Objectives: Fresh osteochondral allografts are well-established treatment for patients who have posttraumatic osteochondral defects over 3cm in diameter and 1cm in depth of the knee. The objective of our study was to investigate the long-term outcome of these grafts and how long they may delay need for arthroplasty in patients with mal-united tibial plateau fractures.

Method: A prospective cohort study of patients who had received fresh osteochondral allografts of the tibial plateau was conducted. 118 patients were identified and survivor ship analysis was performed using conversion to total knee arthroplasty as the end point for graft failure. The Modified Hospital for Knee Surgery Scoring System (MHKSS) was used to clinically assess each patient who had more than five years of follow up. Radiographs were assessed for mechanical axis as well as using the Tonis grade for degenerative change.

Results: 29 of 118 (25%) experienced graft failure and underwent conversion to total knee arthroplasty, at a mean of 12 years (range 3–23) after the index procedure. The remaining 52 patients with a successful graft, and follow up over five years, had a mean MHKSS score of 83 (range 49–100) with a mean follow up of 11.7 years (range 5–34). Kaplan-Meier survivorship analysis of all 118 patients showed that graft survivorship was 94% at 5 years (std err 2.7), 83% at 10 years (std err 4.6), 62% at 15 years (std err 7.4) and 45% at 20 years (std err 8.5). Factors that predicted a successful graft were, using a meniscal allograft in conjunction with the osteochondral graft, and a lateral tibial plateau defect. The age at the time of surgery was no different between the patients that had a successful graft or those that failed.

Conclusion: Fresh osteochondral allografting works well in providing long term treatments for patients with tibial plateau damage. The concurrent use of meniscal allografts is also recommended.

Osteoarthritis (OA) involves pathology in both articular cartilage and subchondral bone. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa beta ligand (RANK-L) balance is known to modulate bone turnover. We compared the bony changes in human total knee arthroplasty (TKA) and cadaveric controls. A qualitative increase in subchondral and ligamentous insertional bone mineral density was observed on micro-CT sections of TKA bone compared with cadaveric controls. In-situ hybridization of digoxygenase (DIG)-labelled OPG riboprobes showed selective uptake in osteoblasts but not osteocytes or osteoclasts in TKA bone. Those data suggested that the upregulation of OPG expression by osteoblasts may have precipitated the bony hypertrophy of end-stage OA.

Altered joint mechanics produced by periarticular bone remodelling may precede the cartilage changes of osteoarthritis (OA). Recently, receptor activator of nuclear factor kappa beta (RANK), along with its soluble ligand (RANK-L), have been shown to induce both maturation and activation of bone-degrading osteoclasts. Activation of RANK on osteoclast cells by RANK-L is opposed by another soluble factor, osteoprotegerin (OPG). Thus RANK/OPG balance is important in regulating bone turnover. Here, we compared periarticular bone from patients with end-stage OA undergoing total knee arthroplasty (TKA) with those of cadaveric controls. We assessed bony, histological and molecular changes that are important in the pathogenesis of OA.

Using in-situ hybridization, we found increased staining of digoxygenase (DIG)-labelled OPG in osteoblasts of TKA bone. A corresponding increase in subchondral and insertional bone was seen on micro-CT (μCT) sections from TKA bone in comparison with cadaveric controls. Those changes were accompanied by marked articular cartilage degeneration on histology.

This study is the first of which we are aware that directly assessed the role of OPG in inducing the bony changes seen in human end-stage OA. We used μCT to compare corresponding samples qualitatively from TKA and cadaveric bone. Adjacent sections underwent hybridization of digoxygenase (DIG)-labelled OPG riboprobes to assess gene expression in situ. Finally, samples were stained and analysed for histology.

Bony hypertrophy may be a result of overexpression of OPG that occurs as an important feature of OA pathophysiology.

Funding: This work was supported by a grant from the Hip Hip Hooray Fund of the Canadian Orthopaedic Research Foundation (CORF) and the Wood Professorship in Joint Injury Research. There was no commercial funding for this research project.