What is the cause of pain in damaged articular cartilage of the TMJ?

The source of pain in damaged articular cartilage of the temporomandibular joint (TMJ) primarily stems from the actions of inflammatory mediators, notably prostaglandin E1 and leukotrienes. When articular cartilage is damaged, it leads to a cascade of inflammatory processes. Prostaglandin E1, specifically, plays a significant role in mediating pain and inflammation. This compound sensitizes nerve endings, which contributes to the perception of pain in the joint.

Furthermore, leukotrienes are part of the inflammatory response and can also enhance pain sensitivity by attracting more inflammatory cells to the site of injury and thus amplifying the inflammatory response. Together, these mediators create an inflammatory environment that leads to the activation of nociceptive pathways, ultimately resulting in the sensation of pain experienced by the patient.

While other factors can contribute to pain in the TMJ, such as histamine release from mast cells or the potential for nerve compression in cases of significant TMJ derangement, these are not the primary mechanisms by which pain is directly induced from damaged articular cartilage. Instead, the involvement of prostaglandin E1 and leukotrienes serves as a more direct link between cartilage damage and the resultant pain, highlighting the inflammatory nature