Arthroscopic Bankart repair with all-suture anchors does not cause important glenoid bone osteolysis: a volumetric CT study of 143 anchors.

PURPOSE: To evaluate with computed tomography (CT) the incidence of anchor-related osteolysis after implantation of two types of all-suture anchors for the management of labral lesions in shoulder instability. METHODS: Single-cohort, observational study with 12-month follow-up. Thirty-three participants (27 males/6 females; age 38.3 years [SD 11.3]) with anterior labral lesions in which 143 all-suture anchors (71 Iconix 1.4 mm and 72 Suturefix 1.7 mm) were implanted were evaluated with a CT performed a mean of 15.4 [3.85] months after surgery. The volume of the bone defects was measured in the CT. Every anchor was classified into one of four groups: (1) no bone defect. (2) Partial bone defect (defects smaller than the drill used for anchor placement). (3) Tunnel enlargement (defects larger than the drill volume but smaller than twice that volume). (4) Cystic lesion (defects larger than twice the drill volume). RESULTS: No bone defect was identified in 16 anchors (11.2%, [95% CI 6.5-17.5%]). A partial bone defect was found in 84 anchors (58.7% [50.2-66.9%]). Tunnel enlargement was found in 43 anchors (30.11% [22.6-37.6%]). No anchor caused cystic lesions (0% [0-2.5%]). The defect volume was a mean of 27.8 mm3 (SD 18.4 mm3, minimum 0 mm3, maximum 94 mm3). Neither the position in the glenoid nor the type of implant used had a significant effect in the type or size of the defects. CONCLUSION: When using all-suture anchors in the glenoid during instability surgery, relevant bone osteolytic defects are rare at 1-year follow-up. Most anchor insertion tunnels will fill completely (11%) or partially (59%) with bone. Tunnel enlargement will develop in 30% of anchors. No cystic defects larger than 0.125 cm3 were observed. There is a low risk that all-suture anchors cause significant osteolytic bone defects in the glenoid. These implants can be used safely. Level of evidence IV.

[Supportive drugs for improved implant healing]. / Medikamentöse Verbesserung der Implantateinheilung.

BACKGROUND: Improvement of implant healing in orthopedic and trauma surgery serves to improve the life expectancy of the implant. Good primary stability by clamping is a prerequisite for secondary stability and for the actual integration and healing of the implant. RESULTS: Possible causes of implant loosening are abrasive particles, which arrive at non-integrated implants at the unsealed prosthesis-bone interface and provoke a macrophage-mediated foreign body reaction, resulting in periprosthetic osteolysis. Numerous animal studies have already described the use of bisphosphonates to inhibit osteolysis induced by abrasion and secondary instability. In patients with total knee arthroplasty, a decrease in prosthetic migration under the influence of bisphosphonates could be shown. The stimulation of bone formation around the implants and the resulting implant healing was demonstrated both in animal experiments for bone morphogenetic proteins (BMP) and in case reports for intermittent parathyroid hormone administration. CONCLUSION: By using supportive drugs, it is possible to achieve an improvement in the osseointegration of implants; thus, more rapid secondary stability and load-bearing are expected.

Propionate and butyrate attenuate macrophage pyroptosis and osteoclastogenesis induced by CoCrMo alloy particles.

BACKGROUND: Wear particles-induced osteolysis is a major long-term complication after total joint arthroplasty. Up to now, there is no effective treatment for wear particles-induced osteolysis except for the revision surgery, which is a heavy psychological and economic burden to patients. A metabolite of gut microbiota, short chain fatty acids (SCFAs), has been reported to be beneficial for many chronic inflammatory diseases. This study aimed to investigate the therapeutic effect of SCFAs on osteolysis. METHODS: A model of inflammatory osteolysis was established by applying CoCrMo alloy particles to mouse calvarium. After two weeks of intervention, the anti-inflammatory effects of SCFAs on wear particle-induced osteolysis were evaluated by Micro-CT analysis and immunohistochemistry staining. In vitro study, lipopolysaccharide (LPS) primed bone marrow-derived macrophages (BMDMs) and Tohoku Hospital Pediatrics-1 (THP-1) macrophages were stimulated with CoCrMo particles to activate inflammasome in the presence of acetate (C2), propionate (C3), and butyrate (C4). Western blotting, Enzyme-linked immunosorbent assay, and immunofluorescence were used to detect the activation of NLRP3 inflammasome. The effects of SCFAs on osteoclasts were evaluate by qRT-PCR, Western blotting, immunofluorescence, and tartrate-resistant acid phosphatase (TRAP) staining. Additionally, histone deacetylase (HDAC) inhibitors, agonists of GPR41, GPR43, and GPR109A were applied to confirm the underlying mechanism of SCFAs on the inflammasome activation of macrophages and osteoclastogenesis. RESULTS: C3 and C4 but not C2 could alleviate wear particles-induced osteolysis with fewer bone erosion pits (P < 0.001), higher level of bone volume to tissue volume (BV/TV, P < 0.001), bone mineral density (BMD, P < 0.001), and a lower total porosity (P < 0.001). C3 and C4 prevented CoCrMo alloy particles-induced ASC speck formation and nucleation-induced oligomerization, suppressing the cleavage of caspase-1 (P < 0.05) and IL-1ß (P < 0.05) stimulated by CoCrMo alloy particles. C3 and C4 also inhibited the generation of Gasdermin D-N-terminal fragment (GSDMD-NT) to regulate pyroptosis. Besides, C3 and C4 have a negative impact on osteoclast differentiation (P < 0.05) and its function (P < 0.05), affecting the podosome arrangement and morphologically normal podosome belts formation. CONCLUSION: Our work showed that C3 and C4 are qualified candidates for the treatment of wear particle-induced osteolysis.

Additive Effect of Parathyroid Hormone and Zoledronate Acid on Prevention Particle Wears-Induced Implant Loosening by Promoting Periprosthetic Bone Architecture and Strength in an Ovariectomized Rat Model.

Implant-generated particle wears are considered as the major cause for the induction of implant loosening, which is more susceptible to patients with osteoporosis. Monotherapy with parathyroid hormone (PTH) or zoledronate acid (ZOL) has been proven efficient for preventing early-stage periprosthetic osteolysis, while the combination therapy with PTH and ZOL has exerted beneficial effects on the treatment of posterior lumbar vertebral fusion and disuse osteopenia. However, PTH and ZOL still have not been licensed for the treatment of implant loosening to date clinically. In this study, we have explored the effect of single or combined administration with PTH and ZOL on implant loosening in a rat model of osteoporosis. After 12 weeks of ovariectomized surgery, a femoral particle-induced periprosthetic osteolysis model was established. Vehicle, PTH (5 days per week), ZOL (100 mg/kg per week), or combination therapy was utilized for another 6 weeks before sacrifice, followed by micro-CT, histology, mechanical testing, and bone turnover examination. PTH monotherapy or combined PTH with ZOL exerted a protective effect on maintaining implant stability by elevating periprosthetic bone mass and inhibiting pseudomembrane formation. Moreover, an additive effect was observed when combining PTH with ZOL, resulting in better fixation strength, higher periprosthetic bone mass, and less pseudomembrane than PTH monotherapy. Taken together, our results suggested that a combination therapy of PTH and ZOL might be a promising approach for the intervention of early-stage implant loosening in patients with osteoporosis.

Osteolytic metastasis in breast cancer: effective prevention strategies.

INTRODUCTION: Breast cancer is the most common cancer in women throughout the world. Patients who are diagnosed early generally have better prognosis and survivability. Indeed, advanced stage breast cancer often develops osteolytic metastases, leading to bone destruction. Although there are select drugs available to treat bone metastatic disease, these drugs have shown limited success. AREA COVERED: This paper emphasizes updated mechanisms of bone remodeling and osteolytic bone metastases of breast cancer. This article also aims to explore the potential of novel natural and synthetic therapeutics in the effective prevention of breast cancer-induced osteolysis and osteolytic metastases of breast cancer. EXPERT OPINION: Targeting TGFß and BMP signaling pathways, along with osteoclast activity, appears to be a promising therapeutic strategy in the prevention of breast cancer-induced osteolytic bone destruction and metastatic growth at bone metastatic niches. Pilot studies in animal models suggest various natural and synthetic compounds and monoclonal antibodies as putative therapeutics in the prevention of breast cancer stimulated osteolytic activity. However, comprehensive pre-clinical studies demonstrating the PK/PD and in-depth understanding of molecular mechanism(s) by which these potential molecules exhibit anti-tumor growth and anti-osteolytic activity are still required to develop effective therapies against breast cancer-induced osteolytic bone disease.

Rapid induction of clinical remission in SAPHO syndrome using high-dose Tripterygium glycosides: A case report.

RATIONALE: Synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is a rare disease without standard treatments. Tripterygium wilfordii hook f (TwHF) is a traditional Chinese herb with anti-inflammatory effect, and 1.0 mg/(kg·d) dose of Tripterygium glycosides has been reported to significantly improve the disease activity of a SAPHO patient in a case report. However, the optimal dose of TwHF is still unclear. Here, we report the first case of SAPHO patient who achieved rapid remission in clinical symptoms after receiving 1.5 mg/(kg·d) dose of Tripterygium glycosides treatment. PATIENT CONCERNS: A 67-year-old woman noted palmoplantar pustulosis and pain in the anterior chest wall and waist. Bone scintigraphy demonstrated the typical tracer accumulation feature and magnetic resonance images showed bone marrow edema in lumbosacral vertebra. DIAGNOSES: The diagnosis was made by dermatological and osteoarticular manifestations and classical signs in bone scintigraphy in accordance with the diagnostic criteria proposed in 2012. INTERVENTIONS: Tripterygium glycosides was given with a primary dose of 1.5 mg/(kg·d) for 1 month and then reduced at a rate of 10 mg every 2 weeks until 1.0 mg/(kg·d) for a long-term maintenance. OUTCOMES: Fast-induced remission on clinical manifestations was achieved and magnetic resonance imaging abnormality was improved significantly. Additionally, no apparent side effects were observed. LESSONS: 1.5 mg/(kg·d) dose of Tripterygium glycosides seems to have fast-induced remission than 1.0 mg/(kg·d) with reliable safety. Besides, Tripterygium glycosides may also have a pharmacological effect of inhibiting osteolysis and enhancing bone strength.

Cup-neck impingement due to the malposition of the implant as a possible mechanism for metallosis in metal-on-metal total hip arthroplasty.

The metal-on-metal bearing total hip prosthesis is expected to reduce the risk of debris-related osteolysis. However, several reports demonstrated that the socket-stem impingement in the metal-on-metal prosthesis due to the implant malposition results in titanium wear debris and secondary metallosis. In this article, we presented a case of massive metallosis due to metal-on-metal impingement. A 60-year woman had severe hip pain due to fracture of the greater trochanter. We planned a revision of the metal-on-metal inlay. Intraoperatively, the trochanteric bursa and joint space were found to be stained black. Black stained granulation tissue was observed between the femoral stem and the great trochanter. Intraoperatively, notching was noticed on both the posteroinferior aspect of the neck of the femoral component and the anterior aspect of the metal liner and polyethylene core. The notch corresponded to the position of impingement between the socket and the femoral neck during the maximum extension of the hip. To clarify the mechanism of cup-neck impingement, the alignment of the prosthesis and pelvic tilt were evaluated. The cup was placed in too much anteverted position. In addition, increased posterior tilt of pelvis in the standing position made the anteversion of the acetabular cup more significant, which enhanced the cup-neck impingement during the gait. Careful attention is necessary for implant alignment and pelvic tilt especially in metal-on-metal-bearing total hip arthroplasty.

Shoulder Acromioclavicular and Coracoclavicular Ligament Injuries: Common Problems and Solutions.

Injuries to the acromioclavicular joint and coracoclavicular ligaments are common. Many of these injuries heal with nonoperative management. However, more severe injuries may lead to continued pain and shoulder dysfunction. In these patients, surgical techniques have been described to reconstruct the function of the coracoclavicular ligaments to provide stable relationship between the clavicle and scapula. These surgeries have been fraught with high complication rates including clavicle and coracoid fractures, infection, loss of reduction and fixation, hardware migration, and osteolysis. This article reviews common acromioclavicular and coracoclavicular repair and reconstruction techniques and associated complications, and provides recommendations for prevention and management.

Femoral osteolysis following total hip replacement.

Total hip replacement represents the most significant advance in orthopaedic surgery in the 20th century. Periprosthetic osteolysis remains the most significant long-term complication with total hip replacement. It has been reported with all materials and prosthetic devices in use or that have been used to date. This paper reviews the current thinking on the aetiology, pathogenesis, management and future treatment options for osteolysis.

[Bisphosphonates in oncology: update 2007]. / Les bisphosphonates en oncologie: incertitudes et controverses en 2007.

Bisphosphonates prevent bone complications induced by cancer. Their low toxicity promoted their extensive use supported by different international recommendations. However the prescription of these therapies is now seriously questioned because of their late and severe toxicity, the osteonecrosis of the jaw, and the growing efficiency of the oncologic therapies. No monitoring method is now available for bisphosphonates therapy. Therefore only a stricter selection of the patients, based on established and well-proven indications, as well as limitation of the administration durations could maintain an adequate risk/benefit ratio.

[Management of complications of bisphosphonates in oncology patients: jaw osteonecrosis]. / Ostéonecrose des maxillaires en rapport avec la prise de bisphosphonates: que faire ?

The first report of jaw osteonecrosis in patients treated with bisphophonates was published in 2003. Since then, not a week goes by without new cases being described in the literature. The vast majority of patients treated with IV bisphosphonates are oncology patients, although numbers of patients with osteonecrosis treated for osteoporosis and Paget's disease are also rising. In the absence of any established treatment, it is generally agreed that initiating pretherapeutic prevention strategies in oncology patients is advisable. Treatment of a recognised osteonecrosis is discussed, with preference being given for a conservative approach rather than aggressive surgical procedures. Our team suggests classifying affected patients into two categories according to the lesions: disabling or non-disabling. An appropriate treatment plan can then be put into place.

Treatment of malignancy-associated hypercalcemia with intravenous aminohydroxypropylidene diphosphonate.

Treatment of malignancy-associated hypercalcemia remains unsatisfactory. We have prospectively treated 26 consecutive hypercalcemic cancer patients with intravenous (IV) aminohydroxypropylidene diphosphonate (APD). The drug was administered daily as a 15-mg two-hour IV infusion until both serum and urinary calcium had been normalized for 48 hours. Twenty-four patients were fully evaluable (eight head and neck tumors, seven breast cancers, three epidermoid tumors of the lung, and six miscellaneous neoplasms). Whereas rehydration had only inconsistent effects, APD normalized serum calcium in all patients after a mean of three daily doses: serum calcium decreased from 13.3 +/- 0.4 mg/dL (mean +/- SEM) before APD to 8.0 +/- 0.1 mg/dL at the end of treatment. Ionized calcium declined in parallel to total calcium. APD was as effective in hypercalcemia due to bone metastases as in paraneoplastic hypercalcemia. The drug was tolerated without toxicity and had a prolonged effect: serum calcium remained normal during 3+ weeks (1 + to 8 +) in 17 patients who did not receive or did not respond to antitumoral treatment. APD normalized serum calcium by inhibiting bone resorption, as evidenced by the dramatic decrease in urinary excretion of calcium and hydroxyproline. Inhibition of bone resorption was probably also responsible for the decrease in serum phosphorus from 2.9 +/- 0.2 to 2.0 +/- 0.1 mg/dL. In summary, IV APD constitutes a major advance in the treatment of malignancy-associated hypercalcemia: it is very effective, well tolerated, and has a prolonged efficacy.

Treatment of hypercalcaemia of malignancy with clodronate.

The bisphosphonate clodronate has been widely used in the treatment of hypercalcaemia and osteolytic bone metastases. It can normalize plasma calcium in most hypercalcaemic, rehydrated cancer patients when increased bone resorption is the prevailing disturbance of calcium metabolism. When given intravenously either as a single infusion or as repeated daily administrations, serum calcium levels fall to normal 3-5 days after the onset of therapy. Long-term maintenance treatment must be adjusted individually since relapse appears to depend upon the tumour type, the degree of malignancy and any anticancer therapy. In patients in whom increased tubular calcium reabsorption is the prevailing disturbance of calcium metabolism, the effect of clodronate on plasma calcium is incomplete, despite the normalization of bone resorption. This type of therapeutic response can be reproduced experimentally in bisphosphonate-treated animals receiving a constant infusion of parathyroid hormone-related peptide, a peptide isolated from various tumour types including lung, kidney, breast and neuroendocrine tumour of the pancreas. In patients having a good response to clodronate, the fall in plasma calcium is accompanied by an increase in the calcium-regulating hormones, parathyroid hormone and 1,25-dihydroxyvitamin D3. This homeostatic response probably explains why hypocalcaemia occurs rarely in clodronate-treated patients. No serious side-effects of treatment have been reported. Clodronate appears to be a safe and effective treatment for the hypercalcaemia of malignancy, where increased bone resorption is the major mechanism disturbing the homeostasis of extracellular calcium.

The pathogenesis of bone loss following total knee arthroplasty.

Bone loss following total knee arthroplasty (TKA) may be focal or diffuse. It may be caused mechanically, either by unloading of the bone leading to disuse osteoporosis, or by overloading of the bone leading to trabecular fractures and bone destruction. Osteolysis, instigated by an inflammatory reaction to particulate wear debris, is an important and common cause of bone loss after TKA. Less common, though sometimes dramatic, causes of bone loss are infection and osteonecrosis.

Hardware complications related to the surgical fixation of slipped capital femoral epiphyses.

Slipped upper femoral epiphysis is a disabling condition with an annual incidence of 2-13 per 100,000. In situ surgical fixation is the preferred initial treatment for both stable and unstable slipped capital femoral epiphysis (SCFE) cases. The main aim is to avoid further slippage and complications such as osteonecrosis and chondrolysis. The choice of medical implants in managing this condition has changed along the years from large nail-like devices to cannulated screws. The biomechanical properties of different fixation techniques have been studied. All implants have been associated with complications that can occur intraoperatively as well as in the early and late postoperative periods. This report examines a number of different implants used and identifies complications and ways on how to avoid such complications. It also looks at the complications directly related to medical implants in the management of SCFE. We looked at published literature in peer-reviewed journals describing the use of the different medical implants and the documented complications. We also examined literature that suggests ways on how to avoid and manage these complications. A review of the current literature is presented in this text.

Moderate zinc supplementation during prolonged steroid therapy exacerbates bone loss in rats.

The present study was conducted to understand the influence of zinc on bone mineral metabolism in prednisolone-treated rats. Disturbance in bone mineral metabolism was induced in rats by subjecting them to prednisolone treatment for a period of 8 weeks. Female rats aged 6-8 weeks weighing 150 to 200 g were divided into four treatment groups, viz., normal control, prednisolone-treated (40 mg/kg body weight orally, thrice a week), zinc-treated (227 mg/L in drinking water, daily), and combined prednisolone + zinc-treated groups. Parameters such as changes in mineral levels in the bone and serum, bone mineral density (BMD), bone mineral content (BMC), and bone 99m-technetium-labeled methylene diphosphonate ((99m)Tc-MDP) uptake were studied in various treatment groups. Prednisolone treatment caused an appreciable decrease in calcium levels both in the bone and serum and also in bone dry weight, BMC, and BMD in rats. Prednisolone-treated rats when supplemented with zinc showed further reduction in calcium levels, bone dry weight, BMD, and BMC. The study therefore revealed that moderate intake of zinc as a nutritional supplement during steroid therapy could enhance calcium deficiency in the body and accelerate bone loss.