Peri-prosthetic osteolysis and subsequent aseptic loosening is the most common reason for revising total hip replacements. Wear particles originating from the prosthetic components interact with multiple cell types in the peri-prosthetic region resulting in an inflammatory process that ultimately leads to peri-prosthetic bone loss. These cells include macrophages, osteoclasts, osteoblasts and fibroblasts. The majority of research in peri-prosthetic osteolysis has concentrated on the role played by osteoclasts and macrophages. The purpose of this review is to assess the role of the osteoblast in peri-prosthetic osteolysis. In peri-prosthetic osteolysis, wear particles may affect osteoblasts and contribute to the osteolytic process by two mechanisms. First, particles and metallic ions have been shown to inhibit the osteoblast in terms of its ability to secrete mineralised bone matrix, by reducing calcium deposition, alkaline phosphatase activity and its ability to proliferate. Secondly, particles and metallic ions have been shown to stimulate osteoblasts to produce pro inflammatory mediators in vitro. In vivo, these mediators have the potential to attract pro-inflammatory cells to the peri-prosthetic area and stimulate osteoclasts to absorb bone. Further research is needed to fully define the role of the osteoblast in peri-prosthetic osteolysis and to explore its potential role as a therapeutic target in this condition. Cite this article: Bone Joint J 2013;95-B:1021–5

The most frequent cause of failure after total hip replacement in all reported arthroplasty registries is peri-prosthetic osteolysis. Osteolysis is an active biological process initiated in response to wear debris. The eventual response to this process is the activation of macrophages and loss of bone.

Activation of macrophages initiates a complex biological cascade resulting in the final common pathway of an increase in osteolytic activity. The biological initiators, mechanisms for and regulation of this process are beginning to be understood. This article explores current concepts in the causes of, and underlying biological mechanism resulting in peri-prosthetic osteolysis, reviewing the current basic science and clinical literature surrounding the topic.

We report the results of using a combination of fixator-assisted nailing with lengthening over an intramedullary nail in patients with tibial deformity and shortening. Between 1997 and 2007, 13 tibiae in nine patients with a mean age of 25.4 years (17 to 34) were treated with a unilateral external fixator for acute correction of deformity, followed by lengthening over an intramedullary nail with a circular external fixator applied at the same operating session. At the end of the distraction period locking screws were inserted through the intramedullary nail and the external fixator was removed.

The mean amount of lengthening was 5.9 cm (2 to 8). The mean time of external fixation was 90 days (38 to 265). The mean external fixation index was 15.8 days/cm (8.9 to 33.1) and the mean bone healing index was 38 days/cm (30 to 60).

One patient developed an equinus deformity which responded to stretching and bracing. Another developed a drop foot due to a compartment syndrome, which was treated by fasciotomy. It recovered in three months. Two patients required bone grafting for poor callus formation.

We conclude that the combination of fixator-assisted nailing with lengthening over an intramedullary nail can reduce the overall external fixation time and prevent fractures and deformity of the regenerated bone.