Volume 6 Supplement 1
Mandibular condyle destruction in juvenile idiopathic arthritis (JIA)
© Zak et al; licensee BioMed Central Ltd. 2008
Published: 15 September 2008
Assessment of destruction of the mandibular condyle in relation to clinical baseline data and disease progression in JIA.
Materials and methods
293 consecutive patients (f = 198; m = 95) diagnosed 1995–2006 participated. Median JIA onset age was 6 1/2 yrs for girls and 8 yrs for boys. ILAR classification: persistent-oligoarticular (p-oligo) 26%, extended-oligoarticular (e-oligo) 24%, polyarticularRF- (poly-) 22%, polyarticularRF+ (poly+) 1%, enthesitis-associated (ERA) 16%, psoriatic (pso) 6% and systemic (sys) 5%. Disease course, uveitis, ANA, IgM-RF and HLA-B27 was recorded. Due to small numbers sys, poly+ and pso were excluded from subtype analysis. Patients with poly- and e-oligo were regarded as polyarticular course. Orthopantomographics was done in all. 79% had 2 or more radiographs. Condylar morphology grading was: 0 = normal; 1 = erosions of the surface; 2 = flattening; 3 = total destruction.
Results and discussion
At the first examination, 28% had radiographic TMJ changes (1:29%; 2:66%; 3:5%). During the observation period, additional 7% developed TMJ changes, increasing the total frequency to 35%. 10 pt. with condylar lesions showed progression during the observation period. TMJ changes were significantly associated with ANA+. No other baseline associations were observed. In logistic regression models for TMJ changes, the following independent variables contributed significantly to the equation: ANA+ (p = 0.01), ILAR subtype (p = 0.009), and age (p = 0.02) at first examination. The OR for polyarticular course vs. ERA was 4.6 (95%CI:1.7–12.5) and p-oligo vs. ERA 2.9 (95%CI:1.0–8.0).
A lower frequency of mandibular condyle destruction in JIA than reported in several previous studies was found. Progression of changes was mild to moderate. The data suggest that condyle destruction in JIA is associated with ILAR subtype, age at disease onset and ANA+.
This article is published under license to BioMed Central Ltd.