Although dysfunction is the major condition affecting the bilateral te
mporomandibular joint (TMJ), it has defied previous attempts to explai
n, predict, or prevent its clinical manifestations. A hypothesis is de
veloped that there is an anatomical predisposition to TMJ dysfunction
which should be sought in the phylogenetic flexing of the hominid basi
cranium. It is argued that the glenoid fossa, caught between an ever-i
ncreasing brain size and more ventrally oriented facial apparatus, has
become deepened and hence labile to dysfunction.