Intact Bone Vitality and Increased Accumulation of Nonmineralized Bone Matrix in Biopsy Specimens of Juvenile Osteochondritis Dissecans: A Histological Analysis

TY - JOUR

T1 - Intact Bone Vitality and Increased Accumulation of Nonmineralized Bone Matrix in Biopsy Specimens of Juvenile Osteochondritis Dissecans: A Histological Analysis

AU - Krause, Matthias

AU - Lehmann, Daniel

AU - Amling, Michael

AU - Rolvien , Tim

AU - Frosch, Karl-Heinz

AU - Püschel, Klaus

AU - Bohndorf, Klaus

AU - Meenen, Norbert M

N1 - © 2015 The Author(s).

PY - 2015/6

Y1 - 2015/6

N2 - BACKGROUND: Although commonly proposed to be the starting point of juvenile osteochondritis dissecans (JOCD), avascular osteonecrosis (AVN) has been an inconsistent finding in histological studies. Analysis of early-stage lesions is required to elucidate the origins of OCD and justify proper treatment.PURPOSE: To analyze histological sections of JOCD lesions with special emphasis on bone vitality.STUDY DESIGN: Cross-sectional study; Level of evidence, 3.METHODS: Of 64 patients with 74 JOCD lesions (20 females, mean age, 11.4 years; 44 males, mean age, 12.7 years), 34 required surgery because of lesion instability or failed nonoperative treatment. From 9 patients, 11 histological specimens were obtained. Lesions were classified according to the International Cartilage Repair Society (ICRS). Two additional histological control sections were harvested from children without JOCD manifestation. Undecalcified histological sections were histomorphometrically analyzed. To analyze the skeletal health of the patients, biochemical analyses with special emphasis on bone metabolism were performed.RESULTS: Histologically, no osteonecrosis was visible in any of the cases. Osteocyte distribution was similar among OCD lesions and controls. ICRS OCD I lesions (n = 6) showed no intralesional separation. In ICRS OCD II and III lesions (n = 5), there was a subchondral fracture concomitant with histological characteristics of active repair mechanism (increased bone formation: osteoid volume P = .008, osteoblast number P = .046; resorption: osteoclast number P = .005; and tissue fibrosis compared with controls). Instead, in ICRS OCD I lesions, subchondral osteoid volume (P = .010) and osteoblast number (P = .046) were significantly increased compared with controls; however, no active repair mechanisms (no increased bone resorption or fibrous tissue) were detected, suggesting a focal lack of mineralization. Fifty-seven of 64 patients (89.1%) showed a vitamin D deficiency. The median vitamin D serum level of the patients with ICRS OCD I lesions was 13.6 µg/L.CONCLUSION: In the present study, osteonecrosis was not found in histological specimens of JOCD. As a secondary finding, focal accumulations of nonmineralized bone matrix indicating a lack of mineralization in ICRS OCD I lesions were revealed. This finding correlated with a low level of vitamin D in the affected children.

AB - BACKGROUND: Although commonly proposed to be the starting point of juvenile osteochondritis dissecans (JOCD), avascular osteonecrosis (AVN) has been an inconsistent finding in histological studies. Analysis of early-stage lesions is required to elucidate the origins of OCD and justify proper treatment.PURPOSE: To analyze histological sections of JOCD lesions with special emphasis on bone vitality.STUDY DESIGN: Cross-sectional study; Level of evidence, 3.METHODS: Of 64 patients with 74 JOCD lesions (20 females, mean age, 11.4 years; 44 males, mean age, 12.7 years), 34 required surgery because of lesion instability or failed nonoperative treatment. From 9 patients, 11 histological specimens were obtained. Lesions were classified according to the International Cartilage Repair Society (ICRS). Two additional histological control sections were harvested from children without JOCD manifestation. Undecalcified histological sections were histomorphometrically analyzed. To analyze the skeletal health of the patients, biochemical analyses with special emphasis on bone metabolism were performed.RESULTS: Histologically, no osteonecrosis was visible in any of the cases. Osteocyte distribution was similar among OCD lesions and controls. ICRS OCD I lesions (n = 6) showed no intralesional separation. In ICRS OCD II and III lesions (n = 5), there was a subchondral fracture concomitant with histological characteristics of active repair mechanism (increased bone formation: osteoid volume P = .008, osteoblast number P = .046; resorption: osteoclast number P = .005; and tissue fibrosis compared with controls). Instead, in ICRS OCD I lesions, subchondral osteoid volume (P = .010) and osteoblast number (P = .046) were significantly increased compared with controls; however, no active repair mechanisms (no increased bone resorption or fibrous tissue) were detected, suggesting a focal lack of mineralization. Fifty-seven of 64 patients (89.1%) showed a vitamin D deficiency. The median vitamin D serum level of the patients with ICRS OCD I lesions was 13.6 µg/L.CONCLUSION: In the present study, osteonecrosis was not found in histological specimens of JOCD. As a secondary finding, focal accumulations of nonmineralized bone matrix indicating a lack of mineralization in ICRS OCD I lesions were revealed. This finding correlated with a low level of vitamin D in the affected children.

U2 - 10.1177/0363546515572579

DO - 10.1177/0363546515572579

M3 - SCORING: Journal article

C2 - 25759459

VL - 43

SP - 1337

EP - 1347

JO - AM J SPORT MED

JF - AM J SPORT MED

SN - 0363-5465

IS - 6

ER -