Histopathology Evaluation of Cartilage Disease and Repair

Pritzker, Kenneth P.H.; Gahunia, Harpal K.

doi:10.1007/978-1-4939-7587-7_15

Cited by 1 publication

(1 citation statement)

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“…To investigate the protective effect of LMCP on cartilage, LMCP was orally administered to rabbits with ACLT-induced OA for 12 weeks. Cartilage damage was evaluated through H&E and Safranin O staining, which accurately confirms cartilage degeneration during OA progression [ 24 ]. According to the H&E staining ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Low-Molecular-Weight Collagen Peptide Ameliorates Osteoarthritis Progression through Promoting Extracellular Matrix Synthesis by Chondrocytes in a Rabbit Anterior Cruciate Ligament Transection Model

Lee

Kim

Chung

et al. 2021

J. Microbiol. Biotechnol.

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This study examined whether the oral administration of low-molecular-weight collagen peptide (LMCP) containing 3% Gly-Pro-Hyp with >15% tripeptide (Gly-X-Y) content could ameliorate osteoarthritis (OA) progression using a rabbit anterior cruciate ligament transection (ACLT) model of induced OA and chondrocytes isolated from a patient with OA. Oral LMCP administration (100 or 200 mg/kg/day) for 12 weeks ameliorated cartilage damage and reduced the loss of proteoglycan compared to the findings in the ACLT control group, resulting in dose-dependent (p < 0.05) improvements of the OARSI score in hematoxylin & eosin (H&E) and Safranin O staining. In microcomputed tomography analysis, LMCP also significantly (p < 0.05) suppressed the deterioration of the microstructure in tibial subchondral bone during OA progression. The elevation of IL-1β and IL-6 concentrations in synovial fluid following OA induction was dose-dependently (p < 0.05) reduced by LMCP treatment. Furthermore, immunohistochemistry illustrated that LMCP significantly (p < 0.05) upregulated type II collagen and downregulated matrix metalloproteinase-13 in cartilage tissue. Consistent with the in vivo results, LMCP significantly (p < 0.05) increased the mRNA expression of COL2A1 and ACAN in chondrocytes isolated from a patient with OA regardless of the conditions for IL-1β induction. These findings suggest that LMCP has potential as a therapeutic treatment for OA that stimulates cartilage regeneration.

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Section: Resultsmentioning

confidence: 99%