In this review, we focus on (i) the physiological basis of joint pH and a concise synthesis of reported pH ranges in OA and RA; (ii) biological sources of acidification in OA; (iii) how acidosis modulates chondrocyte and synovial cell programs (catabolism, survival, inflammation, nociception); and (iv) how joint cells sense acidic cues through acid-sensing G-protein-coupled receptors (GPR4, GPR65/TDAG8, GPR68/OGR1, GPR132/G2A) and ASIC channels, with an emphasis on signaling pathways that reprogram gene expression. Here, GPR68 is linked to rheumatoid arthritis.