My take on the genesis of TMD is not confined to the joint but rather tracks back to large dietary changes that induce HOX genes (HOXa/3 primarily). These genes exclude normal neural crest cells which direct naso-maxillary growth essentially leading to smaller Naso-maxillae. This leads to more tongue-in-pharynx time and intermittent hypoxia which then recruits peptides that 'switch on' the inflammatory cascade as shown in Gozals study of 3-year-olds exhaled breath (CRP TNF etc parallel adults with cardiovascular disease also bloods show early endothelial damage and thickening of intima with an infestation of cholesterol. This is half the explanation of why TMD presents in so many different formats. The other is the entrapped mandible takes the condyle towards the back wall of the fossae and compresses the vascular bed = high volumes of nociception which can overwhelm the CNS. When this is appreciated treatment changes often to a far more targetted modality, rather than just making the joint happy.

What percentage of TMD cases you see have signs of OSA.SDB? The answers to this may give an insight into how to best train dentists and other health professionals. A recent patient to our clinic was prescribed 5 different anti-hypertensives which do interfere with each other and compound their side effects and it appears nobody has asked her if she has OSA or any of the typical signs... She has perio, high abfraction levels and many comorbid conditions.