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Microcracks in subchondral bone plate is linked to less cartilage damage.

Abstract：

OBJECTIVES:Osteoarthritis (OA) is a disease of the whole joint characterized by cartilage loss and subchondral bone remodeling. The role of microcracks in cartilage integrity and subchondral bone homeostasis is not fully understood. The main goal of this work was to evaluate microcrack density in both calcified cartilage and subchondral bone plate in relation to cartilage damage in humans and to better define the association of microcracks and osteocyte density in subchondral bone. METHODS:We investigated 18 bone cores from cadaveric human knees that were stained with En-Bloc Basic Fuchsin. We quantified microcrack density, osteocyte density, cartilage surfaces and cartilage damage. The presence of microcracks was confirmed for each bone core by scanning electron microscopy. Finally, trabecular subchondral bone parameters were measured by micro-CT. RESULTS:Microcracks were detected in both calcified cartilage and subchondral bone plate. The density of microcracks in both calcified cartilage (CC) and subchondral bone plate (SBP) was negatively correlated with cartilage damage (r = -0.45, p < 0.05). The presence of microcracks in SBP was associated with a lower histological OA score. Osteocytes formed a dendrite network that abruptly stopped at the border of calcified cartilage. Osteocyte density in subchondral bone plate was increased in the presence of microcracks in calcified cartilage. CONCLUSIONS:Subchondral bone plate microcracks might be required for maintaining cartilage homeostasis. Microcracks in calcified cartilage may trigger osteocyte density in subchondral bone plate with subsequent regulation of subchondral bone remodeling to prevent cartilage damage.

journal_name

Bone

journal_title

Bone

authors

Zarka M,Hay E,Ostertag A,Marty C,Chappard C,Oudet F,Engelke K,Laredo JD,Cohen-Solal M

doi

10.1016/j.bone.2019.03.011

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

1-7

eissn

8756-3282

issn

1873-2763

pii

S8756-3282(19)30087-0

journal_volume

123

pub_type

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