Our aim was to develop a clinically relevant model of atrophic nonunion in the rat to test the hypothesis that the vessel density of atrophic nonunion reaches that of normal healing bone, but at a later time-point. Atrophic nonunion is usually attributed to impaired blood supply and is poorly understood.

We determined the number of blood vessels at the site of an osteotomy using immunolocalisation techniques in both normally healing bones and in atrophic nonunion. At one week after operation there were significantly fewer blood vessels in the nonunion group than in the healing group. By eight weeks, the number in the atrophic nonunion group had reached the same level as that in the healing group.

Our findings suggest that the number of blood vessels in atrophic nonunion reaches the same level as that in healing bone, but at a later time-point. Diminished vascularity within the first three weeks, but not at a later time-point, may prevent fractures from uniting.

Femoral neck fractures remain the leading cause of early failure after metal-on-metal hip resurfacing. Although its' exact pathomechanism has yet to be fully elucidated, current retrieval analysis has shown that either an osteonecrotic event and/or significant surgical trauma to the femoral head neck junction are the leading causes. It is most likely that no single factor like patient selection and/or femoral component orientation can fully avoid their occurrence. As in osteonecrosis of the native hip joint, a certain cell injury threshold may have to be reached in order for femoral neck fracture to occur. These insults are not limited to the surgical approach, but also include femoral head preparation, neck notching, and cement penetration.

Although some have argued that the posterior approach does not represent an increased risk fracture for ON after hip resurfacing because of the so-called intraosseous blood supply to the femoral head, to date, the current body of literature on femoral head blood flow in the presence of arthritis has confirmed the critical role of the extraosseous blood supply from the ascending branch of the medial circumflex, as well as the lack of any substantial intraosseous blood supply. Conversely, anterior hip dislocation of both the native hip joint as well as the arthritic hip preserves femoral head vascularity. The blood supply can be compromised by either sacrificing the main branch of the ascending medial femoral circumflex artery or damaging the retinacular vessels at the femoral head-neck junction. Thus an approach which preserves head vascularity, while minimizing soft tissue disruption would certainly be favorable for hip resurfacing. This presentation will review the current state of knowledge on vascularity of the femoral head as well as surgical techniques enhancing its preservation.

Two acetabula which contained large bone allografts introduced at revision arthroplasty were obtained at post-mortem. The allografts had been placed in superior defects to support cementless acetabular components, and both hips were functioning well at the time of death. Clinical radiographs demonstrated apparent healing of graft to host bone, no graft collapse and stability of the acetabular components. Microscopic examination of sections through these specimens showed that the bulk allografts were encapsulated in fibrous tissue. Vascularity was increased at the host-graft interface, but there was limited evidence of bone union between the graft and the host. In the few areas where union had occurred, revascularisation extended no more than 2 mm beyond the graft-host interface. Within the body of the graft, the acellular matrix of trabecular bone maintained structural integrity up to 48 months after surgery. In areas where the allograft was adjacent to an implant, there was fibrous tissue orientated parallel to the implant surface. The acetabulum which contained a porous-coated component showed evidence of bone growth into the porous surface where it was in contact with viable host bone. No ingrowth occurred in areas where the porous coating was in contact with the graft. Although the grafts were functioning well, allograft revascularisation and remodelling were minimal, and the radiological appearance of healing did not correlate with histological findings

We assessed the predictive value of the macroscopic and detailed microscopic appearance of the coracoacromial ligament, subacromial bursa and rotator-cuff tendon in 20 patients undergoing subacromial decompression for impingement in the absence of full-thickness tears of the rotator cuff. Histologically, all specimens had features of degenerative change and oedema in the extracellular matrix. Inflammatory cells were seen, but there was no evidence of chronic inflammation. However, the outcome was not related to cell counts.

At three months the mean Oxford shoulder score had improved from 29.2 (20 to 40) to 39.4 (28 to 48) (p < 0.0001) and at six months to 45.5 (36 to 48) (p < 0.0001). At six months, although all patients had improved, the seven patients with a hooked acromion had done so to a less extent than those with a flat or curved acromion judged by their mean Oxford shoulder scores of 43.5 and 46.5 respectively (p = 0.046). All five patients with partial-thickness tears were within this group and demonstrated less improvement than the patients with no tear (mean Oxford shoulder scores 43.2 and 46.4, respectively, p = 0.04). These findings imply that in the presence of a partial-thickness tear subacromial decompression may require additional specific treatment to the rotator cuff if the outcome is to be improved further.