Basic anatomy and physiology of the temporomandibular joint (TMJ)

The tempormandibular joint (jaw joint) is a rather complex aspect of our anatomy.  Its complexity leaves it prone to a number of pain responses and histological (tissue) changes.  The following is a brief description of its anatomy and how it functions in relation to the rest of our skull and central nervous system.

The squamous portion of the temporal bone articulates with the condyle of the mandible at a juncture that is known as a temporomandibular joint (TMJ).  In great apes (man included) the mandible is fused at the midline allowing each of the bilaterally symmetrical TMJ’s to operate as one unit.  Together both TMJ’s are referred to as a single craniomandibular joint (CMJ).  The CMJ encompasses the whole mandible along with both articulating surfaces of the temporal bone (2).  The fact that the CMJ is made up of two joints that work in unison creates a dependence of one on the other.  Any dysfunction experienced on one side is sure to influence the opposite side (5).

The TMJ is extremely complex and is almost constantly in motion.  The TMJ is mobile when we talk, chew, make certain facial expressions; even during sleep, it is activated to some degree. It is composed of two synovial cavities that allow movement of the mandibular condyle over the glenoid fossa of the temporal bone.  The superior portion of the joint is an arthrodial gliding joint and the inferior portion is a ginglymoid hinge joint (5).  The complexity of the TMJ allows lateral movement, elevation, depression, protrusion, and retraction of the mandible (2).  The reduction of the canines in hominids during evolution allowed us the rotary movement that is not possible in most primates.  The drawback is that teeth grinding came with this trait.  Branches of the trigeminal nerve innervate the muscles of mastication that are responsible for movement of the mandible.  The trigeminal nerve is related to the reticular alarm system (RAS) of the central nervous system, which is active during mental stress (1, 3, 4, 5,).  Trigeminal nerve innervates the pons of the brain which is where sympathetic (fight or flight) nerve responses are registered.  This is one of the main reasons that mental stress is a common etiology for temporal mandibular dysfunction.

 

1) Campbell, Bernard G., Loy, James D.: Humankind Emerging, The Concise Edition. Pearson Education Company, Boston, MA; 2002.

2) Elson, Lawrence M., Kapit, Wynn.: The Anatomy Coloring Book, 3rd edition. Benjamin/Cummings Publishing Company Incorporated, Menlo Park, CA; 2002.

3) Henderson, David F., A Comprehensive Overview of the Temperomandibular Joint. 2004.

4) Marieb, Elaine N.: Human Anatomy and Physiology, 4th edition. Benjamin/Cummings Publishing Company, Menlo Park, CA; 1998.

5) Upledger, John E., D.O., F.A.A.O.:  Craniosacral Therapy II, Beyond the Dura. Eastland Press Incorporated, Seattle, WA; 1987.

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Pathology of stress (part 2)

Central Nervous System

In the brain, a potential stressor is first perceived in the thalamus which relays the sensory information via cortical projections to the pre-frontal cortex.  In the pre-frontal cortex the implied stressor is given meaning and is evaluated.  The prefrontal lobe works in consort with the limbic system (principle contributors are the amygdala and the hippocampus along with the insular cortex) via prefrontal-limbic connections (1).  It is these structures where the consequence of the stressor is realized, related to memories, given emotional significance and if necessary acted upon (5).

If the prefrontal-limbic relay integrates the given information as a stressful situation, then sympathetic activity is relayed to rest of the body by increasing the actions of the HPA (2).  When action is required to deal with stressful circumstances, the limbic system takes command of autonomic centers of the hypothalamus and brainstem where nerve and endocrine responses of the sympathoadrenal system begin (5).

Endocrine Response

When the stress response is initiated the hypothalamus responds by stimulating the pituitary, resulting in a release of hormones by the following psychoneuroendocrine response cascade of the HPA.  In the primary response sympathetic preganglionic nerve endings are stimulated resulting in the release of the catecholamines norepinephrine and epinephrine (3, 5).  The circulating catecholamines use glycogen stores from the liver in order to produce glucose, to provide a quick energy source for a “fight or flight” situation (3, 5). Metabolic and motor activities are stimulated and blood flow is increased to the muscles (3, 5 8).

An enhancement of the sympathoadrenal system is provided by adrenal steroid hormones called glucocorticoids.  Glucocorticoids are slower in action than catecholamines, providing a secondary endocrine response to stress.  These adrenal stress hormones are released via the HPA.  The result of this psychoneuroendocrine response cascade results in the release of the adrenocorticoid steroid hormone cortisol.  Cortisol is the most prevalent glucocorticoid released by the adrenal gland (4).  It is a neuromodulatory hormone which either enhances or inhibits the response of neurons to neurotransmitters (4).  The cells of the zona fasciculuta in the adrenal cortex produce cortisol.  This hormone helps the body maintain homeostasis by metabolizing carbohydrates, lipids, and proteins.  In response to stress, it aids in the uptake of glucose in order to provide energy for the body to deal with stressors (3).

Glucocorticoid production is regulated by pituitary adrenocorticotropin (ACTH), whose release is controlled by corticotrophin releasing hormone (CRH) from the hypothalamus.  When stress is realized, CRH is released from the hypothalamus into the specialized portal circulation of the pituitary stalk (3, 5).  CRH causes ACTH to be released into the blood stream.  In turn cortisol production and its release from the adrenal cortex is increased (3, 5)

The HPA axis is a major contributor to the connection of long term psychosocial stress to having negative effects on psychological as well as somatic health (3, 5).  The long-term effects of elevated cortisol levels can be detrimental to the health of all body systems (3, 5, 7).  Cortisol has been found to be the primary mediator of allostatic load in humans. This load is characterized by the collective physiological toll experienced by the body due to adaptaptation to life’s stressors. (5, 6).

If cortisol levels remain high in the body due to a chronic stress response, exhaustion occurs in the body.  Negative feedback to the hypothalamus is continuous, resulting in the constant release of stress hormones (7).  Glucose is inhibited from entering the muscles causing a hindrance of adenine tri-phosphate (ATP) to efficiently synthesize proteins.  The eventual ramifications of a prolonged state of hypercortisolism may be counterproductive to the healing process.  Continuous stress in experimental results found by Selye (1976) when stress is continuous resulted in muscle wasting, hyperglycemia, atrophy of the immune system, vascular derangement, along with a breakdown of fat stores.

The fact that cortisol levels are increased as a result of both physiological as well as psychological stress demonstrates how stress can be one of the etiologies responsible for a number of ailments including temporomandibular joint dysfunction (TMD).  Korzun (2002) found that daytime levels of cortisol have been found to be much higher in people who suffer from chronic facial pain as compared to those who suffered from depression and fibromyalgia.  The presence of raised cortisol levels in chronic facial pain sufferers may demonstrate that TMD sufferers have a high susceptibility to abnormalities in stress hormone responses that result in elevated cortisol levels (4).  Whether somatic (the body’s) structures are the cause of stress, or if stress stems from psychological issues that in turn act on the somatic structures seems to be irrelevant to the process of the stress response.  The cause and effect stress response cycle often expresses itself as symptoms in both aspects.

This explains the body/mind connection.  What we think effects us physically and what we feel effects us mentally.  In some cases It can be either a vicious circle of repetitive negative emotions continuously causing harm to our bodies or our bodies causing harm to our minds.  The contrary  situation a positive cycle of kind emotions and thoughts effecting our bodies for the better.

We are simply a result of how these chemical reactions take place.  It is important that we can break these cycles of negative thoughts that may keep us from a state of homeostasis.  When faced with an onslaught of negativity it is best to try to remove ourselves from the situation or depressor and breathe deeply to counteract the sympathetic (fight or flight) nervous response.  We must try our best to think positive and surround ourselves with good things that make us smile in the face of difficulties.   Some of us will find solace in meditation, working out, or stretching our bodies.  This is also an example of “you are what you eat”.  What we put into our bodies affects how we feel both physically and mentally.  All of these are examples of how the physical can affect the mental and vice versa.

1)  Chrousos, GP, Gold, PW. The concepts of stress and system disorders. Overview of physical and behavioral homeostasis. JAMA 1992; 267; 1244-1252

2)  Everly GS, Lating, JM. A Clinical Guide of the Human Stress Response, 2nd edition. Kluwer Academic / Plenum Publishers., New York, NY; 2002. 178-180

3)  Hadley, Mac E., Endocrinology, 5th edition. Prentice Hall, Inc., Upper Sadler River, NJ; 2000. 364-368

4)   Korzun A. Facial pain depression and stress – connections and directions. Journal of Oral Pathology and Medicine. 2002; Volume 31, Issue 10, 615

5)   Lavallo, William R., Stress and Health, Biological and Psychological Interactions. SAGE Publications, Inc., Thousand Oaks, CA; 1997; 70-101

6)  Seeman et al., 2001. Seeman, B.S., McEwin, J.W., Rowe, Singer, B.H. Allostatic Load as a Marker of Cumulative Biological Risk: MacArthur Studies of Scientific Aging, Proc. Natnl. Acad. Sci. USA 98 (2001), pp. 4770-4775.

7)  Selye H. The Stress of Life, revised edition. McGraw Hill, Inc. New York, NY; 1976. 55-426.

8)  Upledger, John E., D.O., F.A.A.O.:  Craniosacral Therapy II, Beyond the Dura. Eastland Press Incorporated, Seattle, WA; 1987.  15-20; 64-68; 155-207; 234.

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The Pathology of Stress (Part 1)

 

Stressors may be either of physiological or psychological etiology (Lavallo, 1997; Upledger, 1987).  Any threat to the homeostatic mechanisms of the body is considered a stressor (Lavallo, 1997).  Physical stressors are events that directly challenge one’s health, examples being: significant temperature changes, infection, toxic substances, or injuries.  Psychological stressors challenge one’s well being because of how they are perceived by that individual (Lovallo, 1997; Selye, 1976).  Examples of psychological stressors are great disappointment, fear, job or family related demands and so on.  These stressors may be the result of an immediate event or past and future worry that manifests in one’s thoughts, resulting in a stress response that uses the same biological sympathetic responses that would prepare that individual’s body to take action (Selye, 1976). 

Stress is simply a matter of how stressors are perceived, followed by the actions that the Central Nervous System (CNS) imposes on the body (Selye, 1976).  It is non-specific in that it can come from any external or internal factor perceived in the CNS.   The stress response is the body’s compensatory reaction due to interference that a stressor poses (Lovallo, 1997; Selye 1976).

The hypothalamus-pituitary-adrenal axis (HPA) is the homeostatic mechanism that provides living beings with a means to compensate for stressors that come from the external as well as internal environments (Chourosis, 1992).  Through the actions of hormones and nerve activity, modifications are made in all of the bodies systems in order to deal with stressful changes (Lovallo, 1997).  Korszun (2002) found that it is likely craniofacial pain acts as a strong activator of the HPA.  This observation possibly demonstrates that stress can come from physical as well at psychological origins and vice versa.  No matter the cause the body’s biological reaction to stress is essentially the same.

                       

This is how the three glands of the HPA axis work together to produce cortisol.

Photo © HOPES, at Stanford

Definition: The hypothalamic-pituitary-adrenal axis is a complex set of interactions between the hypothalamus (a part of the brain), the pituitary gland (also part of the brain) and the adrenal or suprarenal glands (at the top of each kidney.) The HPA axis helps regulate things such as your temperature, digestion, immune system, mood, sexuality and energy usage. It’s also a major part of the system that controls your reaction to stress, trauma and injury.

Research links fibromyalgia and chronic fatigue syndrome with abnormalities in genes involved in the HPA axis. (Primarily the hypothalamus in fibromyalgia and primarily the adrenals in chronic fatigue syndrome.)

The HPA axis also is involved in anxiety disorder, bipolar disorder, post-traumatic stress disorder, clinical depression, burnout and irritable bowel syndrome.

http://chronicfatigue.about.com/od/cfsglossary/g/hpa_axis.htm

Chrousos, GP, Gold, PW. The concepts of stress and system disorders. Overview of physical and behavioral homeostasis. JAMA 1992; 267; 1244-1252

Henderson, David F., Effectiveness of Manual Therapy on Stress in Temperomandibular Joint Dysfunction. 2005

Korzun A. Facial pain depression and stress – connections and directions. Journal of Oral Pathology and Medicine. 2002; Volume 31, Issue 10, 615

Lavallo, William R., Stress and Health, Biological and Psychological Interactions. SAGE Publications, Inc., Thousand Oaks, CA; 1997; 70-101

Selye H. The Stress of Life, revised edition. McGraw Hill, Inc. New York, NY; 1976. 55-426.

Upledger, John E., D.O., F.A.A.O.:  Craniosacral Therapy II, Beyond the Dura. Eastland Press Incorporated, Seattle, WA; 1987.  15-20; 64-68; 155-207; 234.

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