The prevalence of gluteal tendinopathy (GT) associated with osteoarthritis of the hip is difficult to determine as it is frequently undiagnosed or misdiagnosed as trochanteric bursitis. Its relationship to total hip arthroplasty (THA) outcomes is currently unknown. The aim of this study was to determine the incidence of GT at the time of hip arthroplasty and examine the relationship between GT and patient reported outcomes (PROMS) before and after THA.

Patients undergoing THA for primary osteoarthritis between August 2017 and August 2020 were recruited. Tendinopathy was assessed and graded at time of surgery. PROMS included the Oxford Hip Score (OHS), HOOS JR, EQ-5D, and were collected preoperatively and at one year after THA. Satisfaction with surgery was also assessed at 1 year.

797 patients met eligibility criteria and were graded as Grade 1: normal tendons (n =496, 62%), Grade 2: gluteal tendinopathy but no tear (n=222, 28%), Grade 3: partial/full thickness tears or bare trochanter (n=79, 10%). Patients with abnormal gluteal tendons were older (p=0.001), had a higher mean BMI (p=0.01), and were predominately female (p=0.001). Patients with higher grade tendinopathy had statistically significant inferior PROMS at one year, OHS score (44.1 v 42.9 v 41.3, p 0.001) HOOS JR (89.3 V 86.3 V 85.6 p 0.005). Increasing gluteal tendon grade was associated with a greater incidence of problems with mobility (p=0.001), usual activities (p=0.001) and pain (p=0.021) on EQ5D. There was a 3 times relative risk of overall dissatisfaction with THA in the presence of gluteal tears.

This study demonstrated that gluteal tendinopathy was commonly observed and associated with inferior 1-year PROMS in patients undergoing THA for OA. Increasing degree of tendinopathy was a negative prognostic factor for worse functional outcomes and patient satisfaction.

Hip resurfacing arthroplasty (HRA) is a bone conserving alternative to total hip arthroplasty. We present the early 1 and 2-year clinical and radiographical follow-up of a novel ceramic-on-ceramic (CoC) HRA in a multi-centric Australian cohort.

Patient undergoing HRA between September 2018 and April 2021 were prospectively included. Patient-reported outcome measures (PROMS) in the form of the Forgotten Joint Score (FJS), HOOS Jr, WOMAC, Oxford Hip Score (OHS) and UCLA Activity Score were collected preoperatively and at 1- and 2-years post-operation. Serial radiographs were assessed for migration, component alignment, evidence of osteolysis/loosening and heterotopic ossification formation.

209 patients were identified of which 106 reached 2-year follow-up. Of these, 187 completed PROMS at 1 year and 90 at 2 years. There was significant improvement in HOOS (p< 0.001) and OHS (p< 0.001) between the pre-operative, 1-year and 2-years outcomes. Patients also reported improved pain (p<0.001), function (p<0.001) and reduced stiffness (p<0.001) as measured by the WOMAC score. Patients had improved activity scores on the UCLA Active Score (p<0.001) with 53% reporting return to impact activity at 2 years. FJS at 1 and 2-years were not significantly different (p=0.38). There was no migration, osteolysis or loosening of any of the implants. The mean acetabular cup inclination angle was 41.3° and the femoral component shaft angle was 137°. No fractures were reported over the 2-year follow-up with only 1 patient reporting a sciatic nerve palsy.

There was early return to impact activities in more than half our patients at 2 years with no early clinical or radiological complications related to the implant. Longer term follow-up with increased patient numbers are required to restore surgeon confidence in HRA and expand the use of this novel product.

In conclusion, CoC resurfacing at 2-years post-operation demonstrate promising results with satisfactory outcomes in all recorded PROMS.

Tenomodulin (Tnmd) is the best known mature tendon factor for tendon and ligament tissues with reported important regulatory roles1. In addition, Tnmd C-terminal cysteine-rich domain has been descibed to exert anti-angiogenic functions in in vitro angiogenic assays as well as in vivo models of tendon injury and age-associated cardiac valve diseases1, 2. Interestingly, Tnmd expresson in the intervertebral disc (IVD), which is normally avascular tissue, has been also suggested3. Hence, the purpose of this study was first, to map the exact expression pattern of Tnmd during IVD development and aging and second, by implementing Tnmd-knockout mouse model, to examine if Tnmd plays a role in IVD homeostasis.

Histological analyses (hematoxylin/eosin, Safranin O, CD31 for endothelium, TUNEL for apoptosis and type X collagen and Runx2 for hypetrophy) were performed on Tnmd −/−, Tnmd −/− and chondromodulin I Chmd 1 −/− (Tnmd only homolog) double knockout and wild type mice WT (n = three to five) to examine IVD degeneration. Real time PCR was implemented to explore gene expression chnages in annulus fibrous (AF) between Tnmd −/− and WT mice. In addition, outer AF (OAF) cells were isolated from both genotypes to further determine cellular phenotype and assess effects on co-culture with human umbical vein endothelial cells (HUVECs). Statistical differences between two groups were determined with t-test. In multiple comparisons, one-way ANOVA was followed by Bonferroni post-hoc correction.

Tnmd was expressed in a temporal manner in OAF and to very low extent in NP. Tnmd −/− mice exhibited more rapid progression of age-related IVD degeneration. These signs included smaller collagen fibril diameter, reduced multiple IVD- and tendon/ligament-related gene expression, induced angiogenesis and inflamatory cell infiltration in OAF as well as more hypertrophic-like chondrocytes in the NP. In addition, Tnmd−/− Chm1 −/− mice displayes not only accelerated IVD phenotpye, but also ectopic bone formation in the IVD. Lastly, the abscence of Tnmd in OAF-derived cells significantly promoted HUVECs migratory capacity.

These findings provide clear evidence that Tnmd plays a critical role in IVD homeostasis.

Post-traumatic osteonecrosis of the femoral head (ONFH) is a major complication of femoral neck fractures that require numerous solutions. The purpose of the current study is to investigate the effects of platelet-rich plasma (PRP) incorporated autologous granular bones graft for the treatment of pre-collapse stages (ARCO stage II-III) of post-traumatic ONFH.

A total of 46 patients were eligible and enrolled into the study. 24 patients were treated with core decompression and PRP incorporated autologous granular bones graft (treatment group: 9 females and 15 males, age range, 16–39 years), and 22 patients with core decompression and autologous granular bones graft (control group: 6 females and 16 males, age range, 18–42 years. During a minimum duration of follow-up of 36 months, multiple imaging techniques including X-ray and computed tomography (CT) scanning were used to evaluate the radiological results, and Harris hip score (HHS) and the visual analogue scale (VAS) were chosen to assess the clinical results.

Both treatment group and control group had a significant improved HHS (P < 0.001). The minimum clinically important difference (MCID) for HHS was reached in 91.7% of treatment group and 68.2% of control group (P = 0.0449). HHS in treatment group was significantly higher than control group at the last follow-up (P = 0.0254). VAS score was significantly declined in treatment group when compared with control group (P = 0.0125). Successful clinical results were achieved in 21 of 24 patients (87.5%) in treatment group compared with 13 of 22 patients (59.1%) in control group (P = 0.0284). Successful radiological results were achieved in 19 of 24 patients (79.2%) in treatment group compared with 11 of 22 patients (50%) in control group (P = 0.0380). The survival rates using requirement for further hip surgery as an endpoint were higher in treatment group in comparison to control group (P = 0.0260).

The PRP incorporated autologous granular bones graft is a safe and effective procedure for the treatment of pre-collapse stages (ARCO stage II-III) of post-traumatic ONFH.

Previous studies have shown that Tnmd is important for tendon maturation and has key implications for the residing tendon stem/progenitor cells. The putative signaling in which Tnmd participates is just starting to be better understood (Dex et al. 2016). However, its exact functions during tendon healing process still remain elusive. Therefore, the aims of this study were to perform systematic review of the literature on Tnmd-related research and to investigate the role of Tnmd in early tendon healing by applying a tendon rupture model in Tnmd-deficient mice.

First, we searched in the PubMed database for articles containing “tenomodulin” or its alternative names and abbreviations. After exclusion of papers only available in abstract form and foreign language, we grouped the remaining 128 full-text publications into four study types: 1) looking into functions of Tnmd; 2) using Tnmd as a tendon marker; 3) correlating Tnmd mutations to a variety of diseases; and 4) reviews. Following literature analysis, we carried out a pilot Achilles tendon injury model with Tnmd-knockout (KO) mouse strain. Adult Tnmd-KO (n = 8) and wild-type (WT) (n = 8) mice underwent unilateral surgery of Achilles tendon based on Palmes et al. 2002 and were compared at day 8 postoperatively by: 1) H&E staining for overall assessment; 2) immunohistochemical BrdU analysis for cell proliferation; and 3) Safranin O staining for endochondral formation.

Our literature screen revealed that Tnmd has been strongly justified as the best tendon and ligament marker in more than 90 different studies. Moreover, in vivo and in vitro investigations have demonstrated its positive role on tendon cell proliferation and tissue functions. Our follow up surgical study showed a very different scar organization in Tnmd-KO with a clearly reduced cell density. BrdU analysis confirmed a lower number of proliferating cells in Tnmd-KO scar area. Interestingly, endochondral formation was not observed in the scar tissues in either of the genotypes at day 8.

Taken together, we systematically summarized the current knowledge on Tnmd gene and highlighted several future research perspectives. Lack of studies on the role of Tnmd in tissue healing, motivated our pilot investigation on Achilles tendon rupture, which in turn suggested that loss of Tnmd results in inferior repair process.