To evaluate the effects of 6 and 18 months of abaloparatide (ABL) compared with placebo (PBO) on bone mineral density (BMD) in the acetabular regions of postmenopausal women with osteoporosis (OP).

Acetabular bone loss, as may occur in OP, increases risk of acetabular fragility fractures^a. In total hip arthroplasty (THA), low acetabular BMD adversely affects primary stability, osseointegration, and migration of acetabular cups.^c ABL is an osteoanabolic agent for the treatment of men and postmenopausal women with OP at high risk for fracture. Effects of ABL on acetabular BMD are unknown.

Hip DXA scans were obtained at baseline, 6, and 18 months from a random subgroup of postmenopausal women (aged 49–86 y) from the phase 3 ACTIVE trial randomized to either ABL 80 µg/d or PBO (n=250/group). Anatomical landmarks were identified in each DXA scan to virtually place a hemispherical shell model of an acetabular cup and define regions of interest corresponding to DeLee & Charnley zones 1 (R1), 2 (R2), and 3 (R3). BMD changes compared to baseline were calculated for each zone. Statistical P values were based on a repeated mixed measures model.

BMD in all zones were similar at baseline in the ABL and PBO groups. BMD significantly increased in the ABL group at 6 and 18 months compared with PBO (all P<0.0001 vs PBO). BMD in the PBO group was relatively stable over time.

ABL treatment resulted in rapid and progressive increases in BMD of all 3 acetabular zones. Increasing acetabular BMD has the potential to improve acetabular strength, which may reduce risk of acetabular fragility fractures. In bone health optimization prior to THA, increased acetabular BMD via ABL may provide better primary stability and longevity of acetabular cups in postmenopausal women with OP.

Purpose: Joint cartilage repair is one of the most widely studies aspects of orthopedic care. The tissue’s intrinsic capacity to repair degenerative, inflammatory or trauma-induce damage is low. The purpose of this study was to report early results obtained with an allograft using a hybrid biocartilage in the rabbit.

Material and methods: Chondrocytes obtained by successive enzymatic digestion of joint cartilage from the knee joint were implanted via medial arthrotomy into an osteo-cartilaginous knee defect measuring 4 cm in diameter and 3 mm in depth produced by trepanation of the tronchlea. Both knees were operated in six adult New Zealand rabbits. After eight weeks, the animals were assessed clinically then sacrificed. The femoral condyles were removed for histological study. All grafted joints were mobile and had normal function without risk of self-mutilation.

Results: The joint samples did not show any evidence of effusion. The implant site was still visible macroscopically and presented a cartilaginous surface continuous with the healthy cartilage. After HES staining, the distal pole of the implant was found to be colonised with young cartilage continuous with the trochlear cartilage. Enchondral ossification appeared to be present in the distal part of certain cartilaginous nodules with a bony lamina continuous with the adjacent subchondral bone. There was no evidence of an inflammatory reaction of the synovial and the patellar cartilage was normal.

Discussion: These preliminary results of a hybrid biocartilage graft combined with cartilage surface reconstruction and osteointegration of the deep implant without in vivo supply of growth factors are encouraging. The safety of the supporting material was demonstrated. We are currently working on developing an autograft from progenitor cells.