Relationship between distal radius fracture severity and 25-hydroxyvitamin-D level among perimenopausal and postmenopausal women.

AIMS: Low-energy distal radius fractures (DRFs) are the most common upper arm fractures correlated with bone fragility. Vitamin D deficiency is an important risk factor associated with DRFs. However, the relationship between DRF severity and vitamin D deficiency is not elucidated. Therefore, this study aimed to identify the correlation between DRF severity and serum 25-hydroxyvitamin-D level, which is an indicator of vitamin D deficiency. METHODS: This multicentre retrospective observational study enrolled 122 female patients aged over 45 years with DRFs with extension deformity. DRF severity was assessed by three independent examiners using 3D CT. Moreover, it was categorized based on the AO classification, and the degree of articular and volar cortex comminution was evaluated. Articular comminution was defined as an articular fragment involving three or more fragments, and volar cortex comminution as a fracture in the volar cortex of the distal fragment. Serum 25-hydroxyvitamin-D level, bone metabolic markers, and bone mineral density (BMD) at the lumbar spine, hip, and wrist were evaluated six months after injury. According to DRF severity, serum 25-hydroxyvitamin-D level, parameters correlated with bone metabolism, and BMD was compared. RESULTS: The articular comminuted group (n = 28) had a significantly lower median serum 25-hydroxyvitamin-D level than the non-comminuted group (n = 94; 13.4 ng/ml (interquartile range (IQR) 9.8 to 17.3) vs 16.2 ng/ml (IQR 12.5 to 20.4); p = 0.005). The AO classification and volar cortex comminution were not correlated with the serum 25-hydroxyvitamin-D level. Bone metabolic markers and BMD did not significantly differ in terms of DRF severities. CONCLUSION: Articular comminuted DRF, referred to as AO C3 fracture, is significantly associated with low serum 25-hydroxyvitamin-D levels. Therefore, vitamin D3 supplementation for vitamin D deficiency might prevent articular comminuted DRFs. Nevertheless, further studies must be conducted to validate the results of the current study. Cite this article: Bone Jt Open 2022;3(3):261-267.

Clinical outcome of the chronic flexor tenosynovitis in the hand caused by non-tuberculous mycobacterium treated by extensive tenosynovectomy and drugs.

Chronic flexor tenosynovitis in the hand caused by non-tuberculous mycobacterial (NTM) infection is uncommon. Although some authors have recommended combining surgical and drug therapy, there are few reports about the timing of drug administration after operation. The purpose of this retrospective study was to analyse the clinical outcome of the protocol, which consisted of extensive tenosynovectomy and drug therapy administered after culture results had been obtained. Four men and one woman were included. Average age was 57.4 years and average follow-up period was 46.7 months. Extensive tenosynovectomy was performed and surgical specimen was examined histopathologically and microbiologically. After a positive culture result had been obtained, three kinds of drugs were administered. Clinical outcome including infectious condition, range of motion, and grip strength was examined. All patients were immunocompetent and had no underlying disease. Three patients were diagnosed at first operation and two were diagnosed at second operation. The average period of drug therapy was 5.5 months. In four patients, infection resolved with combination therapy. In one patient with surgical treatment, only swelling remained. Osteomyelitis of the scaphoid was found in one patient to whom systemic steroid had been administered because of a negative culture result at first operation. For immunocompetent patients, flexor tenosynovitis in the hand caused by NTM was resolved with a combination of surgical and drug treatment. Drug treatment seemed to be essential after a reduction of the infectious lesion and the timing of administration was safe enough to resolve in four patients.

Intra-articular fractures of the distal radius evaluated by computed tomography.

PURPOSE: To describe the fracture lines of intra-articular distal radius fractures as evaluated by computed tomography scans. METHODS: With computed tomography, we examined 95 intra-articular fractures of the distal radius from 91 patients. Multiplanar computed tomography images or 3-dimensional images, or both, were assessed. We divided the periphery of the distal articular surface of the distal radius into 6 segments (sigmoid notch, dorsoulnar, dorsoradial, volar radial, volar ulnar, radial styloid) and examined which segment had fracture lines. For fractures involving the sigmoid notch, we divided them by the location and the direction of the fracture lines entering the sigmoid notch. Next, we categorized the fractures into 3 fracture groups (extension group, neutral group, and flexion group) by the dorsal or volar angulation of the cortex of the distal radius. In all the fractures and in each of the 3 fracture groups, we described the frequency of the fracture lines in each segment and the number of the segments with fracture lines. The location and the direction of the fracture lines in the sigmoid notch were analyzed in each of the 3 fracture groups. RESULTS: The most frequent fracture type, seen in 21% of all fractures, had fracture lines in the sigmoid notch and the dorsoulnar segment. The frequency of the fracture lines was 77% in the sigmoid notch, 71% in the dorsoulnar segment, and 57% in the dorsoradial segment. The volar ulnar segment was lowest in frequency, at 13%. The fractures in the extension group were more common in the dorsoulnar segment and less common in the dorsoradial segment and the radial styloid segment. The scaphoid facet always had a fracture in the flexion or neutral group. In the extension group, the direction of the fracture lines from the sigmoid notch was dorsoradial or parallel to the volar articular edge. In contrast, the direction was parallel or volar radial compared to the volar articular edge in the flexion group. CONCLUSIONS: We documented the location and the direction of intra-articular fracture lines of the distal radius. The location and the direction of fractures showed different tendencies related to the volar/dorsal angulation of the distal radius. CLINICAL RELEVANCE: The findings might help in the evaluation, classification, and treatment of intra-articular fractures of the distal radius.

[Role of BMPs and Smads during endochondral bone formation].

Biochemical research has revealed that BMP signals are mainly mediated through ligand binding to the receptors followed by activation of Smad proteins. BMP signaling is subjected to regulation at extracellular level by noggin and at intracellular level by inhibitory-Smads. Analysis of transgenic mice in which BMP signals are activated or inactivated has been clarifying a role of BMP signaling during endochondral bone formation. BMPs promote chondrocyte proliferation and hypertrophy, whereas Smad signaling regulates chondrocyte hypertrophy. Proper regulation of these signals is necessary for normal bone formation.

Localization of RANKL in osteolytic tissue around a loosened joint prosthesis.

Osteoclastogenesis is a key event of the cellular reaction in prosthetic loosening. Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were used to study the localization and expression of receptor activator of nuclear factor kappa B ligand (RANKL), a potent factor for osteoclastogenesis in the membranous tissue formed around loosened prosthetic joint implants. RANKL was identified in a wide variety of cells appearing in this membranous tissue. At least three types of RANKL-positive cells were identified, including prolyl 4-hydroxylase (PH)-positive fibroblast lineage cells, CD68 cells, and tartrate-resistant acid phosphatase (TRAP)-positive mononuclear and multi-nucleated macrophage lineage cells. Tumor necrosis factor (TNF)-alpha-converting enzyme (TACE) was colocalized with RANKL in these cells, suggesting the in-situ release of this factor. RT-PCR confirmed the actual expression of the RANKL and TACE genes in the tissues around the loosened implant. These observational findings indicate the possible synthesis of RANKL by fibroblast and macrophage lineage cells, and suggest the in-situ involvement of RANKL in both osteoclastogenesis and osteoclastic bone resorptive events occurring in prosthetic joint loosening.

Smad6/Smurf1 overexpression in cartilage delays chondrocyte hypertrophy and causes dwarfism with osteopenia.

Biochemical experiments have shown that Smad6 and Smad ubiquitin regulatory factor 1 (Smurf1) block the signal transduction of bone morphogenetic proteins (BMPs). However, their in vivo functions are largely unknown. Here, we generated transgenic mice overexpressing Smad6 in chondrocytes. Smad6 transgenic mice showed postnatal dwarfism with osteopenia and inhibition of Smad1/5/8 phosphorylation in chondrocytes. Endochondral ossification during development in these mice was associated with almost normal chondrocyte proliferation, significantly delayed chondrocyte hypertrophy, and thin trabecular bone. The reduced population of hypertrophic chondrocytes after birth seemed to be related to impaired bone growth and formation. Organ culture of cartilage rudiments showed that chondrocyte hypertrophy induced by BMP2 was inhibited in cartilage prepared from Smad6 transgenic mice. We then generated transgenic mice overexpressing Smurf1 in chondrocytes. Abnormalities were undetectable in Smurf1 transgenic mice. Mating Smad6 and Smurf1 transgenic mice produced double-transgenic pups with more delayed endochondral ossification than Smad6 transgenic mice. These results provided evidence that Smurf1 supports Smad6 function in vivo.