Back pain is common in the general population, but only a subgroup of back pain patients develops a disabling chronic pain state. The reasons for this are incompletely understood, but recent evidence implies that both preexisting and pain-related variations in the structure and function of the nervous system may contribute significantly to the development of chronic pain. Here, we addressed the role of striatal dopamine (DA) D2/D3 receptor (D2/D3R) function in chronic non-neuropathic back pain (CNBP) by comparing CNBP patients and healthy controls using PET and the D2/D3R-selective radioligand [11C]raclopride. D2/D3R availability was measured at baseline and during a pain challenge, yielding in vivo measures of receptor availability (binding potential, BPND) and DA release (change in BPND from baseline to activated state). At baseline, CNBP patients demonstrated reductions in D2/D3R BPND in the ventral striatum compared with controls. These reductions were associated with greater positive affect scores and pain tolerance measures. The reductions in D2/D3R BPND were also correlated with μ-opioid receptor BPND and pain-induced endogenous opioid system activation in the amygdala, further associated with measures of positive affect, the affective component of back pain and pain tolerance. During the pain challenge, lower magnitudes of DA release, and therefore D2/D3R activation, were also found in the ventral striatum in the CNBP sample compared with controls. Our results show that CNBP is associated with adaptations in ventral striatal D2/D3R function, which, together with endogenous opioid system function, contribute to the sensory and affective-motivational features of CNBP. SIGNIFICANCE STATEMENT The neural systems that underlie chronic pain remain poorly understood. Here, using PET, we provide insight into the molecular mechanisms that regulate sensory and affective dimensions of pain in chronic back pain patients. We found that patients with back pain have alterations in brain dopamine function that are associated with measures of pain sensitivity and affective state, but also with brain endogenous opioid system functional measures. These findings suggest that brain dopamine–opioid interactions are involved in the pathophysiology of chronic pain, which has potential therapeutic implications. Our results may also help to explain individual variation in susceptibility to opioid medication misuse and eventual addiction in the context of chronic pain.

The aim of this study was to evaluate the change in thickness of the mouthguard sheet due to different heating conditions during fabrication.Mouthguards were fabricated with ethylene vinyl acetate (EVA) sheets (4.0-mm thick) using a vacuum-forming machine, and six conditions which varied the height of the frame above the surface, reversing the sheet while heating, and controlled power on–off of the heater when a specified level of sagging had been attained were used to determine optimal conditions. The working model was trimmed to a height of 20-mm at the incisor and 15-mm at the first molar. Post-molding thickness was determined for the incisal portion (incisal edge and labial surface) and molar portion (cusp, central groove, and buccal surface). Differences in the change in thickness due to heating condition were analyzed using Scheffé’s multiple comparison tests.The heating condition which the sheet frame was lowered to and heated at 50 mm below the top of the post, the heater was turned off when the sheet sagged by 10 mm, and the sheet was molded when the sagging reached 15 mm showed the thickest, what the decrease in the thickness reduction was approximately 0.40–0.44 mm at the incisal, and that was 0.35–0.40 mm at the molar portions.When molding a mouthguard using an EVA sheet, the thickness of the incisal and molar portions of the mouthguard can be maintained by adjusting the height of the sheet frame and heating conditions, which may be clinically useful.

Context: Placebo and nocebo effects, the therapeutic and adverse effects, respectively, of inert substances or sham procedures, represent serious confounds in the evaluation of therapeutic interventions. They are also an example of cognitive processes, particularly expectations, capable of influencing physiology.Objective: To examine the contribution of 2 different neurotransmitters, the endogenous opioid and the dopaminergic (DA) systems, to the development of placebo and nocebo effects.Design and Setting: Using a within-subject design, subjects twice underwent a 20-minute standardized pain challenge, in the absence and presence of a placebo with expected analgesic properties. Studies were conducted in a university hospital setting.Participants: Twenty healthy men and women aged 20 to 30 years recruited by advertisement.Main Outcome Measures: Activation of DA and opioid neurotransmission by a pain stressor with and without placebo (changes in the binding potential of carbon 11 [C-11]-labeled raclopride and [C-11] carfentanil with positron emission tomography) and ratings of pain, affective state, and anticipation and perception of analgesia.Results: Placebo-induced activation of opioid neurotransmission was detected in the anterior cingulate, orbitofrontal and insular cortices, nucleus accumbens, amygdala, and periaqueductal gray matter. Dopaminergic activation was observed in the ventral basal ganglia, including the nucleus accumbens. Regional DA and opioid activity were associated with the anticipated and subjectively perceived effectiveness of the placebo and reductions in continuous pain ratings. High placebo responses were associated with greater DA and opioid activity in the nucleus accumbens. Nocebo responses were associated with a deactivation of DA and opioid release. Nucleus accumbens DA release accounted for 25% of the variance in placebo analgesic effects.Conclusions: Placebo and nocebo effects are associated with opposite responses of DA and endogenous opioid neurotransmission in a distributed network of regions. The brain areas involved in these phenomena form part of the circuit typically implicated in reward responses and motivated behavior.

PURPOSE:To clarify the section showing minimal intraindividual variations in the movement of the mandibular incisal point during mastication of softened chewing gum.METHODS:Twenty healthy subjects were asked to chew softened chewing gum on the habitual side for 20 seconds. The change in the spatial parameters (gape and masticatory width) and temporal parameter (cycle time) were investigated for 20 cycles from the first cycle. The coefficients of variation of these parameters were investigated for each of 10 consecutive cycles (first to eleventh series).RESULTS:The spatial and temporal parameters were maximal at the first cycle, decreased progressively until the fourth or fifth cycle, and then remained almost unchanged thereafter. The coefficients of variation of the parameters were maximal during the first series, decreased progressively until the fourth to sixth series, and then tended to increase gradually thereafter. Minimal coefficients of variation were observed during the fifth and sixth series for the gape, during the fifth series for the width, and during the fourth series for the cycle time.CONCLUSION:These results suggest that the ten cycles after the fourth to the sixth cycle was the section showing minimal intra-individual variations in the masticatory movement during the chewing of softened chewing gum.

Expectations, positive or negative, are modulating factors influencing behavior. They are also thought to underlie placebo effects, impacting perceptions and biological processes. Using healthy human subjects, we examined the role of the nucleus accumbens (NAC), a region centrally involved in the encoding of reward expectation, in the formation of placebo responses. Employing functional molecular imaging, activation of NAC dopamine (DA) release was observed during placebo administration and related to its anticipated effects, perception-anticipation mismatches, and placebo effect development. In additional functional MRI studies, the expectation of monetary gain increased NAC synaptic activity in a manner proportional to placebo-induced DA release, anticipated effects, perception-anticipation differentials, and actual placebo effects. Individual variations in NAC response to reward expectation accounted for 28% of the variance in the formation of placebo analgesia.

Positron Emission Tomography (PET) with appropriate radiotracers and quantification methods allows the detection of changes in endogenous neurotransmission by determine the reduction in the binding potential (BP) of receptors before and after experimental challenges. These have typically employed psychostimulants and PET with dopamine (DA) receptor radiotracers. However, reductions in BP persist far beyond the increases in the release of the endogenous neurotransmitter, an effect ascribed to receptor internalization and recycling, a possible confound in repeated studies. Here we examined the time‐course of changes in BP during a nonpharmacological challenge, moderate levels of sustained pain, shown to induce robust reductions in μ‐opioid and DA D2 BP, as measured with [ 11 C]carfentanil and [ 11 C]raclopride. It was hypothesized that, contrary to pharmacological probes, the use of a more “physiological” stimulus would not be associated with persistent changes in the BP measures. The pain challenge was associated with reductions in μ‐opioid receptor BP in several cortical and subcortical regions. These did not persist in a subsequent scan. Similar results were obtained for DA D2 receptor BP, where the pain challenge induced significant reductions in the caudate nucleus. These data demonstrate that changes in receptor BP induced by a nonpharmacological challenge did not persist into subsequent scans. They further suggest differences in the effect of pharmacological and nonpharmacological probes on PET BP measures. These may reflect varying levels of change in receptor affinity, receptor internalization, and recycling depending on the type of challenge employed. Synapse 61:707–714, 2007. © 2007 Wiley‐Liss, Inc.

Most practicing dentists perceive the subject of temporomandibular joint (TMJ) diseases and disorders (TMJDs) as one of controversy, fueled by intense arguments about the relationship between the dental occlusion and the state of health of the masticatory system. Will dentistry ever again be able to think freely about this matter? How will we unravel the etiopathogenesis of the TMJDs when faced with strong convictions and consumed by an emotionally charged debate? When are negative results about the link between the occlusion and TMJDs sufficient to examine alternative lines of inquiry of the pathogenesis of TMJDs? How will we ever be in a position to isolate and reevaluate the uncomfortable factual irregularities that do not fit the prevailing explanatory models of TMJDs? How can one practice according to the evidence if the evidence is not predicted by the popular models of disease causation? It appears that we have reached a stage in understanding where the original literature needs to be reassessed based on BMethods and Materials[ and BResults[ rather than the motivations and constructs expressed in the BIntroduction[ and BDiscussion[ sections. Influenced by powerful trends in science at-large, the field of TMJD is at a point where it is expected that traditional concepts will rapidly loose appeal and that the field of TMJD will gain significant new momentum.

Unraveling the pathways and neurobiological mechanisms that underlie the regulation of physical and emotional stress responses in humans is of critical importance to understand vulnerability and resiliency factors to the development of a number of complex physical and psychopathological states. Dysregulation of central stress response circuits have been implicated in the establishment of conditions as diverse as persistent pain, mood and personality disorders and substance abuse and dependence. The present review examines the contribution of the endogenous opioid system and μ-opioid receptors to the modulation and adaptation of the organism to challenges, such as sustained pain and negative emotional states, which threaten its internal homeostasis. Data accumulated in animal models, and more recently in humans, point to this neurotransmitter system as a critical modulator of the transition from acute (warning signals) to sustained (stressor) environmental adversity. The existence of pathways and regulatory mechanisms common to the regulation of both physical and emotional states transcend classical categorical disease classifications, and point to the need to utilize dimensional, “symptom”-related approximations to their study. Possible future areas of study at the interface of “mind” (cognitive–emotional) and “body” (physical) functions are delineated in this context.

The activation of pain-suppressive, endogenous opioid neurotransmission after administration of a placebo with expectation of analgesia has been directly demonstrated in humans using molecular imaging techniques in recent work. Regional effects were described in the dorsolateral prefrontal cortex, pregenual anterior cingulate, anterior insula, and nucleus accumbens. However, it was also observed that the magnitude of these responses was subject to substantial individual and regional variation. The present study was undertaken to examine the contribution of various factors to the observed variability in the neurochemical responses to placebo administration. Multiple regression analyses were conducted on data from 19 healthy males to study to what degree expectations of analgesia and various elements of the experience of pain itself, in the absence of placebo, were associated with the individual and brain regional variability in endogenous opioid neurochemical responses to placebo. A model that included affective qualities of pain, the volume of algesic stimulus required to maintain pain over the experimental period within a moderate range, and the internal affective state of the volunteers contributed to 40–68% of the variance in the regional neurochemical responses to placebo. These initial data suggests that in the case of endogenous opioid mediated placebo analgesic responses, the individual experience of pain, in particular its affective elements, the internal affective state of the individuals during pain and a measure of sustained pain sensitivity are important factors contributing to the formation of a placebo effect. Further examination of individual variations in placebo responding will need to take into account the underlying process for which relief is required.

Objective: Synaptic β -endorphin and μ-opioid receptors are intimately involved in responses to stress. Sex differences noted in opioid-mediated stress response mechanisms may be due to the effects of gonadal steroids on vulnerability factors. We examined the psychophysical and μ-opioid neurotransmitter responses to a model of physical and psychological stress in women under two hormonal conditions. Design: This study was an intrasubject design during low estradiol and high estradiol states with each subject receiving a sustained pain-stress challenge and placebo in a randomized order, in each hormonal condition. Materials and Methods: Eight female healthy volunteers were studied with positron emission tomography (PET) and the selective μ-opioid radiotracer [C-11]carfentanil during the early follicular phase of the menstrual cycle (low estradiol, low progesterone state) and again during the same phase of the cycle after 7–10 days of treatment with transdermal estradiol patches (0.4 mg/day) (high estradiol, low progesterone state). Two experimental conditions were employed during each hormonal condition: a non-painful saline control state, and a 20 minute moderate pain state induced by the infusion of small amounts of hypertonic saline into the masseter (jaw) muscle. Pain was maintained at a constant level (40 VAS units) by the use of an adaptive computer controlled infusion system and every 15 second ratings of current pain by the volunteers. Measures of μ-opioid receptor binding potential (BP) were obtained with Logan plots with the occipital cortex as the reference region. μ-Opioid system activation was quantified as the reductions in BP from saline control to pain conditions. Results: Hormone treatment elevated estradiol plasma concentrations to levels comparable to those achieved during the periovulatory period. Estradiol treatment was associated with significant increases in baseline μ-opioid receptor BP in the anterior thalamus, nucleus accumbens, ventral pallidum and amygdala, bilaterally (z-values 4.0–6.6, p<0.05 after correction for multiple comparisons). Mu-opioid system activation in response to the pain challenge was enhanced after treatment with estradiol. Significantly higher μ-opioid system activation in the high estradiol, compared to the low estradiol studies, was detected in the anterior and posterior thalamus, nucleus accumbens and amygdala, bilaterally (z-values 4.8–6.7, p<0.05 after correction for multiple comparisons). Conclusion: These data demonstrate that estradiol has important effects on neurotransmitter systems, such as the endogenous opioid, which is involved in the regulation of stress and affective responses and reproduction.

Responses to pain and other stressors are regulated by interactions between multiple brain areas and neurochemical systems. We examined the influence of a common functional genetic polymorphism affecting the metabolism of catecholamines on the modulation of responses to sustained pain in humans. Individuals homozygous for the met(158) allele of the catechol-O-methyttransferase (COMT) polymorphism (val(158)met) showed diminished regional mu-opioid system responses to pain compared with heterozygotes. These effects were accompanied by higher sensory and affective ratings of pain and a more negative internal affective state. Opposite effects were observed in val(158) homozygotes. The COMT val(158)met polymorphism thus influences the human experience of pain and may underlie interindividual differences in the adaptation and responses to pain and other stressful stimuli.

In their critical analysis of the literature, Maekawa et al examine available data regarding the connection among fibromyalgia, Raynaud-like symptoms, cardiovascular dysfunction, and altered intramuscular perfusion. They identified many shortcomings of the clinical literature, which caused them great difficulty in sorting and summarizing of the available information. This process represents the major contribution of this critical review. Factors of concern with studies reviewed by Maekawa et al dealt with matters of experimental study design, case definition, and level of comorbidity of study samples, concomitant medication effects, and variations in the study environment and examination techniques to which patients were subjected. After recognizing, acknowledging, and weighting inherent study limitations and judging the evidence by using best clinical judgment, the authors draw conclusions that should spark discussion and hopefully further investigation. Unlike Raynaud-like symptoms and cardiovascular dysfunction, intramuscular hypoperfusion appeared to be a prominent and consistent feature of fibromyalgia syndrome for which, according to deductions presented by the authors, “agonist-induced β-adrenergic receptor desensitization” appears as the most likely mechanism explaining the change in muscle perfusion. Overall, the critical review deals with the contribution of the autonomic nervous system to fibromyalgia syndrome, a subject matter that is clearly not receiving as much consideration in research as it should. Scientific advancement has been slow because of the phenomenologic complexity and the lack of suitable investigative tools for human use and/or the absence of exciting animal models mimicking critical features of the human pathology. Although microneurography has provided important insight into autonomic control mechanisms in humans, few laboratories and investigators have reached the necessary technologic sophistication. On the other hand, the most established animal model involving adrenergic receptors, the β3AR knockout mouse, is suitable for hypothesis testing with respect to the maintenance of body temperature and obesity. However, it offers little for the kind of questions that the authors of the critical review have posed, but more suitable model systems are being developed. Maekawa et al should be commended for raising the awareness of processes mediated by adrenoceptors, particularly regarding the control of blood vessel diameter in skeletal muscle. Although the tight focus of this critical review represents its most significant strength, it also constitutes its weakness. The authors recognize this fact by briefly acknowledging a number of potentially important downstream effects or interactions in peripheral tissue in support of alternative interpretations. The dismissal of factors that would otherwise shift attention away from their hypothesis of agonist-induced β-adrenergic receptor desensitization can be justified for reasons of stimulating interest for an understudied subject matter. In view of possible alternative interpretations, it remains to be seen, however, whether agonist-induced β-adrenergic receptor desensitization plays a causal role in the initiation or persistence of pain associated with fibromyalgia syndrome. One of the key questions that enter my mind relates to the nature of the link between the proposed phenomenon of agonist-induced β-adrenergic receptor desensitization and the hallmark feature of fibromyalgia syndrome, mechanical allodynia. According to Maekawa et al, the weighted evidence moderately supports the view of altered muscle hemodynamics, notably a state of muscle hypoperfusion. This finding triggered the authors to ask (1) how muscle hypoperfusion may be caused and (2) how a reduced state of muscle perfusion may cause pain. Research performed in the laboratory convincingly shows that hypoxia or ischemia causes significant increases in neuronal discharges in muscle afferents.5Mense S Stahnke M Responses in muscle afferent fibres of slow conduction velocity to contractions and ischaemia in the cat.J Physiol (Lond). 1983; 342: 383-397Google Scholar However, there remains the question whether the conditions studied in the laboratory approximate the situation encountered in the painful muscle of fibromyalgia patients with respect to the magnitude of the altered hemodynamics. Unlike the acute effects produced in the laboratory, the idea has been put forth in the clinical literature that (1) anatomic abnormality of the capillary bed and (2) abnormality of the control system underlying the adjustment of the vascular diameter may be the reasons for altered hemodynamics in persistently painful muscle. However, definitive answers will not be obtained from studies involving patients because of the unavoidable, complicating, and confounding factors also encountered by Maekawa et al in the process of sorting the clinical evidence. These issues constitute a major impediment to the advancement of the respective clinical science. For example, causality issues are not easily resolved by comparing the vascular system of patients and matched control subjects because confounding factors, such as muscle deconditioning associated with states of persistent pain, are likely to alter the capillary bed of the affected muscle. Clearly, an appropriate model system is required to address issues of causality involving anatomic blood vessel abnormality. As far as the presence of abnormality in the control mechanism of the vascular diameter is concerned, clinical investigators are not only faced with almost insurmountable complexity but also with the lack of convenient research tools. Therefore, it should be obvious that appropriate model systems are needed to reduce the naturally occurring complexity to reach the next level of system's understanding. It is important to recognize that the effect of stimulation (agonist) of β1- and β2-adrenoceptors is tissue specific, involving increased contractility of the myocardium, relaxation of the intestine, and dilation of blood vessels as examples. On the other hand, blockade (antagonist) of β1- and β2-adrenoceptors causes reduced contractility of the myocardium, and constriction of blood vessels, however, has no effect on the intestine. Tissue-specific densities of adrenoceptor subtypes appear to be in support of the behavioral and physical adaptation to pain-stress, including increased arousal and alertness, focused attention, increased temperature, suppression of appetite, feeding and reproduction, increased blood pressure, heart rate and respiratory rate, increased gluconeogenesis and lipolysis, and the direction of oxygen and nutrients to the central nervous system and the affected body site(s).1Chrousos GP Gold PW The concepts of stress and stress system disorders: Overview of physical and behavioral homeostasis.JAMA. 1992; 267 ([erratum JAMA 268:200, 1992]): 1244-1252Crossref PubMed Scopus (3186) Google Scholar Indeed, adrenoceptors are implicated in all of these processes. I would like to finish with a few comments regarding the central hypothesis put forth by Maekawa et al. Although not involving skeletal muscle, down-regulation of β1- and β2-adrenoceptors has been observed in advanced cases of coronary heart disease in terms of a reduction of both adrenoceptor subtypes in the myocardium. It has been postulated that elevated norepinephrine levels in plasma could be responsible for the down-regulation of myocardial β-adrenoceptors.2Hajjar RJ Muller FU Schmitz W Schnabel P Bohm M Molecular aspects of adrenergic signal transduction in cardiac failure.J Mol Med. 1998; 76: 747-755Crossref PubMed Scopus (50) Google Scholar, 3Kawai H Fan TH Dong E Siddiqui RA Yatani A Stevens SY Liang CS ACE inhibition improves cardiac NE uptake and attenuates sympathetic nerve terminal abnormalities in heart failure.Am J Physiol. 1999; 277: H1609-H1617PubMed Google Scholar, 4Khamssi M Brodde OE The role of cardiac beta1- and beta2-adrenoceptor stimulation in heart failure.J Cardiovasc Pharmacol. 1990; 16: S133-S137Crossref PubMed Scopus (33) Google Scholar Maekawa et al seem to extend this hypothesis from myocardium to skeletal muscle, proposing that the increased availability of norepinephrine results in the down-regulation of likely β2-adrenoceptors in blood vessels of muscle. As illustrated in Fig 1, which diagrammatically depicts the controlling elements in the diameter of blood vessels in muscle, muscle hypoperfusion can be mediated by a number of potential neuronal signals and signaling molecules, including the postulated agonist-induced β-adrenergic receptor desensitization by the authors of the critical review.Unclear is whether the stated hypothesis is consistent with epidemiologic and phenomenologic facts, such as the preponderance of women in the reproductive years and the predilection of specific muscle groups in fibromyalgia syndrome. At the local level, as shown in Fig 1, plasma factors, endothelium-derived molecular signals, and both prejunctional and postjunctional effects can potentially modulate the vascular diameter. Distant effects at the level of the central nervous system, mediated by heavy or prolonged barrage of vascular afferent fibers (or other primary muscle afferent), could result in neuroplastic changes within the central nervous system, which, in turn, would cause pathologic sympathetic activity. However, there is one important point to keep in mind in this discussion. If changes in vessel diameter, caused by any of these presumed effects, do not produce a state of muscle hypoperfusion, which, in turn, contributes to the onset and persistence of pain, the phenomenon discussed here may have little causal significance. Instead, it could represent nothing but one of the many adaptive consequences of pain. According to Maekawa et al, only research will provide the answer.

The processing of noxious and non-noxious sensations differs between chronic pain syndromes, and we believe that studies of sensory processing in the presence of pain will help to clarify the aetiology of the conditions. Here we measured in humans the threshold-level mechanosensitivity in tonic experimental muscle pain. We found (1) that muscle pain induced by hypertonic saline reduced cutaneous threshold-level mechanosensitivity at the site of pain and at the mirror site in the contralateral face, (2) that this effect outlasted the sensation of pain, (3) that it was more pronounced when the painful area was reported to be large, and (4) that the loss of mechanosensitivity was greater in males than females. Comparing our findings to results obtained with other pain models, all classes of nociceptors do not seem to have the same effect on cutaneous mechanosensitivity. The observed threshold-level hypoesthesia is consistent with the hypothesis that the increased mechanical thresholds found in clinic cases of temporomandibular disorders and cervicobrachialgia are a direct result of the activation of muscle nociceptors.

Conditions involving chronic orofacial pain represent a major health problem, and patients with persistent pain are difficult to manage successfully. These conditions are often comorbid with additional health issues such as sleep disturbances, cardiovascular, gastrointestinal and reproductive system complaints, weight loss or weight gain, swelling, numbness, sweating and flushing, and concerns regarding loss of libido, drive, attention, and memory. Neuroendocrine and autonomic pain-stress responsivity and the consequences of pain for sensory, motor, immune and reproductive functions, and mood seem to account for the broad range of comorbid complaints. Susceptibility to a particular response appears to explain intra-individual differences in disease expression. Understanding of these regulatory, mostly adaptive processes will support novel treatments to manage many troublesome comorbid complaints for which current approaches are unsatisfactory.

Although epidemiologic work has shown great success in diseases that are caused by a single pathogen, the socioeconomic impact created by chronic, debilitating conditions calls for the use of the epidemiologic method in these diseases to arrive at a better understanding of the web of events in their causation. Considering the topic of interest, current knowledge does not support the notion that the masticatory muscle disorders are any different from the painful muscle afflictions in other regions of the human body. However, the tactile sensibility of the tooth support makes the masticatory apparatus unique in that significantly smaller differences can be perceived in this region than in any other musculoskeletal system of the body. Therefore it is not surprising that bi te shifts or teeth no longer fitting r ight have been reported by patients with temporomandibular disorders (TMDs). As a result, the dental profession has had a long-standing interest in these disorders and a plethora of occlusal treatments have been developed to address the bite complaints. It is the belief of many providers that most cases with masticatory myalgia are treated effectively by managing the dental occlusion. Therefore, failure to resolve a jaw pain problem is perceived by some as a clinician' s inadequacy to provide the patient with an acceptable occlusal scheme. In recent years, however, a reassessment of this point of view was triggered by epidemiologic work and the impression gained in tertiary-care clinics that there exists a group of patients withj aw muscle pain for whom this treatment paradigm does not bring any lasting relief. I f the problem did not resolve with a proper occlusion, psychological reasons are typically used to explain the failure. The question arises as to whether we should pursue more aggressively the popular occlusaltreatment paradigm or whether we should abandon this paradigm, which appears to be incorrect. This issue has become a counterproductive controversy.