Subchondral bone remodeling is related to clinical improvement after joint distraction in the treatment of ankle osteoarthritis.

Published

Journal Article

OBJECTIVE: In osteoarthritis (OA), subchondral bone changes alter the joint's mechanical environment and potentially influence progression of cartilage degeneration. Joint distraction as a treatment for OA has been shown to provide pain relief and functional improvement through mechanisms that are not well understood. This study evaluated whether subchondral bone remodeling was associated with clinical improvement in OA patients treated with joint distraction. METHOD: Twenty-six patients with advanced post-traumatic ankle OA were treated with joint distraction for 3 months using an Ilizarov frame in a referral center. Primary outcome measure was bone density change analyzed on computed tomography (CT) scans. Longitudinal, manually segmented CT datasets for a given patient were brought into a common spatial alignment. Changes in bone density (Hounsfield Units (HU), relative to baseline) were calculated at the weight-bearing region, extending subchondrally to a depth of 8mm. Clinical outcome was assessed using the ankle OA scale. RESULTS: Baseline scans demonstrated subchondral sclerosis with local cysts. At 1 and 2 years of follow-up, an overall decrease in bone density (-23% and -21%, respectively) was observed. Interestingly, density in originally low-density (cystic) areas increased. Joint distraction resulted in a decrease in pain (from 60 to 35, scale of 100) and functional deficit (from 67 to 36). Improvements in clinical outcomes were best correlated with disappearance of low-density (cystic) areas (r=0.69). CONCLUSIONS: Treatment of advanced post-traumatic ankle OA with 3 months of joint distraction resulted in bone density normalization that was associated with clinical improvement.

Full Text

Duke Authors

Cited Authors

  • Intema, F; Thomas, TP; Anderson, DD; Elkins, JM; Brown, TD; Amendola, A; Lafeber, FPJG; Saltzman, CL

Published Date

  • June 2011

Published In

Volume / Issue

  • 19 / 6

Start / End Page

  • 668 - 675

PubMed ID

  • 21324372

Pubmed Central ID

  • 21324372

Electronic International Standard Serial Number (EISSN)

  • 1522-9653

Digital Object Identifier (DOI)

  • 10.1016/j.joca.2011.02.005

Language

  • eng

Conference Location

  • England