Pentti Kemppainen

Review of aetiological concepts of temporomandibular pain disorders: towards a biopsychosocial model for integration of physical disorder factors with psychological and psychosocial illness impact factors

Several studies have reported that musculoskeletal disorders of the stomatognathic system, commonly known as temporomandibular disorders (TMD) resemble musculoskeletal disorders and chronic pain disorders in general. There is also general consensus that combined biomedical and biopsychosocial methods best support the assessment and management of the cardinal features of TMD, i.e., pain and dysfunction or physical (peripheral) and psychosocial (central) factors. This overview of the aetiology of TMD will outline conceptualizations of past models and present the current view that patients with TMD should be assessed according to both the physical disorder and the psychosocial illness impact factors. The conceptual theories outlined in this review include biomedical models related to temporomandibular joints, muscles of mastication and occlusal factors, psychological models and the biopsychosocial models. An integrated and multidimensional approach concerning physical and psychosocial factors in temporomandibular pain and dysfunction is presented as an example of how the biopsychosocial model and information processing theory may apply in the conceptualization and management of TMD for various health care professionals.

Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: A selective role for endogenous opioids

Ischemic pain was produced by a blood pressure cuff placed to the arm of healthy human subjects for 15 min which produced a mean pain score of 59% (visual analogue scale). Ischemia induced a significant dental pain threshold elevation (mean 67%) and 2 mg of naloxone did not reduce it. Thermal sensitivity of the upper lip had a tendency to reduction during ischemia and 2 mg of naloxone reduced this effect. Tactile thresholds in the forehead or in the contralateral arm were not markedly elevated. Neither ACTH nor prolactin level in the plasma was related to the dental pain threshold elevation during ischemia. The findings of the present study suggest that ischemic pain nonsegmentally produces a predominant inhibition of responses to thin afferents. Endogenous opioids may markedly contribute to the reduction of thermal sensitivity induced by ischemia, but their contribution to dental pain threshold elevations seems to be less important. Stress or other adenohypophyseal mechanisms involving the release of ACTH or prolactin do not explain the effects of ischemia found in the present study.

Modification of dental pain and cutaneous thermal sensitivity by physical exercise in man

The effect of physical exercise on dental pain thresholds, the release of pituitary stress hormones and thermal sensitivity of skin was tested in healthy human subjects. Different levels of exercise (100-300 W) at different pedal frequencies were produced by a cycle ergometer. Thermal limen (the interval between warm and cool thresholds) determined from glabrous hand, hairy forearm and leg was used as a parameter of thermal sensitivity. In all subjects the heart rate and blood pressure were increased with increasing work load. Dental pain thresholds were elevated at high work loads with a concomitant activation of pituitary stress hormone (especially growth hormone) release. Thermal limens at all 3 sites were increased work load, too, independent of the pedal frequency. The increase of thermal limen was most marked in the leg and least in the glabrous hand. The results indicate that physical exercise produces a non-segmental, load-dependent decrease of pain and thermal sensitivity with a concomitant activation of pituitary stress mechanisms. The magnitude of modification varies with skin region. Activation of inhibitory mechanisms at spinal levels via muscle and proprioceptive afferents, in a way suggested by the gate control theory of pain mechanisms, seems to have only a minor, if any, contribution to the present findings, since a higher pedal frequency did not produce a more marked decrease of sensitivity.

A comparative prospective clinical study of two single-tooth implants: A preliminary report of 102 implants

STATEMENT OF PROBLEM Treatment of tooth loss in the anterior maxilla can involve difficult functional, esthetic, and psychologic problems, especially in young patients with otherwise good dentition. PURPOSE The purpose of this study was to provide a preliminary comparative evaluation of two implants (ITI and Astra) in single-tooth restorations. MATERIAL AND METHODS This prospective study of 102 single-tooth replacements with 56 ITI and 46 Astra dental implants was performed in 82 patients at the Finnish Student Health Service Foundation. One Astra implant was lost before loading. The overall survival rate of the implants was 97.8% for Astra implants and 100% for the ITI system. After the initial healing period of at least 6 months, the remaining 101 implants (56 ITI, 45 Astra) were free of periimplant infection and revealed no detectable mobility. Radiographs did not reveal signs of periimplant radiolucencies. All 101 implants received single-tooth crowns. RESULTS Periimplant parameters and acceptable implant function were examined and demonstrated satisfactory results with preestablished clinical parameters and radiographs at 1 year. During the observation time the mean marginal bone loss was 0.13 mm with Astra implants and 0.11 mm with ITI implants. Subjectively all patients were satisfied with their single-tooth restorations supported by either ITI or Astra dental implants. CONCLUSION The favorable results of this short-term study support the application of the two implant systems for single-tooth restorations, especially in the anterior region of the maxilla.

Effect of systemic medetomidine, an alpha2 adrenoceptor agonist, on experimental pain in humans

The effect of systemic (intravenous) medetomidine, an alpha-2 adrenoceptor agonist, on pain thresholds was studied in healthy human subjects (n = 6). Medetomidine produced a dose-dependent (cumulative doses: 25 and 50 micrograms) sedative effect evaluated by visual analog scale. Also, a dose-dependent decrease of blood pressure but not of heart rate was seen after administration of medetomidine. Pain threshold to electric stimulation of the tooth pulp and cutaneous heat pain threshold were uninfluenced by medetomidine. An index of cutaneous thermal sensitivity to innocuous stimuli, the width of the thermoneutral zone, also was uninfluenced by medetomidine. Medetomidine produced a significant attenuation of the affective-motivational component (unpleasantness) of tourniquet-induced ischemic pain, whereas the sensory-discriminative component (pain magnitude estimate) of the ischemic pain was not attenuated. The results suggest that systemic medetomidine alone at subanesthetic but sedative and hypotensive doses does not significantly influence the intensity and thresholds of experimental pain, whereas the affective-motivational component of pain can be attenuated.

Dexamethasone attenuates exercise-induced dental analgesia in man

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.

Cortical representation of experimental tooth pain in humans

&NA; Cortical processing of electrically induced pain from the tooth pulp was studied in healthy volunteers with fMRI. In a first experiment, cortical representation of tooth pain was compared with that of painful mechanical stimulation to the hand. The contralateral S1 cortex was activated during painful mechanical stimulation of the hand, whereas tooth pain lead to bilateral activation of S1. The S2 and insular region were bilaterally activated by both stimuli. In S2, the center of gravity of the activation during painful mechanical stimulation was more medial/posterior compared to tooth pain. In the insular region, tooth pain induced a stronger activation of the anterior and medial parts. The posterior part of the anterior cingulate gyrus was more strongly activated by painful stimulation of the hand. Differential activations were also found in motor and frontal areas including the orbital frontal cortex where tooth pain lead to greater activations. In a second experiment, we compared the effect of weak with strong tooth pain. A significantly greater activation by more painful tooth stimuli was found in most of those areas in which tooth pain had induced more activation than hand pain. In the medial frontal and right superior frontal gyri, we found an inverse relationship between pain intensity and BOLD contrast. We concluded that tooth pain activates a cortical network which is in several respects different from that activated by painful mechanical stimulation of the hand, not only in the somatotopically organized somatosensory areas but also in parts of the ‘medial’ pain projection system.

The importance of stimulus site and intensity in differences of pain-induced vascular reflexes in human orofacial regions.

&NA; Studies in anaesthetized animals have indicated that noxious stimulation may produce marked blood flow changes in various orofacial structures, but the influence of painful stimulation on the blood flow regulation of the orofacial area of humans has been studied only to a limited extent. The purpose of this investigation was to study whether there are differences in temporal and spatial patterns of pain‐induced vasoactive reflexes between various orofacial regions and hand in healthy human volunteers. Dynamic changes in blood flow in various orofacial regions elicited by painful stimulation of the tooth and finger were measured by means of Laser Doppler imaging (LDI) and computer‐assisted infrared thermography (IRT). Blood flow of the finger was recorded by laser Doppler flowmetry (LDF) and plethysmography (PLET). During both stimulus paradigms there was a transient elevation in heart rate (HR) and blood pressure (BP). At the same time there was a significant blood flow decrease in the finger (LDF, PLET) and in the nose (LDI, IRT). In contrast to tooth stimulation, finger stimulation caused a more marked blood flow reduction in the finger. Only high intensity tooth stimulation, but not finger stimulation, caused a long‐lasting vasodilatation both in lower and upper lip. The blood flow changes in the lips were not correlated with changes in systemic blood pressure or heart rate. In the cheek, there were no marked flow changes during either finger or tooth stimulation. These data indicate that painful tooth (regional) stimulation, but not finger (remote) stimulation, can induce a long‐lasting vasodilatation in parts of orofacial tissues which cannot be explained by changes in central cardiovascular parameters. This tooth‐stimulation‐induced blood flow increase supports the hypothesis of a special vasodilator reflex mechanism in the orofacial area. Furthermore, tooth‐stimulation‐induced vasoconstriction in the nose and dilatation in the lips indicate that separate vasoactive reflex mechanisms may exist for different orofacial regions.

Blood flow increase in the orofacial area of humans induced by painful stimulation

The purpose of this study was to investigate if painful stimulation produces blood flow changes in the tooth pulp and the facial skin in humans. Also, we attempted to find out if the possible blood flow changes induced by painful stimulation could be explained by central sympathetic and parasympathetic reflex mechanisms, by an antidromic activation of nociceptive axons (axon reflex), or by a change in central cardiovascular parameters. Laser Doppler flowmeter was used to assess the blood flow changes. Electrical tooth pulp stimulation at painful intensities induced a blood flow increase in the ipsilateral lip adjacent to the stimulus site, and vice versa. Nonpainful stimulation had no effects. Painful thermal stimulation of the upper lip also produced an increase in the blood flow of the ipsilateral upper incisor. The blood flow changes in the lip produced by dental stimulation were not correlated with changes in systemic blood pressure or heart rate. Painful electrical stimulation of the hand did not induce any changes in the pulpal blood flow, whereas painful dental stimulation produced a blood flow decrease in the finger but no change in the contralateral lip or cheek. In monkey experiments a regional block of the central conduction of the inferior alveolar nerve at the level of the mandibular foramen produced varying results: the blood flow increase in the lower incisor produced by noxious thermal stimulation of the ipsilateral lower lip was not abolished in two experiments but was abolished in other two experiments. It is concluded that painful stimulation can induce significant increases in the blood flow of the orofacial regions in humans. This increase is predominantly restricted to the region adjacent to the stimulus site and cannot be explained by changes in the central cardiovascular parameters. Central neuronal reflex mechanisms and an axon reflex may both underlie these blood flow increases.

Lowered cutaneous sensitivity to nonpainful electrical stimulation during isometric exercise in humans.

SummaryThe effect of isometric exercise on cutaneous sensitivity to nonpainful electric stimulation was studied in human subjects. The exercises consisted of brief (duration: 1–10 s) palmar flexions of the hand or foot against varying loads (10–30% of the maximal force). A visual “go” cue was used to indicate the start and end of the exercise. Isometric hand exercise produced a load-dependent increase of electrotactile thresholds of the fingers. The threshold elevation was rapidly attenuated with prolonged duration of the exercise. The hand exercise-induced threshold elevation was of equal magnitude in the glabrous and hairy skin of the fingers. Thresholds were not changed for the hand contralateral to the exercising hand. Passive static pressure of the hand did not produce threshold changes, whereas activation of afferent inhibition by a vibrotactile stimulus (100 Hz, 0.1 mm) did produce a significant threshold elevation. Exerciseinduced threshold elevation was also significant immediately prior to the EMG response of the arm but not at the time of the visual “go” signal, or before it. The threshold increase found during the EMG response was not significantly stronger than that found prior to the EMG response. These results suggest that isometric exercise load-dependently produces a phasic, rapidly attenuating increase in cutaneous tactile thresholds in the exercising limb but not multisegmentally. Corollary efferent barrage from motor to sensory structures of the brain could be underlying the threshold changes produced by isometric exercise, whereas afferent inhibitory mechanisms seem to have only a minor role.