There is still no clear consensus regarding which cup position might provide better functional performance for developmental dysplasia of the hip (DDH). This study aimed to evaluated the feasibility and efficacy of acetabular mirroring reconstruction for DDH in total hip arthroplasty (THA).

The study reviewed 96 patients (96 hips) with unilateral Crowe type-II/III DDH undergoing either visualized navigation-assisted mirroring reconstruction with augment according to the rotation center and biomechanical structure of the contralateral normal hips (Mirroring group, 51 hips) or high hip center reconstruction (HHC group, 45 hips) in THA from 2020 to 2023. The functional and radiographic results were analyzed between the groups during a mean follow-up period of 27.5 and 28.9 months (a minimum follow-up of 12 months).

The Harris hip score at the last follow-up significantly improved in both groups, while it was significantly higher in the mirroring group (P<0.001). In the HHC group, the rotation center height and greater trochanter height were significantly increased in the affected hip (P<0.001; P<0.001) and the abductor lever arm was significantly decreased in the affected hip compared to that in the contralateral normal hip (P<0.001), whereas in the mirroring group no significant statistical differences were observed between two sides. The limping occurred in 7 patients (13.7%) in the mirroring group and 14 patients (31.1%) in the HHC group (P=0.040). A multiple logistic regression demonstrated mirroring reconstruction could reduce the incidence of postoperative limping (P=0.020).

Both mirroring and HHC reconstruction could improve the functional performance of THA, whereas mirroring reconstruction could offer superior biomechanical results and gait improvement as compared with HHC reconstruction, meeting the higher requirements of functional recovery.

Osteocytes are terminally differentiated long-lived cells and account for greater than 95% of the bone cell population. It has been established that osteocytes are connected through their highly developed dendritic network, which is necessary for the maintenance of optimal bone homeostasis. However, little is known on how osteocytes use the network to coordinate their cellular function and communication that requires energy and protein turnover. Here using super-resolution confocal imaging on both live and fixed osteocytes, we demonstrated conclusively that mitochondria are widely distributed and dynamically shared between osteocytes. Using confocal live cell imaging analysis we showed that inhibiting the contact between mitochondria and endoplasmic reticulum (ER) by the knockdown of MFN2 in osteocytes impedes the transfer of mitochondria suggesting the involvement of ER contact with mitochondria in the transfer process. Moreover, we showed that transport of mitochondria between osteocytes within the network enables rescue of osteocytes with dysfunction of mitochondria. Using the 3D tetraculture system with confocal imaging, we identify the transfer of mitochondria from healthy osteocytes enables recovery of mitochondria activities in osteocytes that devoid of mitochondrial DNA by ethidium bromide. The results indicated that when osteocytes are depleted of functional mitochondria, normal parental osteocytes can transfer mitochondria to these stressed osteocytes to provide them with energy. Collectively we show for the first time that the utilisation of mitochondrial transfer enables osteocytes to function with a network and coordinate their cellular activities in response to different energy demands.

Mechanical loading plays an essential role in both tendon development and degradation. However, the underlying mechanism of how tendons sense and response to mechanical loading remains largely unknown. SPARC, a multifunctional extracellular matrix glycoprotein, modulates cell extracellular matrix contact, cell-cell interaction, ECM deposition and cell migration. Adult mice with SPARC deficiency exhibited hypoplastic tendons in load-bearing zone. By investigating tendon maturation in different stages, we found that hypoplastic tendons developed at around postnatal 3 weeks when the mice became actively mobile. The in vitro experiments on primary tendon derived stem cells demonstrated that mechanical loading induced SPARC production and AKT/S6K signalling activation, which was disrupted by deleting SPARC causing reduced collagen type I production, suggesting that mechanical loading was harmful to tendon homeostasis without SPARC. In vivo treadmill training further confirmed that increased loading led to reduced Achilles tendon size and eventually caused tendon rupture in SPARC-/− mice, whereas no abnormality was seen in WT mice after training. We then investigate whether paralysing the hindlimb of SPARC-/− mice using BOTOX from postnatal 2 weeks to 5 weeks would delay the hypoplastic tendon development. Increased patellar tendon thickness was shown in SPARC-/− mice by reducing mechanical loading, whereas opposite effect was seen in WT mice. Finally, we identified a higher prevalence of a missense SNP in the SPARC gene in patients who suffered from a rotator cuff tear. In conclusion, SPARC is a mechano-sensor that regulates tendon development and homeostasis.