Weightbearing ovine osteochondral defects heal with inadequate subchondral bone plate restoration: implications regarding osteochondral autograft harvesting

Abstract

Purpose: It is unknown what causes donor site morbidity following the osteochondral autograft transfer procedure or how donor sites heal. Contact pressure and edge loading at donor sites may play a role in the healing process. It was hypothesized that an artificially created osteochondral defect in a weightbearing area of an ovine femoral condyle will cause osseous bridging of the defect from the upper edges, resulting in incomplete and irregular repair of the subchondral bone plate.

Methods: To simulate edge loading, large osteochondral defects were created in the most unfavourable weightbearing area of 24 ovine femoral condyles. After killing at 3 and 6 months, osteochondral defects were histologically and histomorphometrically evaluated with specific attention to subchondral bone healing and subchondral bone plate restoration.

Results: Osteochondral defect healing showed progressive osseous defect bridging by sclerotic circumferential bone apposition. Unfilled area decreased significantly from 3 to 6 months (P = 0.004), whereas bone content increased (n.s.). Complete but irregular subchondral bone plate restoration occurred in ten animals. In fourteen animals, an incomplete subchondral bone plate was found. Further common findings included cavitary lesion formation, degenerative cartilage changes and cartilage and subchondral bone collapse.

Conclusions: Osteochondral defect healing starts with subchondral bone plate restoration. However, after 6 months, incomplete or irregular subchondral bone plate restoration and subsequent failure of osteochondral defect closure is common. Graft harvesting in the osteochondral autograft transfer procedure must be viewed critically, as similar changes are also present in humans.

Level of evidence: Prognostic study, Level III.

Fig. 1

Subchondral bone plate restoration stages. In these Safranin O/Fast Green stained samples, mineralized bone and fibrous tissue appear bluish green, whereas (fibro)cartilage appears red. Scale bars represent the diameter of the initial osteochondral defect. a In stage 1 (n = 3), the defect was continuous with the synovial cavity, with no signs of defect bridging. Notice the extensive (fibro)cartilage collapse (white horizontal arrows) and erosion of bone outside the perimeters of the initially created defect (black vertical arrows). b In stage 2 (n = 5), fibrous tissue bridging or minor circumferential subchondral bone plate restoration was present. The main difference with stage 1 was the formation of fibrous strands in an attempt to partially close the created defect (white vertical arrow). Again, collapse of (fibro)cartilage (white horizontal arrow) and subchondral bone (white arrowhead), coupled to osseous erosion (black vertical arrows), was seen frequently. Already, the first signs of a central irregularly shaped cavitary lesion were seen. This lesion was either empty or filled with connective tissue. In some samples, central vacuolization of the fibrous tissue was present. c In stage 3 (n = 6), there was still inward collapse of subchondral bone and (fibro)cartilage. Progressive subchondral bone plate restoration was observed. Notice the evident subchondral bone sclerosis (black arrowhead). The central cavitary lesion, which was nearly closed, either was lined with fibrous tissue or showing exposed bone. d In stage 4 (n = 10), there was complete sclerotic osseous bridging of the defect, with mostly a concave fibrocartilaginous articular surface, and a central cavitary lesion which was either empty or filled with fibrous tissue. Again, cartilage flow and subchondral bone sclerosis were present

Fig. 2

Subchondral bone plate restoration in stage 4 Safranin O/Van Kossa stained samples. Mineralized bone appears black, and (fibro)cartilage and fibrous tissue appear red. Scale bars represent the diameter of the initial osteochondral defect. The subchondral bone plate was characterized by irregular restoration, compromised by fibrocartilage flow (white arrows), the underlying cavitary lesion (black arrow) and subchondral bone plate advancement (arrowheads)