Osteoarthritis of the jaw joint is more than simple wear and tear. Inflammation, cellular ageing and immune responses together contribute to damage to cartilage and bone. This suggests that treatments should not only target pain, but also address the underlying disease processes, according to surgeon Antong Wu.
‘My study focuses on osteoarthritis of the temporomandibular joint, the jaw joint that enables chewing, speaking and opening the mouth. This condition can cause persistent pain, restricted movement and progressive damage to cartilage and bone,’ explains Wu.
Current treatments are mainly aimed at relieving symptoms, while the biological processes that cause the disease and determine its progression are still not fully understood.
‘That is why I investigated whether osteoarthritis of the jaw joint should not only be seen as mechanical wear and tear, but as a condition influenced by an interplay of abnormal loading, inflammation, cellular ageing and systemic immune factors,’ Wu continues.
Wu’s central question was whether understanding these mechanisms could lead to more precise and disease-targeted treatments. ‘The aim was to move beyond short-term pain relief and find practical ways to protect the joint, slow structural damage and tailor treatments to different patient profiles.’
From mechanical loading to targeted treatment
Wu’s findings indicate that osteoarthritis of the jaw joint develops through an interplay of mechanical and biological factors.
‘One part of my research focuses on oral splints, a custom-made plastic appliance that supports the teeth and jaw joint. I investigated how accurately these appliances are manufactured. The studies showed that accurately milled oral splints were generally closer to their original design than 3D-printed splints,’ says Wu.
Possible treatments for inflammation and cellular damage
In addition to mechanical factors, Wu investigated possible ways of limiting biological damage in the joint. In experimental models, metformin, a medicine used among other things to treat type 2 diabetes, reduced joint damage.
He also investigated a compound that can be administered locally into the joint and releases hydrogen sulphide. This treatment reduced inflammation by shifting immune cells from a state that promotes damage towards one that is more supportive of repair.
In addition, Wu observed more signs of iron-related cellular damage under ageing-like conditions. This process could also represent a potential target for future treatments.