It appears most probable that immediate damage to the temporomandibular joints themselves is produced by a combination of mechanical forces resulting from the vehicular collision and abnormal or accelerated muscular forces acting during joint movement produced by the collision. That is, abnormal muscular forces encountered during the collision are capable of producing injurious forces within the joint which may be disproportionate to the force of the impact of the collision. Certain predisposing factors such as pre-impact disc position may also effect the nature and degree of injury.
Normally, the mechanics of mouth opening occurs so as to protect the internal environment of the temporomandibular joint from undue compression during both rotation and translation.
The first movement which occurs during mouth opening is depression of the mandible secondary to relaxation of the elevator muscles and the effect of gravity. This allows for a minimum of joint compression during condyle rotation and translation thereby minimizing wear and tear on, or even frank injury to, the discal and cartilaginous components of the joint. Theoretically, if mouth opening, even partial opening, occurred without this decompression then forces would be placed on the components of the temporomandibular joint which could produce tissue damage in the joint. In point-of-fact, during the whiplash event it is quite possible that the elevator muscles contract as both rotational and translatory movements take place between the condyles and their respective mandibular fossae. This then would increase rather than decrease joint compression as the mandible and skull move relative to each other during the whiplash event. However, even if muscular tonicity was only maintained during joint movement, this would represent abnormal joint mechanics.
Furthermore, during the whiplash event, it is the 8 to 14 pound skull which moves relative to a less actively displaced 4 to 6 ounce mandible which is held in place by the hyoid muscles and other anchoring tissues. This is the reverse of the normal kinematics for the temporomandibular joint. Finally, these movements occur at an accelerated rate which adds to the stress on the region. The whiplash event then most probably produces frank tissue damage to the temporomandibular joints by:
I would note here that the investigation into the mechanics of the mechanism of temporomandibular joint injury from whiplash is ongoing. Please note that in the UCLA computer model, while abnormal mechanics were noted which support the statement that abnormal temporomandibular joint mechanics were observed, questions concerning tissue tolerances remain. Once again, while the mechanics of the injury are interesting, the historical relationship of symptoms to event remains at the heart of the causation statement.
Frank tissue damage is not the only factor involved in the mechanism of injury for the temporomandibular joints however, although it is the most immediate. Other factors may subsequently act on the inflamed temporomandibular joint and perpetuate or even escalate what then becomes an inflammation/scarring process. Some of these factors are a result of the whiplash event e.g. cervical injury, and yet other influences may represent predisposing architectural, psychological, chemical and postural qualities possessed by the individual injured prior to the whiplash event. These predisposing and/or perpetuating factors frequently involve the very same patient profile pointed to by the defense as causative: malocclusion, bruxism, psychometric profile, tissue weakened by prior injury, arthritides, allergies and chronic pain issues. Care taken in identifying these factors will improve your treatment results and sustain your causation statement.
MECHANISM OF TMJ INJURY FROM A WHIPLASH EVENT SHOULD BE VIEWED AS A FUNCTION OF THE FOLLOWING FORMULA: Frank tissue damage to TMJ apparatus affected by:Many medical/legal arguments concerning the proposed pathogenesis for a temporomandibular disorder center around radiography of the temporomandibular joints. Radiography (tomograms, transcranial views, panographic views, etc.) may provide useful information concerning fracture, tumor invasion and specific arthritides. Absent these factors x-rays should not be used to make a statement concerning the prior existence of, presence of or probable development of a temporomandibular disorder. While this is clearly referenced in the literature, x-rays are routinely used inappropriately to discount trauma as the causation in a temporomandibular disorder. Specific statements generally reference alterations in cortical bone shape of the mandibular fossa and condylar head despite the fact that longitudinal studies as well as electron microscopic studies of the temporomandibular joints have stated clearly that alteration in bone shape within the temporomandibular joints will occur within a normally functioning joint and that these joints are capable of extensive remodeling without pathologic process. Temporomandibular joint tomograms have demonstrated a statistically significant relationship between posterior condyle position in centric occlusion and anterior disc position. This has not however been linked to the symptom expression of TMD.
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