Primary cilia regulate limb and axial skeletal formation and hedgehog signaling, but their roles in temporomandibular joint (TMJ) development are unknown. Thus, we created conditional mouse mutants deficient in ciliary transport protein Kif3a in cartilage. In post-natal wild-type mice, primary cilia were occasionally observed on the superior, inferior, or lateral side of condylar cells. Cilia were barely detectable in mutant chondrocytes but were evident in surrounding tissues, attesting to the specificity of chondrocyte Kif3a ablation. Mutant condyles from 3-month-old mice were narrow and flat along their antero-posterior and medio-lateral axes, were often fused with the articular disc, and displayed an irregular bony surface. The polymorphic layer in P15 mutants contained fewer Sox9-expressing chondroprogenitor cells because of reduced mitotic activity, and newly differentiated chondrocytes underwent precocious hypertrophic enlargement accompanied by early activation of Indian hedgehog (Ihh). Interestingly, there was excessive intramembranous ossification along the perichondrium, accompanied by local expression of the hedgehog receptor Patched-1 and up-regulation of Osterix and Collagen I. In summary, Kif3a and primary cilia are required for coordination of chondrocyte maturation, intramembranous bone formation, and chondrogenic condylar growth. Defects in these processes in Kif3a condylar cartilage are likely to reflect abnormal hedgehog signaling topography and dysfunction.

In this paper, we report two cases of dislocation of the hallux interphalangeal joint with interposition of the plantar plate including the sesamoid bone. These dislocations were treated with open reduction: one through lateral approach and the other through plantar approach. Plantar approach afforded repair of the plantar plate with preservation of the sesamoid bone and satisfactory result.

Objective: This study aimed to characterize the process of disease progression in the early stage of rapidly progressive osteoarthritis of the hip (RPOH) and clarify its association with potential pathological factors of RPOH. Methods: This monocentric retrospective study included 41 female patients who met the criteria for RPOH, chondrolysis >2 mm during 12 months from the onset of hip pain based on a series of radiographs and computed tomography. This study also included 9 female patients with osteoarthritis secondary to developmental dysplasia of the hip (DDH) who demonstrated chondrolysis >2 mm during 12 months from the onset of hip pain. Cortical thickness index (CTI) correlated with bone mineral density of the hip, pelvic tilt, and serum concentrations of matrix metalloproteinase (MMP)-3 were analyzed. Results: RPOH was classified into two types based on the absence (type 1, n=17) and presence (type 2, n=24) of subsequent femoral head destruction within 12 months after the onset of hip pain. MMP-3 significantly increased in RPOH type 2 compared with type 1 and DDH. Increased posterior pelvic tilt was found in RPOH type 2 compared with DDH. Logistic regression and receiver operating characteristic curve analyses indicated that MMP-3 may be associated with differentiation between RPOH types 1 and 2. No difference was found in the CTI between the RPOH types and DDH. Conclusion: Disease progression of RPOH during 12 months after the onset of hip pain could be classified into two distinct types based on the absence (type 1) and presence (type 2) of femoral head destruction in association with MMP-3 and pelvic tilt as biological and mechanical factors, respectively. MMP-3 may be helpful to differentiate these two types in the early stage of RPOH. Cite this article as: Yasuda T, Matsunaga K, Hashimura T, Tsukamoto Y, Sueyoshi T, Ota S, et al. Characterization of rapidly progressive osteoarthritis of the hip in its early stage. Eur J Rheumatol 2020; 7(3): 130-4.

Background: There has been widespread use of short-segment posterior fixation (SSPF) for traumatic thoracolumbar burst fractures. The relationship between the destruction of the vertebral endplate and adjacent disc and postoperative correction loss has been studied in only a few studies. This study investigated the risk factors for correction loss following SSPF. Methods: Forty-eight patients (mean age 35.0 years) who underwent SSPF for thoracolumbar burst fractures were enrolled. The mean follow-up period was 25.7 months (12–98 months). The neurological status and postoperative back pain were assessed by the medical records. Segmental kyphotic angle (SKA) and anterior vertebral body height ratio (AVBHR) were measured radiographically to assess indirect vertebral body reduction and local kyphosis. Preoperative Sander’s traumatic intervertebral disc lesion (TIDL) classification and AO classification were used to evaluate the severity of disc and vertebral endplate injury. The corrective loss was considered present if ΔSKA was ≥10°. A multivariate logistic regression analysis was performed to identify the risk factors associated with postoperative loss of correction. Results: The fracture distribution was as follows: 10 at T12, 17 at L1, 10 at L2, 9 at L3, and 2 at L4. Vertebral fractures were classified in the following way: A3 in 13 patients, A4 in 11, B1 in 11, and B2 in 13. In 47 patients (98%), a union of the fractured vertebrae was achieved. SKA and AVBHR improved significantly after surgery from 11.6° to 3.5° and from 67.2 to 90.0%, respectively. However, the correction loss at follow-up was 10.4° and 9.7%, respectively. Twenty patients (42%) had severe TIDL (grade 3). Postoperative ΔSKA and ΔAVBHR were significantly higher in patients with TIDL grade 3 than with TIDL grade 0–2. The presence of cranial TIDL grade 3 and older age were significant risk factors for ΔSKA ≥10° on multivariate logistic regression analysis. All patients could walk at follow-up. TIDL grade 3 and ΔSKA ≥10° were associated with severe postoperative back pain. Conclusions: Risk factors for loss of correction after SSPF for thoracolumbar burst fractures were severe disc and endplate destruction at the time of injury and older age.

Objective: Previous reports have demonstrated that patients with end-stage rapidly progressive osteoarthritis of the hip (RPOH) show significantly higher serum levels of bone turnover markers than those with osteoarthritis (OA). However, the characteristics of bone turnover markers in the early stage of RPOH remain unclear. This study aimed to elucidate the association of bone turnover markers with disease progression in the early stage of RPOH. Methods: This study included 29 postmenopausal female patients with joint space narrowing >2 mm demonstrated on a series of radiographs and computed tomography within 1 year following the onset of hip pain. The study also included 9 postmenopausal female patients with hip OA secondary to developmental dysplasia showing femoral head destruction. Cortical thickness index (CTI) associated with bone mineral density of the hip was analyzed. Serum concentrations of tartrate-resistant acid phosphatase-5b (TRACP-5b) and bone alkaline phosphatase (BAP) were evaluated. Results: RPOH was classified into two types on the basis of the absence (type 1, n=13) or presence (type 2, n=16) of subsequent destruction of the femoral head within 1 year following disease onset. TRACP-5b and BAP significantly increased in RPOH type 2 compared with type 1 and OA. Receiver operating characteristic curve analyses indicated that TRACP-5b and BAP could differentiate RPOH type 2 from type 1 within 1 year following the onset. CTI showed no difference among the RPOH types 1 and 2 and OA. Conclusion: High serum levels of bone turnover markers may be associated with destruction of the femoral head in the early stage of RPOH. Cite this article as: Yasuda T, Matsunaga K, Hashimura T, Tsukamoto Y, Sueyoshi T, Ota S, et al. Bone turnover markers in the early stage of rapidly progressive osteoarthritis of the hip. Eur J Rheumatol 2021; 8(2): 57-61.