Our results provide the first direct evidence of accelerated joint tissue turnover in a mouse model responding to acute joint injury. These data strongly suggest that mouse SF recovery is feasible and that biomarker analysis of collected SF samples can augment traditional histological analyses in mouse models of arthritis.

Only the age and weight-independent associations of IL-6 and G-CSF with histological OA were significant under the conditions imposed by the Holm step-down adjustment for multiple comparisons. Though the observed changes of these cytokine levels may be due to a correlation with age, it is highly unlikely given the significant difference between Hartley and Strain 13 age-matched cohorts.

This is a prospective, open-label, proof-of-concept study of tofacitinib, a Janus kinase inhibitor, as a steroid sparing therapy in corticosteroid-dependent pulmonary sarcoidosis. 5 patients with corticosteroid-dependent pulmonary sarcoidosis were treated with tofacitinib 5 mg twice daily. The primary endpoint was a ≥50% reduction in corticosteroids at week 16 with no worsening in pulmonary function or respiratory symptoms. 60% of patients (3/5) met the primary endpoint. One patient was lost to follow up prior to steroid taper, and another was withdrawn due to worsening of known neurosarcoidosis. The three patients who met the primary endpoint each tapered to ≤5 mg/day prednisone, respiratory symptoms improved, and spirometry remained stable. In this proof-of-concept study, the addition of a JAK-inhibitor allowed 60% of patients with pulmonary sarcoidosis to successfully taper corticosteroids. JAK-inhibitors are a promising therapy for pulmonary sarcoidosis, which require further investigation in randomized trials.