STUDY DESIGN: A retrospective cohort analysis. OBJECTIVE: To determine the effect of biological agents (BAs) on the development and progression of cervical spine lesions and identify predictors of lesion progression. SUMMARY OF BACKGROUND DATA: The introduction of BAs has facilitated advances in the treatment of rheumatoid arthritis (RA). BAs reduce disease activity and limit structural joint damage. However, the effect of BAs on cervical spine lesions remains unclear. METHODS: Thirty-eight subjects who received more than 2 years of continuous BA treatment were enrolled. The mean x-ray interval was 4.4 years. RA activity was evaluated by disease activity score (DAS)-C reactive protein (CRP) and matrix metalloproteinase (MMP)-3. Radiographical definitions of cervical lesions were atlanto-dental interval (ADI) more than 3 mm for atlanto-axial subluxation (AAS), Ranawat value less than 13 mm for vertical subluxation (VS), and anterior or posterior listhesis more than 2 mm for subaxial subluxation (SS). Definitions of radiographical progression were an increase of ADI more than 2 mm for AAS, a decrease of both Ranawat and Redlund-Johnell values more than 2 mm for VS, and an increase of listhesis more than 2 mm for SS. RESULTS: RA activity responded dramatically to BA therapy (DAS-CRP from 4.3 to 2.3, P < 0.01; MMP-3 from 207.9 ng/mL to 105.6 ng/mL, P < 0.01). Baseline radiographical evaluation showed no pre-existing cervical spine lesions in 12 cases, AAS in 15 cases, and VS in 11 cases. Radiological progression was found in 1 (8%) patient in the no lesion group, 12 patients (80%) in the AAS group, and 9 patients (80%) in the VS group. The incidence of progression was significantly lower in the no lesion group compared with the other groups. Multivariate regression analysis showed that the presence of pre-existing cervical lesions was the single greatest predictor of progression. CONCLUSION: BAs prevented the development of de novo cervical spine lesions in patients with RA, but failed to inhibit progression of pre-existing RA lesions.
STUDY DESIGN: A retrospective cohort analysis. OBJECTIVE: To determine the effect of biological agents (BAs) on the development and progression of cervical spine lesions and identify predictors of lesion progression. SUMMARY OF BACKGROUND DATA: The introduction of BAs has facilitated advances in the treatment of rheumatoid arthritis (RA). BAs reduce disease activity and limit structural joint damage. However, the effect of BAs on cervical spine lesions remains unclear. METHODS: Thirty-eight subjects who received more than 2 years of continuous BA treatment were enrolled. The mean x-ray interval was 4.4 years. RA activity was evaluated by disease activity score (DAS)-C reactive protein (CRP) and matrix metalloproteinase (MMP)-3. Radiographical definitions of cervical lesions were atlanto-dental interval (ADI) more than 3 mm for atlanto-axial subluxation (AAS), Ranawat value less than 13 mm for vertical subluxation (VS), and anterior or posterior listhesis more than 2 mm for subaxial subluxation (SS). Definitions of radiographical progression were an increase of ADI more than 2 mm for AAS, a decrease of both Ranawat and Redlund-Johnell values more than 2 mm for VS, and an increase of listhesis more than 2 mm for SS. RESULTS: RA activity responded dramatically to BA therapy (DAS-CRP from 4.3 to 2.3, P < 0.01; MMP-3 from 207.9 ng/mL to 105.6 ng/mL, P < 0.01). Baseline radiographical evaluation showed no pre-existing cervical spine lesions in 12 cases, AAS in 15 cases, and VS in 11 cases. Radiological progression was found in 1 (8%) patient in the no lesion group, 12 patients (80%) in the AAS group, and 9 patients (80%) in the VS group. The incidence of progression was significantly lower in the no lesion group compared with the other groups. Multivariate regression analysis showed that the presence of pre-existing cervical lesions was the single greatest predictor of progression. CONCLUSION: BAs prevented the development of de novo cervical spine lesions in patients with RA, but failed to inhibit progression of pre-existing RA lesions.