In osteoarthritis (OA), bone changes are radiological hallmarks and are considered important for disease progression. The C-C chemokine receptor-2 (CCR2) has been shown to play an important role in bone physiology. In this study, we investigated whetherCcr2osteoblast-specific inactivation at different times during post-traumatic OA (PTOA) progression improves joint structures, bone parameters, and pain. We used a tamoxifen-inducibleCcr2inactivation in Collagen1α-expressing cells to obtain osteoblasts lackingCcr2(CCR2-Col1αKO). We stimulated PTOA changes inCCR2-Col1αKOandCCR2+/+ mice using the destabilization of the meniscus model (DMM), inducing recombination before or after DMM (early- vs. late-inactivation). Joint damage was evaluated at two, four, eight, and twelve weeks post-DMM using multiple scores: articular-cartilage structure (ACS), Safranin-O, histomorphometry, osteophyte size/maturity, subchondral bone thickness and synovial hyperplasia. Spontaneous and evoked pain were assessed for up to 20 weeks. We found that early osteoblast-Ccr2inactivation delayed articular cartilage damage and matrix degeneration compared toCCR2+/+, as well as DMM-induced bone thickness. Osteophyte formation and maturation were only minimally affected. Late Collagen1α-Ccr2deletion led to less evident improvements. Osteoblast-Ccr2deletion also improved static measures of pain, while evoked pain did not change. Our study demonstrates thatCcr2expression in osteoblasts contributes to PTOA disease progression and pain by affecting both cartilage and bone tissues.