitonin receptor expressed by the porcine LLC-PK1 renal tubule cells is a seven-transmembrane domain, G protein-coupled receptor activating adenylyl-cyclase and phospholipase C. Salmon calcitonin stimulated dose- and time-dependent release of the phospholipase D-dependent phosphatidylcholine product [3H] choline with an EC50 = 2.5 +/-0.3 x 10(-8) M, similar to that determined for phosphoinositide metabolism (EC50 = 4.5 +/-1.0 x 10(-8)M). The hormone failed to induce release of [3H]phosphocholine and [3H]glycerophosphocholine, ruling out activation of phosphatydilcholine-specific phospholipase C and phospholipase A. Calcitonin stimulated phosphatidic acid, a product of phospholipase D-dependent phosphatydilcholine hydrolysis. Activation of phospholipase D was confirmed by release of [3H]phosphatydilethanol, a specific and stable product in the presence of a primary alcohol. Activation of calcitonin receptor induced diacylglycerol formation, with a rapid peak followed by a prolonged increase, due to activation of phospholipase C and of phospholipase D. Consequently, the protein kinase-C alpha, but not the delta isoenzyme, was cytosol-to-membrane translocated by approximately 50% after 20 min exposure to calcitonin, whereas protein kinase-C zeta, which was approximately 40% membrane-linked in unstimulated cells, translocated by approximately 19%. The human calcitonin receptor expressed by BIN-67 ovary tumor cells, although displaying higher affinity for calcitonin, failed to activate phospholipase D and protein kinase-C in response to the hormone. This receptor lacks the G protein binding consensus site due to the presence of a 48-bp cassette encoding for a 16-amino acid insert in the predicted first intracellular loop. This modification is likely to prevent the calcitonin receptor from associating to phospholipase-coupled signaling.

Molecular characterization of two novel isoforms of the human calcitonin receptor.

Calcitonin inhibits bone resorption by acting on osteoclasts via a specific receptor. The calcitonin receptor (CTR) is also found in many other normal and malignant tissues and cell lines. It has been cloned and sequenced in several species including humans. It belongs to a subclass of seven-transmembrane G protein-coupled receptors. Four human CTR (H-CTR) isoforms generated by alternatively spliced mRNA have previously been described. Two H-CTR encoding DNAs containing an unidentified 50-bp insert are now reported from T47D cells. The 50-bp insert corresponds to a DNA region located between exon 9 and exon 10, and appears to originate from an alternative splicing process. The two H-CTR cDNAs encode 274 and 290 aa long isoforms. Both are deleted from the putative fourth transmembrane domain to C-tail. They differ by the presence (H-CTR5) or absence (H-CTR6) of a previously known 16-aa insert in the putative first intracellular loop. Cell- and tissue-distribution analysis using RT-PCR demonstrates that the shorter one, HCTR6, is more prevalent. The mRNA of both isoforms was detected in giant cell tumor, whereas only H-CTR6 mRNA was detected in TT cells and kidney tissue. Neither H-CTR5 nor H-CTR6 could be detected in peripheral blood mononuclear cells cultured in the presence of RANKL, in MCF7 cells, and in cortical brain and ovarian tissues. When H-CTR6 was transiently expressed in HEK293 cells, CT failed to induce production of cAMP or to bind to the receptor. These suggest either an intrinsic loss of ligand binding function, or an altered intracellular trafficking. Our findings therefore indicate the existence of two novel splice variants of the H-CTR and confirm that multiple splicing patterns could be involved in the post-transcriptional regulation of the gene.

Osteoclast formation from human cord blood mononuclear cells co-cultured with mice embryonic metatarsals in the presence of M-CSF.

Investigating the potentiality of cord monocytes to differentiate toward osteoclast-like cells (OCL) in vitro, we previously reported that in the presence of 1,25(OH)2 vitamin D3 (1,25-(OH)2D3), multinucleated-cells generated by cord monocyte cultures though displaying morphological features of OCL failed to resorb devitalized bones. We thus hypothesized that full differentiation of cord monocytes toward bone-resorbing cells may require the presence of factors released from and/or direct interactions with living osteogenic cells. In the present study, we tested these hypotheses using two culture systems supporting the development of bone-resorbing cells in the presence of bone matrix. First, cord mononuclear cells were co-cultured with murine fetal metatarsals depleted of osteoclast progenitor cells (stripped metatarsals) in the presence of 1,25-(OH)2D3. We found that cord mononuclear cells failed to differentiate toward OCL as indicated by the absence of the release of 45Ca previously incorporated in fetal bones and by the absence of formation of TRAP-positive (TRAP[+]) multinucleated cells which have invaded mineralized cartilage during the co-culture period. In the same model, we then investigated the effect of some soluble factors known as stimulators of osteoclast differentiation. Whereas exogenous rhIL6 and rhIL3 were ineffective in this assay, rhM-CSF consistently increased both the number of TRAP(+) multinucleated cells inside the mineralized cartilage and the release of 45Ca into the culture media. The effects of rhM-CSF were time-dependent reaching the maximum after 3 weeks of culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitonin receptor mRNA in mononuclear leucocytes from postmenopausal women: decrease during osteoporosis and link to bone markers with specific isoform involvement.

Calcitonin inhibits bone resorption via its receptor (CTR) on osteoclasts. Two hCTR isoforms, hCTR1 and hCTR2, give proteins that differ in their structure and signaling pathways. We investigated whether specific isoforms or quantitative changes in total hCTR mRNA were associated with high bone resorption and turnover in menopause or osteoporosis. The hCTR mRNA in mononuclear blood cells of premenopausal (PreM), healthy (PostM), and osteoporotic (OsteoP) postmenopausal women was assessed using reverse-transcriptase polymerase chain reaction. hCTR1 and hCTR2 were investigated for 59 total RNA samples, and semiquantitative analysis of total hCTR mRNA was performed for 71. Serum calcitonin, free urinary deoxypyridinoline (D-Pyr), serum bone alkaline phosphatase (SBAP), and osteocalcin (SOC) were also evaluated. Serum calcitonin levels did not differ in PostM and OsteoP. The prevalence of each isoform was similar in the three groups. Healthy postmenopausal women and OsteoP with hCTR2 had lower bone turnover (D-Pyr: 6.79 +/- 0.54, n = 25; SBAP: 11.63 +/- 1.47, n = 26; SOC: 8.31 +/- 0.58, n = 26) than those without hCTR2 (D-Pyr: 9.90 +/- 1.95, n = 5; SBAP: 21 +/- 5.19, n = 5; SOC: 11.9 +/- 2.10, n = 5; p < 0.05). Total hCTR mRNA levels were not different in PreM and PostM. By contrast, values were strikingly lower in OsteoP (0.57 +/- 0.17, n = 28) than in PostM (2. 25 +/- 0.61, n = 19, p < 0.05) and negatively correlated with bone markers values in both. We suggest that a specific isoform and amounts of total hCTR mRNA are linked to increased bone resorption in postmenopausal osteoporosis.

[Steroid induced osteoporosis: prevention and treatment]. / Prévention et traitement de l'ostéoporose cortisonique.

PURPOSE: Corticosteroid induced osteoporosis (CIO) is the most frequent complication of long-term corticosteroid therapy, and the most frequent cause of secondary osteoporosis. New data from biological, epidemiological and therapeutic studies provide basis for optimal management of this bone disease. MAIN POINTS: Corticosteroids are responsible for both quantitative and qualitative deleterious effects on bone, through their effect on bone cells, mainly on osteoblasts (with both a decrease in osteoblast activity and an increase in apoptosis). Epidemiological studies have shown an increased risk of fractures related to CIO, even for low doses, and during the first 6 months of treatment. Relative risk is 1.3 and 2.6 for peripheral and vertebral fractures respectively. Bone mineral density, measured by dual-energy X-ray absorptiometry, is decreased at spine and hip; the risk of fracture is higher in CIO as compared to post-menopausal osteoporosis, for a similar bone density. Prevention of CIO needs the use of the minimal efficacious dose, and treatment of calcium, vitamin D and gonadal hormones insufficiencies. Patients at risk of fracture, as post-menopausal women with prevalent fractures, should receive a bisphosphonate. PERSPECTIVE: It may be possible to reduce the fracture risk in patients on long-term corticosteroid therapy.

[Bone hyperresorption in multiple myeloma]. / L'hyperrésorption osseuse au cours du myélome multiple.

OSTEOLYSIS AND HYPERCALCEMIA: Multiple myeloma is a type B high-grade lymphoproliferative syndrome with bone tropism. Bone-related manifestations--osteolysis and hypercalcemia--are observed in 80 and 30% of cases respectively. Excessive bone resorption subsequent to destruction of the bone matrix by osteoclasts is associated with insufficient bone formation. This process plays a determining role in the development of osteolysis and hypercalcemia in multiple myeloma patients. MECHANISM OF BONE DESTRUCTION: The reality and intensity of bone destruction is clearly demonstrated by histomorphometric studies and more recently by biochemical methods using markers of bone resorption. The excessive bone resorption results from complex interactions between tumor plasma cells, bone cells, and stem cells and involves local factors and adhesion molecules. BISPHOSPHONATES: Bisphosphonates are powerful inhibitors of bone resorption. They constitute a substantial advance in the management of bone manifestation in patients with multiple myeloma. Bisphosphonates not only have a well-established curative effect in patients with tumor-induced hypercalcemia, but also inhibit disease progression in bone.

[Spontaneous fissures and fractures of the legs in patients with osteoporosis treated with sodium fluoride]. / Fissures et fractures spontanées des membres inférieurs chez des ostéoporotiques traités par fluorure de sodium.

Thirteen cases of spontaneous fissure or fracture of the lower limbs observed in 8 patients under treatment with sodium fluoride are reported; 7 of these patients were being treated for osteoporosis. The fissures occurred after 20 months of treatment on average and were revealed by pain in the metaphysis with early high radionuclide uptake. Three to 4 weeks later, X-ray films showed a linear bone condensation area, involving in most cases, the tibial metaphysis, the femoral neck and the calcaneum. The prognosis was usually favourable, but 2 patients required surgery for fissure of the femoral neck with rupture of the cortex. Fluor seems to be responsible for the fissures which cannot be avoided by calcium and/or vitamin D intake. The main pathogenic hypotheses are excessive bone resorption, large amounts of poorly mineralized osteoid tissue and architectural abnormalities of the trabeculae. When such fissures occur, fluoride therapy must be discontinued and the limb put at rest, but since this side-effect is rare and usually benign the principle of a treatment that is beneficial in many cases of osteoporosis need not be revised.

[Risk factors and prevention of postmenopausal osteoporosis]. / Facteurs de risque et prévention de l'ostéoporose post-ménopausique.

Preventing postmenopausal bone loss and osteoporotic fractures (vertebral crush fractures and femoral neck fractures) is an important challenge for the next decades. This goal should be achieved by developing screening strategies and deploying established preventive measures. The risk assessment is currently based on densitometric measurements of bone mass and knowledge of risk factors for low bone mass and/or exaggerated bone loss. Hormone replacement therapy is the only well established treatment for preventing osteoporotic fractures. Therefore, it should be recommended to many women. It is important to associate a progesterone derivative with the oestrogen, to exclude patients with breast cancer history and to ensure a follow up by a gynaecologist. Alternative regimens could be useful in patients with low acceptance or contraindication to oestrogens. The long term antifracture efficacy of these molecules remains to be determined, and they have yet, at least in France, no marketing authorization for this purpose.

Diagnostic value of clinical tests for degenerative rotator cuff disease in medical practice.

OBJECTIVES: To assess the diagnostic value of clinical tests for degenerative rotator cuff disease (DRCD) in medical practice. METHODS: Patients with DRCD were prospectively included. Eleven clinical tests of the rotator cuff have been done. One radiologist performed ultrasonography (US) of the shoulder. Results of US were expressed as normal tendon, tendinopathy or full-thickness tear (the reference). For each clinical test and each US criteria, sensitivity, specificity, negative predictive value and positive predictive value, accuracy, negative likelihood ratio (NLR) and positive likelihood ratio (PLR) were calculated. Clinical relevance was defined as PLR ≥2 and NLR ≤0.5. RESULTS: For 35 patients (39 shoulders), Jobe (PLR: 2.08, NLR: 0.31) and full-can (2, 0.5) test results were relevant for diagnosis of supraspinatus tears and resisted lateral rotation (2.42, 0.5) for infraspinatus tears, with weakness as response criteria. The lift-off test (8.50, 0.27) was relevant for subscapularis tears with lag sign as response criteria. Yergason's test (3.7, 0.41) was relevant for tendinopathy of the long head of the biceps with pain as a response criterion. There was no relevant clinical test for diagnosis of tendinopathy of supraspinatus, infraspinatus or subscapularis. CONCLUSIONS: Five of 11 clinical tests were relevant for degenerative rotator cuff disease.

Minimally invasive management of thoraco-lumbar fractures: combined percutaneous fixation and balloon kyphoplasty.

STUDY DESIGN: Retrospective review of prospectively collected data. BACKGROUND: There is no consensus regarding the ideal treatment of thoraco-lumbar spine fractures without neurological compromise. Many surgical techniques have been described but none has proved its definite superiority. The main drawback of these procedures is directly related to the morbidity of the approach. As minimally invasive fixation combined with balloon kyphoplasty for treatment of thoraco-lumbar fractures is gaining popularity, its efficacy has yet to be established. PURPOSE: The purpose of this study is to report operative data, clinical and radiological outcomes of patients undergoing minimally invasive management of thoraco-lumbar fracture at our institutions. METHODS: Forty-one patients underwent percutaneous kyphoplasty and stabilization for treatment of single-level fracture of the thoracic or lumbar spine. All patients were neurologically intact. There were 20 males and 21 females with an average age of 50 years. RESULTS: The mean follow-up was 15 months (3-90 months). The mean operative time was 102 minutes (range 35-240 minutes) and the mean blood loss was <100mL. VAS was significantly improved from 6.7 to 0.7 at last follow-up. Vertebral kyphosis decreased by 16° to 7.8° postoperatively (P<0.001). Local kyphosis and percentage of collapse were also significantly improved from 8° to 5.6° and from 35% to 16% at last follow-up. Fifteen leaks have been identified, three of which were posterior; all remained asymptomatic. No patient worsened his or her neurological condition postoperatively. CONCLUSION: Percutaneous stabilization plus balloon kyphoplasty seems to be a safe and effective technique to manage thoraco-lumbar fractures without neurological impairment.

Medical management following an osteoporotic fracture.

Osteoporotic fractures are common and account for an important medical impact and high induced health-related costs. The most common fracture sites are the vertebra, wrist, proximal humerus and proximal femur. Osteoporosis must benefit from a medical treatment after a fragility fracture. This management is currently insufficient in France, although diagnostic tools (DEXA scan), effective treatments and guidelines are available and have been widely disseminated. Orthopaedic and trauma surgeons must emphasize to patients with a fracture that they need to consult their general practitioner or rheumatologist to decide how their osteoporosis will be diagnosed and treated.