Why can pain sensations be detected in cartilage without direct nerve supply?

The ability to detect pain sensations in cartilage, despite the lack of direct nerve supply, is most accurately attributed to swelling or inflammation around the tissue. When cartilage experiences injury or stress, it can become inflamed, leading to the release of biochemical substances that stimulate pain receptors in nearby tissues. This process often involves surrounding connective tissues that are innervated, which can then relay pain signals to the nervous system.

In situations where there is swelling, the pressure within the tissue increases and can irritate surrounding tissues that do contain sensory nerve fibers. This indirect mechanism highlights that while cartilage itself does not contain nerve endings, the inflammatory response can create conditions that activate pain pathways.

The other options, while relevant in different contexts, do not directly explain how pain can be perceived in cartilage. For example, the regeneration of nerve endings typically does not occur in cartilage, and while sensory receptors are crucial for pain detection, they are not present in cartilage itself. Pressure changes may be a factor in systems with nerve endings, but in the case of cartilage, it is the associated inflammation and the resulting pressure on nearby tissues that primarily lead to pain sensation.