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Ramfjord and Ash

1995, W. B. Sanders, 13

Occlusion – 4th Ed, p 33

In the periphery, substance P and calcitonin gene-related peptide (CGRP), having been synthesized in the cell body of the afferent nerve fiber act with other mediators to stimulate histamine release from mast cells thereby promoting vasodilation and plasma extravasation. The vasodilative effect of substance P suggests that migraine (headache pain) would be strongly influenced by the axon reflex phenomenon.


As described previously, sympathetic-sensory influences relate to the release of substances at sympathetic nerve terminals and to the sensitization of sensory nerve endings. These influences may involve inflammation and sympathetic hyperactivity in cluster headaches and the clinical aspects of arthritis.


Agents that block the synthesis of prostaglandins, or block the actions of histamine or substance P are important for their anti-inflammatory activities. Aspirin-like drugs (acetylsalicylic acid, Naproxen, Ibuprofen) possess these types of activities. Aspirin-like drugs and nonsteroidal anti-inflammatory drugs (NSAIDS) exert their influence by blocking the nociceptive input at receptors through blockade of prostaglandin synthesis.97

Central Modulation

Neurons subserving the transmission of nociceptive impulses can be modulated by superior influences on trigeminal nociceptive neurons from higher brain centers, including those involved in cognition and in motivational and emotional behaviors. The recognition that mind-set can influence pain perception makes the existence of descending modulation from brain centers seem reasonable. These local circuits and neurochemicals appear to be influenced by both descending influences and peripheral sensory inputs.


Ramfjord and Ash

1995, W. B. Sanders, 14

Occlusion – 4th Ed, p 34-5

Referred Pain

Muscles as well as other structures are sources of referred pain69”’2’’9’ and the patterns of referred pain from jaw and neck muscles have been experimentally mapped.”’





Convergence of cutaneous, tooth pulp. viscera] (e.g., X. IX), neck, and muscle afferents onto nociceptive and non-nociceptive neurons in the trigeminal subnucleus caudalis is considered to underlie the referral of pain from one site (e.g., tooth pulp) to nearby sites such as the neck and larynx. The convergence theory of pain.”

Such convergent afferent inputs may contribute to the spread of pain and are involved in deafferentation-induced changes of chronic pain.272

Pain may also be referred to the sites of prior surgical procedures, traumatic injury, or pathologic processes rather than to the usual point of reference. Habital reference appears to be a learned phenomenon;



Pain is referred from the teeth to the eyes, ears, and nasopharyngeal regions. In fact, the ear is a common site for referred pain from the lower molars. No exact guidelines exist for correlating specific teeth with their referral sites in the head and neck. Referral of pain should not be confused with the extension of pain from an area where it is most intense, i.e., pain extending diffusely to involve the whole side of the face. Pain may also radiate from a highly localized point of maximum intensity, such as a jaw muscle, to another localized area, such as an ear.


Ramfjord and Ash

1995, W. B. Sanders, 15

Occlusion – 4th Ed, p 34-6

The convergence of cutaneous, tooth pulp, visceral, joints, and neck and muscle afferents onto nociceptive and non-nociceptive neu­rons in the n. caudalis is likely to be a key to the mechanism of some types of referred pain. On the basis of convergence, input from the pathologic site and from the area (e.g., skin, mucous membrane, and so on) to which the pain is referred, summate to produce pain. Thus, a masticatory muscle disorder can result in summation with pain referred to the teeth or gingiva.53


Sympathetic System

Pain of trigeminal origin appears to be aggravated by sympathetic hyperactivity; the effect may be secondary to circulatory changes. The sympathetic nervous system also appears to exert an influence on motor activity as well. The mechanism may be directly on muscle or indirectly on motoneurons through control effects mediated by the limbic brain.




The nerve pathways to the salivary glands are generally assumed to be by way of the auriculotemporal nerve (parotid) and by way of the adventitia of the blood vessels for the sympathetic nervous system. . However, many parotid, postganglionic, parasympathetic, secretory fibers may accompany the internal maxillary artery. There is an impression that the autonomic innervation of the TMJ capsule is provided through the auriculotemporal nerve and the plexus of the superficial temporal artery.


Deafferentation

Deafferentation refers to a partial or total loss of a sensory nerve supply to a particular region of the body’ resulting in changes in brain stem neurons and leading to pain. The phenomenon is said to be possible following trauma to nerve tissue during extraction of a tooth. Verifying the link requires attention when making a diagnosis of chronic pain and a conservative approach to dental procedures relative to prevention of potential trauma to nerves.


Ramfjord and Ash

1995, W. B. Sanders, 16

Occlusion – 4th Ed, p 36-7

Muscle Tenderness

Localized muscle tenderness refers to an unpleasant pressure sensation or muscle pain that occurs when a pressure stimulus of innocuous intensity is applied to a muscle. Such tenderness can occur as a consequence of unaccustomed exercise or mechanical injury. A hypothesis for the cause proposes that there is sensitization of muscle nociception as well as other mechanosensitive afferents. Factors that are known to have sensitizing action on muscle nociceptors include bradykinin, prostaglandin E2, 5-HIT, hypoxia, and others such as substance P (SP).




Muscle Contraction and Pain

During changes in muscle length, such as with mastication, the generated forces usually change and the contractions that occur may he concentric, excentric, or isometric. In isometric contractions, static work is produced with no change in the length of the muscle fibers; in concentric contractions, positive work is produced with shortening of muscle fiber and in excentric contractions, negative work is produced with lengthening of the muscle fibers. Concentric and excentric contractions are considered as dynamitic activity and isometric contractions as static activity or static work. Fatigue and pain associated with such contractions have been of interest for some




In maintained isometric contractions, depending on the tension level, an onset of fatigue occurs in seconds or minutes. When an isometric contraction is maintained beyond the onset of fatigue, discomfort becomes more intense relevant to the isometric force level.

During prolonged submaximal isometric contraction of the masseter and temporalis muscles, there is a migration of activity from one muscle to the other. Muscles that are in an active state while lengthening perform excentric or negative work.’” A person jogging down a steep incline may be injured when the anterior thigh muscles are instantaneously tensed during lengthening.




Prolonged negative work (10—30 min) is injurious and results in aseptic inflammation of the muscle tissues. It has been shown that 20 grinding excursions per minute involve negative work by the masseter muscle when the mandible moves away from centric occlusion (intercuspal position) and positive work on the return movement. Spontaneous pain sites include the temporal regions, joints, supraorbital regions, zygomatic arches, cheeks, molar and premolar teeth, as well as deep inside the ears and eyes.

On the basis of integrated and cumulative EMG of maximum voluntary tooth grinding, t it has been shown that negative as well as positive work efforts of group function exceeded those of canine function. It has been suggested that the Michigan occlusal bite plane splint exerts its palliative effect through reduction of the number of motor units activated for grinding, mastication, and other functional activities.


Ramfjord and Ash

1995, W. B. Sanders, 17

Occlusion – 4th Ed, p 37-9.

Muscle splinting occurs as a protective reflex to limit movement of a painful joint. e.g., with jaw fracture and acute degenerative osteoarthritis. Muscle contracture refers to painful contraction of muscles such as McArdle’s syndrome where there is a deficiency of myophosphorylase.

The precise nature and mechanisms of the pain from clenching hyperactive jaw muscles is not clear. Muscle pain and poor sleep commonly occur together. The pains induced by dynamic muscle activities have been attributed to direct lesions in the contractile and noncontractile parts of muscle tissue caused by discrepancies between active and passive tensions and negative work loads. To relieve muscular pains there should be a decrease in the level and duration of active and passive tension development and an increase in afferent muscle blood flow.




Hyoid Bone (Pain) Syndrome

The hyoid bone syndrome” is of importance to the clinician because of dental and non-dental pain reference sites. The cause appears to be a focal degenerative injury of the middle pharyngeal constrictor muscle as a consequence of injury to the hyoid greater cornu. Symptoms include pain radiating to the ear, throat, temple, TMJ, molar teeth, and zygomatic arch. A vertical axis of pain extends from the temple down through the TMJ to the clavicle and further inferiorly to the middle of the chest wall.




Toothache — Earache Syndrome
In one report,1 it was found in human specimens that minor branches of the auricu­lotemporal nerve entered the posterior aspect of the joint capsule; that there was an anastomosis of the inferior alveolar, auriculotemporal and facial nerves: and that a branch of the auriculotemporal nerve entered the man­dibular canal along with the inferior alveolar nerve and artery. From anatom­ical and physiologic findings it was suggested that an answer could be provided for the often puzzling toothache—earache syndrome.


Tension-Type Headaches

Headaches may be symptoms of underlying disease or dysfunction. Until recently, tension headaches have been thought to be caused by tonically elevated activity of the head and neck muscles. This concept led to the use of biofeedback therapy to detect EMG evidence of hyperactivity and “learning” to relax the muscle(s) to control headache pain.



Ramfjord and Ash

1995, W. B. Sanders, 18

Occlusion – 4th Ed, p 39, 40

Vascular Headaches

Sensory afferents from the trigeminal nerve supply the intracranial blood vessels (pial arteries) and the dural blood vessels. It is thought that activation of nociceptors innervating these vessels is responsible for migraine and cluster headaches.. This phenomenon results in vasodilatation of vessels and plasma extravasation. There is an increase in bradykinin along with a release of histamine from mast cells and a release of 5-hydroxy-tryptamine from platelets.




Chronic Muscle Pain

Chronic pain is often related to the muscles, joints, tendons, and periarticular tissues.

Deep pain from muscles spreads to other muscles that are close by, as well as to deeper tissues. This pain is associated with auto­nomic symptoms, and exhibits referral phenomena. Muscle pain is perceived to be diffuse and difficult to locate.

Several chronic muscle pain syndromes including fibrositis, tendonmyopathy, temporal tendonitis, TMJ and muscle disorder, myofascial pain syndrome, and fibromyalgia, have been assumed to be clinical entities; however, the absence of specific diagnostic criteria has made differential diagnosis somewhat arbitrary




Fibromyalgia

Fibromyalgia (FM) is considered to be a syndrome (not a disease) characterized by widespread musculoskeletal pain and tenderness, fatigue, and disturbances of sleep. As in some patients with temporomandibular disorders, maximum voluntary clenching (MVC) is reduced. Comparisons of symptoms for primary fibromyalgia, MPD syndrome, and TMD with joint pathology suggest that these diagnostic parameters are not specific for a particular disorder





Myofascial Pain

The pain of an active rnyofascial pain syndrome (MPS) is found localized in one or more areas of a muscle and which when palpated is the trigger point for referral of pain to a specific site. These MPS trigger points are located within a taut band of muscle. However, trigger points and tender points are also present in fibromyalgia. Active trigger points are always tender but tender points are not always trigger points.


Ramfjord and Ash

1995, W. B. Sanders, 19

Occlusion – 4th Ed, p 40, 41

Myofascial Pain Dysfunction

(MPD Syndrome)
The myofascial pain dysfunction syndrome (MPD) has been called a debatable diagnosis because the concept contends that muscle spasms occur in response to psychologic stress even though no true muscle spasms have been observed. The term myofascial was added to the description symptom-triad described at first as pain-dysfunction syndrome,262 but the term should not be confused with myofascial pain. The concept of MPD proposes that muscle pain and muscle hyperactivity constitute what has been termed a viscous cycle causality. Recently this causality model has been questioned.



Adaptation to Pain

The adaptation to pain model proposes that chronic pain from joints, teeth, and other orofacial tissues can cause the same signs of dysfunction as muscle pain. There is evidence that inputs from the various sites do converge on the same groups of interneurons in the intertrigeminal area. Thus, the Group II interneurons proposed for the adaptation model include a mix of inputs that control V motoneurons. These also in­clude inputs in the rostral trigeminal nuclei, reticular nuclei, and small cutaneous, joint and muscle afferents. It has been called the “pain adaptation” model’ because the motor signs of MPD (e.g., decrease in maximal biting force, increase in activity in elevator muscles during jaw opening) appear to be reflex adaptations.




The link between myofascial pain and muscle dysfunction’” of the MPD syndrome is proposed to be a useful reflex adaptation to reduce jaw motion, further injury, or pain arising from the joints and teeth.

Although damage to muscle fibers occurs and algesic substances are released by ischemia, feedback from muscle spindle and tendon organ afferents does not appear to be affected. Motor output of painful muscles ap­pears to be changed by Group III and IV afferents that are activated or sensitized by neurohumoral changes or tissue damage.




One approach to support the model has been reported. The model does not provide any insight into what causes the pain, why it persists, nor if the avoidance behavior is a reflection of a higher substrate involved only in modulation. However, it has been concluded that chronic pain reduces muscle outputs acting as agonists and increases muscle outputs acting as antagonists. It has also been concluded that muscle hyperactivity is not a basis for a viscous-cycle-causality concept of MPD.


Ramfjord and Ash

1995, W. B. Sanders, 20

Occlusion – 4th Ed, p 41

Psychologic Aspects of Chronic Pain
The complexity of the various psychologic factors involved in the perception of pain and behavior has been discussed in a number of reports. There is often a confusing relationship between the intensity of the documentable physical changes, and the patients’ complaints and behavior.


Illness behavior may be normal or abnormal, and assessment includes all aspects of biologic, psychologic, and social functioning, Dysfunctional chronic pain is a subset of illness behaviors inconsistent with medically documented findings, even though the complaints of pain are prominent..


Changes occurring in emotional status include mood and behavioral changes associated with depression such as demoralization, helplessness, and social isolation

A number of factors relate to the pain experience and behavior including anxiety, depression, attention, perceived control, tissue damage, past pain experience, culture, personality, past history with health professionals, and several others. The mechanisms by which these factors operate are complex and the assessment of the patient with abnormal illness behavior usually involves professionals capable of evaluating the physical and psychologic aspects of behavior.


Ramfjord and Ash

1995, W. B. Sanders, 21

Occlusion – 4th Ed, p 50, 51

Clinical Occlusion, Chapter 2
Although the development of occlusion is often over­looked, some of the more important aspects of occlusal disorders had their beginning during the long period of time when the primary and permanent dentitions were being developed. Therefore, some of these areas will be considered in this chapter.

Of particular importance to an understanding of clinical occlusion is the kinesiology of occlusion where function (rather than static relationships), is stressed.




In this respect, descriptions and illustrations of mandibular po­sitions and movements must be related to guidance by the teeth and joints, and to neuromuscular mechanisms underlying such functions as mastication and swallowing.

The response of the periodontal tissues to occlusal forces, including adaptation, is also important for an understanding of clinical practice. Concepts of normal versus idea! oc­clusion provide the clinician with practical goals for occlusal therapy.



DEVELOPMENT OF OCCLUSION

The emergence (eruption) of the primary dentition (Fig. 2—I) into the oral cavity is an important time for the development of oral motor behavior and the acquisition of rnasticatory skills.”

Maturation of oral function beyond obligate nasal breathing in newborn infants re­quires suckling and swallowing. As more solid foods are taken in. the young child frequently opens laterally toward contact on the working side and then back toward contact on the midline so that the teeth make contact as the food is chewed. However, in the young adult without TMJ and muscle dysfunction there is a tendency to open the mandible symmetrically.


By the advent of the primary molars, the juvenile pattern of chewing has been established. With the development of more complex movements of the tongue, pharyngeal wall, and mandible (development which is consistent with an anteroposterior maturation of oral motor behavior), there is a transition away from the infantile swallow. By 6 years of age about one half of the children have achieved an adult swallow. The transition to the adult type of chewing ap­pears to develop in conjunction with the emergence of the canines into occlusion at about the age of 12.


Ramfjord and Ash

1995, W. B. Sanders, 22

Occlusion – 4th Ed, p 51, 53

At the completion of the emergence of the primary teeth, occlusal contact relations occur. It is not unusual to note extensive wear of the anterior primary teeth and the incisors in an edge-to-edge relationship. The significance of such wear in terms of later neurobehavioral patterns of bruxism has not been clarified.


The growth of the jaw provides space for the teeth to erupt and emerge into the mouth. Forward rotation of the maxillo-mandibular complex, which is the more usual pattern, influences the magnitude of tooth eruption, as well as the ultimate anteroposterior position of the incisors.


Primary molar relationships have been described as the flush terminal plane, mesial step, and distal step. The flush terminal plane is considered to be normal for the primary dentition. The transition from the flush terminal plane to the permanent dentition often results in an Angle Class I (normal) molar relationship).


The mesial step relationship may also lead to a normal permanent molar relationship; however, where there is a distal step relationship, the transition to the permanent dentition often results in an Angle Class II molar relationship.

Ramfjord and Ash

1995, W. B. Sanders, 23

Occlusion – 4th Ed, p 55, 57

Significance of Occlusal Development

It is of particular importance to point out that functional disturbances of the masticatory system may have had their beginning during the development of occlusion; including perhaps tongue and swallowing habits, chewing patterns, tooth clenching and bruxism, absence of occlusal continuity and occlusal interferences to function and occlusal stability. As a result of an appropriate development of occlusion, a stable occlusion consistent with the adaptive capacity of the masticatory system should develop, and the possibility for problems of occlusal dysfunction should be minimized.




Malocclusion in the sense of an orthodontic classification such as the Angle Classification is not generally considered to be a cause of clinically recognized temporomandibular and muscle disorders. However, malocclusion is a disturbance of occlusion and may be related to dysfunction via tongue posture (activity) and skeletal anterior open bite.



Changes in Occlusion

After the occlusion has developed initially into good alignment, there is a tendency for crowding of the mandibular incisor teeth during the late teens and early-to-late twenties. Several explanations have been given for such changes. Some evidence for why this occurs has been related to the growth pattern of the jaw, e.g., when late mandibular growth occurs



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