Joint-dependent response to impact and implications for post-traumatic osteoarthritis.
OBJECTIVE
The prevalence of osteoarthritis (OA) varies between joints. Cartilage in eight different joints was evaluated to elucidate the disparate susceptibilities between joints to post-traumatic OA (PTOA) and provide evidence for joint-specific clinical treatments. The hypothesis was that cartilage in different joints would have varying cell death and anabolic gene expression profiles after injury.


METHODS
Adult equine cartilage explants were harvested from shoulder (SH), elbow (EL), carpal (CA), metacarpophalangeal (MC), patellofemoral (FP), tarsal (TA), metatarsophalangeal (MT), and proximal interphalangeal (PP) joints, and injured by loading with 30 MPa within 1 s. Fractional dissipated energy, cell density, cell death, and gene expression were quantified.


RESULTS
PP had the highest fractional dissipated energy (94%, 95% confidence interval [CI] 88 to 101%). Cell density was highest in the superficial zone in all samples, with MC and MT having the highest peak density. Injured samples had significantly increased cell death (13.5%, 95% CI 9.1 to 17.9%) than non-injured samples (6.8%, 95% CI 2.5 to 11.1%, P = 0.016); however, cell death after injury was not significantly different between joints. Gene expression was significantly different between joints. CD-RAP expression in normal cartilage was lowest in FP (Cp = 21, 95% CI -80 to 122). After injury, the change in CD-RAP expression increased and was highest in FP (147% relative increase after injury, 95% CI 64 to 213).


CONCLUSIONS
Different joints have different baseline characteristics, including cell density and gene expression, and responses to injury, including energy dissipation and gene expression. These unique characteristics may explain differences in OA prevalence and suggest differences in susceptibility to PTOA.


CONCLUSIONS
Understanding differences in the response to injury and potential susceptibility to OA can lead to the development of preventative or treatment strategies.


BACKGROUND
Gene expression, cartilage injury, chondrocyte, multiphoton microscopy, cartilage biomechanical properties, PTOA.
The prevalence of OA is variable among joints; however, most laboratory studies are performed on a single joint - most commonly the knee, and extrapolated to other joints such as the ankle or shoulder. A small number of studies have compared knee and ankle cartilage and reported differences in mechanical properties and gene expression.


CONCLUSIONS
There are differences in baseline cell density and gene expression, and differences in response to injury, including gene expression and cell death. This suggests that there are inherent differences leading to varying susceptibilities in OA prevalence among joints. Joint-specific treatments may improve OA therapies.
Department of Clinical Sciences, Cornell University, Ithaca, NY, USA.
K D
KD
Novakofski
Department of Clinical Veterinary and Animal Science, University of Copenhagen, København, Denmark.
L C
LC
Berg
Department of Comparative Biomedicine and Food Science, University of Padova, Padova, Italy.
I
I
Bronzini
Department of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
E D
ED
Bonnevie
Department of Clinical Sciences, Cornell University, Ithaca, NY, USA.
S G
SG
Poland
Department of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
L J
LJ
Bonassar
Department of Clinical Sciences, Cornell University, Ithaca, NY, USA. Electronic address: laf4@cornell.edu.
L A
LA
Fortier
D000818:Animals; D001169:Arthritis, Experimental / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002358:Cartilage, Articular / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology; D016923:Cell Death; D019902:Chondrocytes / Q000473:pathology; D015870:Gene Expression; D020869:Gene Expression Profiling / Q000379:methods; D006734:Horse Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D006736:Horses; D010003:Osteoarthritis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary*; D012333:RNA, Messenger / Q000235:genetics; D013314:Stress, Mechanical
D012333:RNA, Messenger
Cartilage biomechanical properties; Cartilage injury; Chondrocyte; Gene expression; Multiphoton microscopy; PTOA