Axons arising from neurons in motor V constitute the bulk of the motor root of the trigeminal and supply the muscles of mastication (masseter, temporalis and lateral and medial pterygoid muscles), as well as the tensor tympani, tensor veli palatini, anterior belly of digastric and the mylohyoid muscles.
Lesions involving motor V or the motor fibers in the trigeminal nerve result in ATROPHY of the muscles listed above ipsilateral to the lesion. Since the pterygoids OPEN the jaw in concert with a downward and opposing inward motion, when they are weak on one side the inward vector of the opposing pterygoid is unopposed. Thus, the jaw deviates toward the WEAK SIDE (i.e., lesion side) upon opening.
You Med1s are lucky that corticobulbar input to motor V (like that to nucleus ambiguus) is BILATERAL. Therefore lesions of this system (i.e., in motor cortex) DO NOT cause obvious defects of jaw function. (Remember, lesions of the corticobulbar input to the hypoglossal nucleus and motor VII DO cause observable deficits, and you should know them COLD!)