Subchondral bone trauma causes cartilage matrix degeneration: an immunohistochemical analysis in a canine model.
Joint instability was believed to be the main cause of osteoarthritis following non-fracture articular trauma. However, sudden high impact load through articular cartilage onto subchondral bone may also cause osteoarthritic changes.


OBJECTIVE
We asked whether early osteoarthritic changes following transarticular impact may be depicted using immunofluorescence on unfixed cryosections to contribute to a more detailed understanding of degenerative processes of joint impaction.


METHODS
Transarticular impacts were applied to patellofemoral joints of 12 skeletally mature beagle dogs (age: 15-16 months) using a drop tower. Biopsies of impact areas were sampled after 6 months and processed for standard light microscopy on formalin-fixed sections and for immunofluorescence for collagen type I (col I), type II (col II) and aggrecan (AC) on unfixed cryosections. Gross morphology and immunofluorescence on cryosections were documented using a semi-quantitative scaling system, compared to healthy controls and to standard light microscopy.


RESULTS
Four biopsies showed almost entirely fibrocartilaginous morphology, four appeared to be of preserved hyaline morphology with only minor signs of fibrocartilaginous remodelling and four showed preserved hyaline appearance. We found decrease in col II and AC expression in highly degenerative specimens as well as increase of col I expression. Increased col I expression in the pericellular matrix could even be depicted in specimens with intact hyaline morphology.


CONCLUSIONS
Observations suggest that joint impaction causes early osteoarthritic changes after 6 months. Collagen network disruption seems to lead to AC loss, although other researchers found isolated AC loss without denaturation of col II using immunofluorescence in formalin-fixed specimens. This is the first study on effects of transarticular impact using immunofluorescence on unfixed cryosections.
Mrosek
E H
EH
Department of Orthopaedic Surgery, Mayo Clinic College of Medicine, 200 1st Street SW, Rochester, MN 55905, USA. mrosek@cartilage-engineering.com
Lahm
A
A
Erggelet
C
C
Uhl
M
M
Kurz
H
H
Eissner
B
B
Schagemann
J C
JC
D053674:Aggrecans; D000818:Animals; D002358:Cartilage, Articular / Q000378:metabolism* / Q000473:pathology; D011508:Chondroitin Sulfate Proteoglycans / Q000032:analysis / Q000378:metabolism; D024042:Collagen Type I / Q000032:analysis / Q000378:metabolism; D024043:Collagen Type II / Q000032:analysis / Q000378:metabolism; D004285:Dogs; D005109:Extracellular Matrix / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D016326:Extracellular Matrix Proteins / Q000032:analysis / Q000378:metabolism; D005260:Female; D005455:Fluorescent Antibody Technique; D006614:Hindlimb; D007596:Joints / Q000293:injuries* / Q000378:metabolism / Q000473:pathology; D037181:Lectins, C-Type / Q000032:analysis / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D008297:Male; D023421:Models, Animal; D010003:Osteoarthritis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D013314:Stress, Mechanical; D013997:Time Factors; D014949:Wounds, Nonpenetrating / Q000150:complications* / Q000378:metabolism / Q000473:pathology
D053674:Aggrecans; D011508:Chondroitin Sulfate Proteoglycans; D024042:Collagen Type I; D024043:Collagen Type II; D016326:Extracellular Matrix Proteins; D037181:Lectins, C-Type