TMJ Surgery: Chronic Derangement and associated “TMJ” headache, Part I

The above photo is of the intact disc/capsule adapted over the mandibular condyle. The previous blog shows the disc/capsule divided  in the mid sagittal plane.

The above photo is from a patient with not only significant orthopedic dysfunction of the jaw joint but chronic, daily and unremitting headache that lasted for years until finally referred for surgery.  The view is of the superior disc surface which will articulate with the glenoid fossa.

This is the inferior disc surface of the same specimen.  This surface articulates with the condyle of the jaw.  Note the differences int the two surfaces.  Note the significant amount of inflammation present in the entire disc tissue and the effects of longstanding  destructive shear and translational damage throughout the entire specimen.  After surgery, joint function improved significantly. But relative to pain and headache, the most satisfying result in this case and hundreds like it was the significant decrease in headache frequency, duration and intensity that was part of a satisfying long term result of appropriate early  diagnosis and treatment.

The presence of this degree of inflammation in the fibrocartilage  TMjoint disc/capsule tissues is significant due to a number of factors. The synovial nature of the TM joint and the highly vascular posterior  attachment of the disc/capsule to the tympanic plate of the temporal bone (that separates the ear from the TM joint) is a direct conduit that allows access of biochemicals produced by inflammation and tissue destruction into the regional blood supply with many potential effects. 

When the mouth opens and the jaw joint translates, the tissues that compose the posterior joint attachment fill with blood very rapidly.  As the jaw closes and the teeth engage, this blood is compressed rapidly out of the attachment.  The posterior attachment is like a sponge  actually is what is referred to biologically as an arterial-venous fistula (A-V fistula).  This mechanism allows a rapid clearance of metabolites through a healthy synovial lining and system which is necessary to protect the integrity of a fibrous tissue system that is required to maintain its natural elasticity for life long function.  After injury and onsent of chronic instability, infection, other systemic arthritic disease processes  (rheumatoid arthritis, psoriatic arthritis, connective tissue diseases etc) inflammation begins to be a part of the destructive process along with unbalanced shear and torque forces in a progressively unstable joint.  Patients with longstanding  orthopedic joint disease and advanced arthritis almost always have increased volume and diameter of vascular structures surrounding the joint capsule. This is most likely due to an elevation of substances that cause vasodilitation as explained below. 

Significant headache is a common complaint of patients with progressive and longstanding instability or derangement of the jaw joint.  Surprisingly, in the neurological classifications of headache and etiologies of headache requiring the expertice of neurologic specialists in medicine, rarely is chronic TM joint arthritis or the effects of longstanding derangement acknowledged as a potential primary cause of unremitting headache pain, and the condition considered as a viable mechanism of recalcitrant headache treatment.   This is unfortunate and is a primary example of a significant disconnect in the training of physicians and dentists in this area. Headache issues with “TMJ syndrome” are generally described in dental education as being due to chronic “muscle spasm” from various causes varying from malocclusion induced myospasm to bruxism induced muscle tetany producing excessive lactic acidosis, similar to what happens when we excercise beyond our abilities at the time.  Neurological medicine for some mysterious reason has not paid much attention to over 20 years of evidence based data and studies provided by biochemical assays and joint fluid analysis studies compiled by surgical data, most of the early data produced by members of the American Society of TM joint surgeons and reproduced and recomfirmed multiple times and independently  by other researchers in the oral and maxillofacial surgical field  throughout the world.

A second mechanism is true vascular cephalgia or vascular headaches which are complex neurological and biochemical phenomena.  Migraine headache is the extreme neurobiological bad actor that is the prototype vascular headache phenomenon.  In inflamed TM Joints, many different biochemicals that are “vasoactive” substances have been identified… Substance P, is just one of many vasoactive substances that is elevated in the central nervous system blood supply in many types of vascular headaches.   It is found in significantly elevated quantities within joint fluids in cases of TM joint arthropathy as exhibited in these specimens. The centenal work by Moskowicz in the the 80s directed neurologic and pharmacologic research on the development of  medications whose mechanisms are to minimize the effects of these incapacitating headaches.

Substance P is produced in relatively high quantities in the Trigeminal nerve, or the complex motor and sensory nerve that supplies most of the neurologic innervation of structures from beneath the jaw line to the forehead, scalp, ear regions, the teeth, sinuses, eyes.  There are portions of this formidable cranial nerve system that surround arteries in the brain.  Mechanisms of vascular headache can be kicked into gear when Substance P and other biochemicals are elevated in all types of inflammatory disease processes that occur along the paths of this complex cranial nerve system (the 5th). which is a mixed motor (movement) and sensory (feeling) system.   Consequently, “TMJ headache” as reported by patients can be a very troublesome and complex mixed headache of both muscular tension and vascular components.

Often, muscle relaxants are sole prescribed for “TMJ headache” felt to be due to muscle spasm.  The mechanism for many of these drugs (Flexeril, Valium, Soma) work relatively well for muscle spasm induced conditions in muscle groups innervated by the spinal nerves.  Unfortunately, they do not seem to work as well  with the Trigeminal or cranial nerve muscles  because of the complex nature of this part of the nervous system….these drugs just work better with back, neck and extremity muscle spasm conditions. …not so great with the jaw…..this is most likely due, again, to the complex nature of the nerve itself being a complicated  mixed motor and sensory  dually dependent components .  Chronic headache medical management should include consideration of medication designed to reduce the effects of Substance P and other similar substances in this clinical setting.

Chronic headache from cervical disc disease of the neck is accepted as a condition of etiology. Consideration of the evidence in the literature in oral and maxillofacial surgery of repeated studies demonstrating destructive and vasoactive substances in diseased jaw joints should be given consideration as well.

References:  (The following references are some of the classics from neurological research concerning Substance P and its effects in cranial vascular circulation, vasoactivity, and the trigeminal nerve system that is the complex portion of the nervous systems operating in this area of the body.)

1. Moskowitz,MA:  The Neurobiology of Vascular Head Pain.  Annals of Neurology1984; 16: 157-168.

2. Lembeck F.  Peripheralo substance P neuronsL  afferent, efferent or both functions?  In Skrabanek P, Poell D (eds):  Substance P. Dublin: Dublin Press, 1983, pp 81-5.

3. Schellhas KP, Wilkes CH, Baker CC.  Facial pain, headache, and temporomandibular joint inflammation.  Headache 1989; 29:229-32.

4. Schellhas KP, Internal derangement of the temporomandibular joint: radiologic staging with clinical, surgical, and pathologic correlation.  Magnetic Resonance Imaging 1989: 7: 495-515.

5.  Evinsson L, McCullough J, Uddman R. :  Substance P, immunohistochemical localization and effect upon cat pial arteries in vitro and in vivo.  J Physiology 1981;  318: 251-8.

6.  Godsby PJ, Edvinsson L, Ectman R.  Release of vasoactive peptides in the extracerebral circulation of humans and the cat during activation of the trigeminovascular system.  Annals of Neurology, 1988;  23: 193-6.

7. Bereiter DA, Standord LF, Barker DJ:  Hormone induced enlargement of receptive fields in trigeminal mechanoreceptive neurons. II.  Possible mechanisms.  Brain Research 1980;  184;  411-423.

Tags: Add new tag, Substance P and TMJ disease, TMJ headache, TMJ Surgery