Long-term side effects on the temporomandibular joints and oro-facial function in patients with obstructive sleep apnoea treated with a mandibular advancement device.

Patients with obstructive sleep apnoea (OSA) in long-term treatment with a mandibular advancement device (MAD) to increase the upper airway space may develop changes in the temporomandibular joint (TMJ) and the oro-facial function due to the protruded jaw position during sleep. The aim was to investigate the influence of long-term MAD treatment on the TMJs, oro-facial function and occlusion. This prospective study included 30 men and 13 women (median age 54) with OSA [Apnoea-Hypopnoea Index (AHI): 7-57]. They were examined with the Nordic Orofacial Test Screening (NOT-S), the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) and cone beam computed tomography (CBCT) of the TMJs. The examination was performed before MAD treatment (T0), and 3-6 months (T1, no CBCT), 1 year (T2) and 3 years (T3) after treatment start. The results were analysed as long term (T0-T3, n = 14) and short term (T0-T2, n = 24) by t-test, Fisher's exact test and anova. Both long- and short-term analyses revealed a reduction in AHI (P < 0·002). Significant long term were increased scores in the NOT-S Interview (P < 0·045), reduced vertical overbite (P < 0·031) and increased jaw protrusive movement (P < 0·027). TMJ changes were found as joint sounds in terms of reciprocal clicking and crepitus, short term as a decrease and subsequent recurrence (P < 0·053; P < 0·037). No significant radiological changes were found. In conclusion, MAD treatment is beneficial to some OSA patients, but might induce changes in the TMJs, the oro-facial function and the occlusion. However, these changes seemed to be less harmful than previously reported with careful adaptation, control and follow-ups.

Repeated treatments of drooling with botulinum toxin B in neurology.

OBJECTIVES: To investigate efficacy, saliva flow, and composition in repeated BoNT-B treatments of drooling. MATERIALS AND METHODS: Seventeen neurological patients (median 66 years), referred for treatment of drooling participated in this observational study. Median total doses of 4000 units botulinum toxin type B (BoNT-B, Neurobloc(®)) were injected with at least 3 months intervals into parotid and submandibular glands using ultrasound guidance. Measures of drooling and saliva collection for analysis were obtained before treatment, and 6, 12, and eventually 18 weeks after. RESULTS: Number of treatment series in each patient was 1-7. Compared to baseline, saliva flow rate and drooling were reduced 30-70% 6 weeks after treatment in the first series, while sodium, chloride, and total protein increased 20-80% (t-tests; P < 0.05). After 12 weeks, drooling was still significantly reduced, saliva flow tended to be, and saliva composition was back to baseline. Frequent side effects were viscous saliva and dry mouth. Due to fading effect in eight patients, individual decisions were taken to change from BoNT-B to BoNT-A. Similarly, the outcome was significantly reduced over time in six patients completing five subsequent BoNT-B treatment series (ANOVA; P < 0.05). CONCLUSION: In the first series, BoNT-B treatment resulted in marked reduction of drooling and saliva flow rate with some relapse after 12 weeks. The viscous saliva was ascribed to increased total protein content and compensatory mechanisms related to ß-adrenergic receptor-specific actions. With patients needing long-term treatment, it should be noted that the efficacy of repeated BoNT-B may fade with time.

Evaluation of the total adenylate (ATP + ADP + AMP) test for cleaning verification in healthcare settings.

INTRODUCTION: Evaluation of cleaning methods is the first step in the prevention of healthcare-associated infections. ATP hygiene monitoring tests are widely used for assessing the effectiveness of cleaning procedures. The test is easy to use and gives immediate results, however, ATP can be metabolized and degraded to ADP and AMP. Recently, a total adenylate [ATP + ADP + AMP(A3)] monitoring test has been developed. Our objective was to evaluate the usefulness of the A3 test for cleaning verification in healthcare settings. METHODS: The detection sensitivities of the ATP and the A3 tests were compared using blood, and debris derived from gloved-hand method and endoscopes immediately after endoscopic examination. The performance of the A3 test in monitoring cleanliness of high touch surfaces in the hospital and endoscopes at each cleaning step was also evaluated. RESULTS: For the hemolysate, the measurement values of the A3 test were stable, although ATP was promptly degraded. In debris from hands, the amount of A3 was 20 times higher than that of ATP. The detection sensitivities of the A3 test on residues derived from gastroscopes and colonoscopes were 3 and 8 times higher, respectively, than those from the ATP test. A field study indicated that a large number of microorganisms tend to show high A3 values on high touch surfaces in the hospital and on endoscopes. CONCLUSIONS: The A3 test showed higher detection sensitivities than the conventional ATP test for organic debris associated with healthcare settings.

Increased microvascular permeability in mice lacking Epac1 (Rapgef3).

AIM: Maintenance of the blood and extracellular volume requires tight control of endothelial macromolecule permeability, which is regulated by cAMP signalling. This study probes the role of the cAMP mediators rap guanine nucleotide exchange factor 3 and 4 (Epac1 and Epac2) for in vivo control of microvascular macromolecule permeability under basal conditions. METHODS: Epac1-/- and Epac2-/- C57BL/6J mice were produced and compared with wild-type mice for transvascular flux of radio-labelled albumin in skin, adipose tissue, intestine, heart and skeletal muscle. The transvascular leakage was also studied by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) using the MRI contrast agent Gadomer-17 as probe. RESULTS: Epac1-/- mice had constitutively increased transvascular macromolecule transport, indicating Epac1-dependent restriction of baseline permeability. In addition, Epac1-/- mice showed little or no enhancement of vascular permeability in response to atrial natriuretic peptide (ANP), whether probed with labelled albumin or Gadomer-17. Epac2-/- and wild-type mice had similar basal and ANP-stimulated clearances. Ultrastructure analysis revealed that Epac1-/- microvascular interendothelial junctions had constitutively less junctional complex. CONCLUSION: Epac1 exerts a tonic inhibition of in vivo basal microvascular permeability. The loss of this tonic action increases baseline permeability, presumably by reducing the interendothelial permeability resistance. Part of the action of ANP to increase permeability in wild-type microvessels may involve inhibition of the basal Epac1-dependent activity.

Long-term consumption of an obesogenic high fat diet prior to ischemia-reperfusion mediates cardioprotection via Epac1-dependent signaling.

BACKGROUND: Obesity is still considered a risk factor for cardiovascular disease, although more recent knowledge also suggests obesity to be associated with reduced morbidity and mortality - the "obesity paradox". This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling. METHODS: Wild type (wt), Epac1 (Epac1-/-) and Epac2 (Epac2-/-) deficient mice were fed a high fat (HFD) or normal chow diet (ND) for 33 ± 1 weeks. Six experimental groups were included: (1) control wt ND (wt ND), (2) control wt HFD (wt HFD), (3) Epac1-/- mice on ND (Epac1-/-ND), (4) Epac1-/- mice on HFD (Epac1-/-HFD), (5) Epac2-/- mice on ND (Epac2-/-ND), and (6) Epac2-/- mice on HFD (Epac2-/-HFD). Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. Endpoints were infarct size and functional recovery. RESULTS: All groups fed a HFD presented with significantly enhanced body weight, visceral fat content and reduced glucose clearance compared to corresponding ND groups. Although the HFD cohorts presented with an overall comparable systemic capability to clear glucose, the Epac1-/- HFD group presented with glucose levels slightly above the human diabetes criteria at the end of the intraperitoneal glucose tolerance test (ipGTT). Moreover, the HFD significantly reduced infarct size in both wild type (wt HFD 41.3 ± 5.5% vs. wt ND 58.0 ± 9.8%, p < 0.05) and Epac2-/- cohorts (Epac2-/-HFD 34.4 ± 7.2% vs. Epac2-/-ND 56.5 ± 3.8%, p < 0.05). Interestingly, however, the HFD did not reduce infarct size in Epac1-/- deficient mice hearts (Epac1-/-HFD 65.1 ± 5.1% vs. Epac1-/-ND 56.1 ± 3.5%, ns.). CONCLUSION: Epac1-dependent signaling is involved in mediating the cardioprotection afforded by long-term feeding of an obesogenic high fat diet in mice hearts.

Mutually exclusive interactions of two nuclear orphan receptors determine activity of a cyclic adenosine 3',5'-monophosphate-responsive sequence in the bovine CYP17 gene.

ACTH-dependent transcriptional activation of the bovine CYP17 gene (the gene encoding cytochrome P450 steroid 17 alpha-hydroxylase) involves two cAMP-responsive sequences (CRS1 and CRS2) located in the promoter region. Here we demonstrate that two nuclear orphan receptors, chicken ovalbumin upstream promoter transcription factor (COUP-TF) and steroidogenic factor-1 (SF-1), bind to the part of the CRS2 element that contains the repeated sequences AAGTCA and AGGTCA spaced by six nucleotides (repCRS2). Overexpression of COUP-TF and SF-1 in both steroidogenic and nonsteroidogenic cells demonstrated that SF-1 is an activator of repCRS2-dependent transcription of reporter genes. Furthermore, the SF-1-dependent transcription could be further stimulated by activation of the cAMP-dependent protein kinase. In contrast, COUP-TF alone had no effect on repCRS2-dependent reporter gene activity. Mutations that interfere with the binding of SF-1 to repCRS2 in vitro abolished the cAMP-induced activities mediated by the element in transfected Y1 cells. The mutational analysis of repCRS2 further indicated that the binding sites for the two receptors overlap, and electrophoretic mobility shift assays demonstrated that the receptors bound in a mutually exclusive manner. Overexpression of both SF-1 and COUP-TFI simultaneously demonstrated that COUP-TFI inhibited SF-1-dependent activation of reporter genes. Transient transfection experiments with a construct containing a -100/+19 base pair fragment from the bovine CYP17 gene demonstrated that SF-1 and COUP-TF had similar effects on the intact promoter as on the repCRS2/reporter gene constructs. Our data suggest that the two orphan receptors bind in a mutually exclusive manner to repCRS2 and that SF-1 is involved in the activation and COUP-TF in the repression of repCRS2-dependent transcription.

A novel 3',5'-cyclic adenosine monophosphate-responsive sequence in the bovine CYP17 gene is a target of negative regulation by protein kinase C.

The bovine 17 alpha-hydroxylase cytochrome P450 gene (CYP17) contains at least two cAMP-responsive sequences (CRS) within its 5'-flanking region. In this study it is demonstrated that one of the sequences, CRS1, is also a target for protein kinase C (PKC)-mediated regulation. Forskolin-induced, CRS1-dependent transcription of a heterologous minimal promoter/structural gene which had been transfected into the mouse adrenocortical tumor cell line Y1 was suppressed by activation of PKC by phorbol esters such as 12-O-tetradecanoyl phorbol-14-acetate and phorbol 12,13-didecanoate-beta (PDD beta). Use of the active and inactive forms of PDD (PDD alpha and PDD beta) as well as down-regulation of PKC by prolonged treatment of the cells with 12-O-tetradecanoyl phorbol-14-acetate demonstrated that the effect of phorbol esters on transcription conferred by CRS1 was mediated through the PKC pathway and not a consequence of general toxicity to the cells. Analysis of the different steps in the signal transduction pathway between the adenylate cyclase and the CRS1 element suggests that phrobol esters do not exert their effect by altering the forskolin-induced cAMP production, activation of PKA, or the binding of nuclear proteins to CRS1. These results establish the CRS1 element as a target not only for PKA, but also for the PKC-mediated signal transduction pathway. They further suggest that PKC interferes with the transcriptional activation competence of factors bound to CRS1 and the minimal promoter.

Involvement of NK-1 and NK-2 tachykinin receptor mechanisms in jaw muscle activity reflexly evoked by inflammatory irritant application to the rat temporomandibular joint.

An electromyographic (EMG) study was carried out in 51 anesthetized rats to assess if neurokinin, NK-1 and NK-2, receptor mechanisms and tachykinins were involved in the increased jaw muscle activity which can be reflexly evoked by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint (TMJ) region. A baseline level of EMG activity was recorded bilaterally for 20 min from digastric (DIG) and masseter (MASS) muscles and then each animal was treated with NK-1 or NK-2 antagonist or vehicle. In one series of experiments either the NK-1 antagonist CP-99,994 (20 microg approximately 54 nmol), the NK-2 antagonist MEN-10,376 (10 microg approximately 9 nmol or 20 microg approximately 18 nmol) or vehicle (control) was administrated into the lateral ventricle (i.c.v.); in another series the NK-1 antagonist (4 mg/kg approximately 3-4 micromol/rat) or vehicle (control) was given intravenously (i.v.). After 10 min, MO (20 microl, 20%) was applied to one TMJ (first injection) and 45 min later, MO was applied to the opposite TMJ (second injection). Pretreatment with neurokinin antagonists had little effect on the incidence of the MO-evoked EMG responses but did significantly reduce the EMG magnitude and duration. In the animals pretreated with NK-1 antagonist only the responses to the second MO injection was significantly affected whereas NK-2 pretreatment reduced the EMG responses to both MO injections to the TMJ. The systematic depression of the MO-evoked EMG responses by the NK-2 antagonist suggests that neurokinin A may be involved in the EMG responses. Since the NK-1 antagonist produced no systematic changes in responses elicited by the first MO injection, substance P does not seem to be associated directly with the initiation or maintenance of the EMG responses but may be involved if a 'central sensitization' has been induced by the first MO injection to the TMJ.

Pituitary-specific knockout of steroidogenic factor 1.

Knockout mice lacking the orphan nuclear receptor steroidogenic factor 1 (SF-1) revealed its essential roles at multiple levels of endocrine development and function. These SF-1 knockout mice lacked adrenal glands and gonads, thereby manifesting adrenal insufficiency and sex reversal of their internal and external genitalia. Their pituitary gonadotropes failed to express several markers of normal differentiated function, and they lacked a specific hypothalamic nucleus, the ventromedial hypothalamic nucleus (VMH). Using the Cre-loxP system, we generated mice whose gene encoding SF-1 was inactivated specifically in the anterior pituitary. These pituitary-specific SF-1 knockout mice were sterile and never matured sexually. Their gonads weighed only approximately 5% of the weight of wild-type gonads. SF-1 immunoreactivity was absent in the anterior pituitary but was unaffected in the adrenal cortex, validating the selectivity of the gene targeting strategy. Consistent with an important role of SF-1 in gonadotropes, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were markedly decreased in the pituitary-specific SF-1 knockout mice. The pituitary-specific SF-1 knockout mice are a novel genetic model of hypogonadotropic hypogonadism and establish essential roles of SF-1 in gonadotropin expression.

Approaches to define the role of SF-1 at different levels of the hypothalamic-pituitary-steroidogenic organ axis.

Targeted gene disruption has produced knockout mice lacking the orphan nuclear receptor steroidogenic factor 1 (SF-1). These SF-1 knockout mice lacked adrenal glands and gonads, resulting in adrenocortical insufficiency and sex reversal of their internal and external genitalia. They also had impaired expression of pituitary gonadotropins and agenesis of the ventromedial hypothalamic nucleus (VMH), confirming roles of SF-1 at multiple levels of the hypothalamic-pituitary-steroidogenic tissue axis. Using the Cre-loxP system, we now have generated mice in which SF-1 is inactivated selectively in the anterior pituitary. These pituitary-specific SF-1 knockout mice were sterile and failed to exhibit sexual maturation. Histologically, their gonads were markedly hypoplastic, weighing only approximately 5% of the gonads of wild-type mice. Consistent with an important role of SF-1 in gonadotropes, there were no cells in the pituitary gland that expressed either follicle-stimulating hormone (FSH) or luteinizing hormone (LH). These pituitary-specific SF-1 knockout mice are a novel genetic model of hypogonadotropic hypogonadism and establish essential roles of SF-1 in gonadotropin expression.

SF-1: a critical mediator of steroidogenesis.

Studies in knockout mice have established that the orphan nuclear receptor steroidogenic factor 1 (SF-1) plays essential roles in the development and function of the primary steroidogenic organs. These SF-1 knockout mice lacked adrenal glands and gonads, causing adrenocortical insufficiency and sex reversal of their internal and external genitalia. They also had impaired expression of pituitary gonadotropins and agenesis of the ventromedial hypothalamic nucleus (VMH), confirming roles of SF-1 at all three levels of the hypothalamic-pituitary-steroidogenic organ axis. Ongoing experiments are directed at developing methods to inactivate SF-1 in a tissue-specific manner.

Morphine application to peripheral tissues modulates nociceptive jaw reflex.

This study assessed the effect of peripherally applied opioids on the electromyographic activity reflexly evoked in digastric and masseter muscles by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint. In 39 anaesthetized rats, local pretreatment of joint tissues with morphine (15 nmol) significantly depressed the jaw muscle responses compared with saline, and the depression was antagonized by simultaneous local injection of the opiate antagonist naloxone (2.7 nmol); systemic morphine pretreatment (15 nmol, i.v.) did not influence the muscle responses. The naloxone-reversible depression of the MO-evoked muscle responses by local, but not systemic morphine, supports the presence of peripheral opioid receptors that may have a role in modulating nociceptive responses.

Transcriptional regulation of the bovine CYP17 gene by cAMP.

The transcription of steroid hydroxylase genes is controlled by ACTH and cAMP in the adrenal cortex. In most instances the regulation appears to rely on transcription factors traditionally not associated with cAMP-dependent gene expression. For the non-traditional factors it remains necessary to elucidate the coupling of increases in intracellular cAMP and cAMP-dependent protein kinase (PKA) activity to the function of these proteins. The bovine CYP17 gene, which encodes the steroid 17 alpha-hydroxylase, contains two discrete DNA elements within its promoter and upstream region (CRS1 and CRS2) that individually can confer cAMP responsiveness. The CRS1 element is a target for PKA signalling and for negative regulation via the protein kinase C signal transduction pathway. The homeodomain protein Pbx1 enhances CRS1-dependent transcription, but additional CRS1-binding proteins remain to be identified. Furthermore it is not known how PKA regulates the activity of Pbx1 or its possible binding partners. Closer to the promoter, the nuclear orphan receptors SF-1 and COUP-TF have overlapping binding sites in CRS2 and they bind in a mutually exclusive manner with very similar affinities; 8 and 10 nM, respectively. SF-1 stimulates whereas COUP-TF inhibits transcription from the bovine CYP17 promoter. Together, the data suggest that cAMP-dependent control of the amounts of the activator SF-1 vs. the repressor COUP-TF could influence CRS2-dependent transcription. In addition, PKA may influence the phosphorylation of SF-1, thus increasing its activity. In vitro, PKA will elicit phosphorylation of SF-1. However, although SF-1 can be immunoprecipitated from adrenocortical cells as a phosphroprotein, we have not been able to show cAMP-dependent increase in net phosphorylation in intact cells. More careful examination of individual phosphorylation sites in SF-1 may still reveal hormone- and cAMP-induced phosphorylation of SF-1.

Histochemical characterization of masseter muscle fibres in a biopsy study of normal young women.

Muscle fibres from biopsies of the anterior part of the masseter muscle (pars superficialis) were histochemically characterized in 13 healthy female students. They were 21-28 yr old with a full complement of teeth, and normal facial and occlusal relations. Before surgery, normal masseter muscle function was demonstrated by bite-force measurements and recordings of electromyographic activity. After staining for myosin ATPase activity, the relative mean areas of muscle fibres were: type I 82.9%, type IM 9.5% and type II 8.3%. The intraindividual (18-155% of mean) and interindividual (0-216% of mean) variation of the fibre size was large. The type I fibres had the largest diameter (10-80 microns, mean: 39 microns), the type II fibres (6-47 microns, mean: 21 microns) and the IM fibres (8-54 microns, mean: 28 microns) the smallest. The biopsy technique and the histochemical characterization will be suitable for reference in women with functional changes or diseases of the masseter muscle.

Comparative data from young men and women on masseter muscle fibres, function and facial morphology.

The primary aim was to relate information about masseter muscle fibres and function to aspects of facial morphology in a group of healthy young men. The secondary aim was to investigate possible sex differences using data previously obtained from a comparable group of age-matched, healthy women. Dental status and facial morphology were recorded in 13 male students aged 20-26 years. Functional examinations included bite-force measurements and electromyographic recordings of masseter activity. A biopsy was removed from the masseter of each participant during surgical extraction of a wisdom tooth, and the tissue examined for myosin ATPase activity. Further, the cross-sectional areas of the different fibre types were measured. In spite of using age-matched healthy men and women with a full complement of teeth, statistically significant sex differences were found among measures related to muscle function and some measures of facial morphology. Thus data from men and women should not be pooled uncritically. The greater bite force in men than women corresponded with the greater diameter and cross-sectional area of type II fibres. Further, the males had more anteriorly inclined mandibles and shorter anterior facial height, suggesting a relation between the greater muscle force and the shape of the face. However, linear regression analysis failed to demonstrate any significant association between bite force and facial morphology among men and women. Thus, craniofacial morphology could be a result of far more contributing factors than previously believed.

Cardiovascular responses in humans to experimental chewing of gums of different consistencies.

Although the cardiovascular effects of exercise have been extensively investigated in man, little attention has been paid to such responses to jaw muscle activity. The aim here was to investigate the general cardiovascular effects of chewing activity in a single-blind, cross-over design. Ten healthy individuals performed one of the following chewing tasks in four separate sessions: chewing a very hard gum, chewing a moderately hard gum, chewing a soft gum, and "empty chewing" without a bolus. Unilateral chewing of gum or empty chewing was performed for 20 min on the participant's most convenient chewing side at a constant rate of 80 cycles/min. In each session, heart rate and arterial blood pressure were recorded together with electromyographic activity in the masseter and anterior temporalis muscles on the chewing side. Ratings of perceived masticatory fatigue were recorded with visual analogue scales. The heart rate and blood pressure were significantly increased (ANOVA; p < or= 0.01) during the chewing tasks and the increases were, in parallel with the muscle activity, more pronounced the harder the gum. With the very hard gum, heart rate increased by up to 11 beats/min, the systolic blood pressure was 14 mmHg (1.9kPa) higher, and the diastolic blood pressure was 11 mmHg (1.5kPa) higher. The perceived fatigue was proportional to the level of muscle activity. After 10 min of recovery from exercise, heart rate and arterial blood pressures were slightly but still significantly elevated. The results demonstrate that chewing is associated with general circulatory effects proportional to the bolus resistance.

Ultrasonographic assessment of the swelling of the human masseter muscle after static and dynamic activity.

Work-related fatigue, pain and disorders in skeletal muscles have been related to prolonged static and dynamic activity. Such contractions have been shown to impair blood flow and increase muscle thickness and fluid. In the present study the effect of static and dynamic activity was evaluated from changes in masseter thickness as a measure of oedema, simultaneously with assessment of perceived pain/discomfort and cardiovascular responses. As static activity, fourteen young healthy women bit at 15% maximal voluntary contraction on bite-force transducers in the molar regions until exhaustion or 20 min at maximum (median endurance time 7.1 min). For dynamic activity, the same individuals chewed gum unilaterally until exhaustion or 40 min at maximum (all endured 40 min) with a cycle time of 725 ms, an average load of 9.3% of maximal electromyographic activity (maxEMG) and a peak mean voltage of 54.3% of maxEMG. Muscle thickness was measured by ultrasonography at the mid-portion of the ipsilateral masseter. Immediately after exercise, muscle thickness was significantly increased, more after static (14.0%) than dynamic (8.6%), and returned to pre-exercise values after 20-min recovery. Visual analogue scales (VAS) revealed the concomitant occurrence of pain (static 11.9 VAS%; dynamic 5.9 VAS%), and discomfort (static 8.1 VAS%; dynamic 5.9 VAS%), and both sensations decreased to pre-exercise values after 20-min recovery. Systolic blood pressure increased significantly, more during static (12.5%) than dynamic activity (4.3%), whereas heart rate rose significantly only during dynamic exercise (13.3%). Hence, activity was associated with muscular swelling and pain, and, despite the relatively small size of the masticatory muscles, also with general cardiovascular responses.

Orofacial pain, jaw function, and temporomandibular disorders in women with a history of juvenile chronic arthritis or persistent juvenile chronic arthritis.

OBJECTIVES: We sought to study the long-term outcome of juvenile chronic arthritis (JCA) in the temporomandibular joint (TMJ). STUDY DESIGN: Temporomandibular disorders, including TMJ involvement, were assessed in 42 women with pauciarticular or polyarticular JCA--on average 25.8 years from disease onset--and compared with those found in matched control subjects. Disease-related parameters associated with temporomandibular disorders were identified. RESULTS: The TMJ was involved in 66.7% of the patients, most severely in extended pauciarticular JCA. Temporomandibular disorders were more frequent in the patients than in the control subjects, especially in those with persistent disease. The TMJ involvement was positively correlated with disease duration and negatively correlated with jaw opening and occlusal support. Duration of active JCA and history of functional pain were identified as predictors of present TMJ involvement. CONCLUSION: In a long-term follow-up, TMJ involvement proved frequent in the studied patients and was associated with long disease duration and previous pain on jaw opening. The findings suggest that patients with JCA should undergo orofacial evaluation on a regular basis.

Quantitative ultrasound image analysis of the supraspinatus muscle.

OBJECTIVE: To develop and validate a method, based on quantitative ultrasound image analysis, to objectively analyse and characterize the ultrasound images of m. supraspinatus. DESIGN: Quantitative ultrasonography was performed on the supraspinatus muscle of 14 healthy subjects. METHODS: A computerized analysis using first-order grey-scale statistics to evaluate the muscle tissue composition was developed and validated. RESULTS: Data from one scanning site were not representative for the whole muscle due to muscle inhomogenity. Using first-order grey-scale statistics the scanning direction was of no importance. By using a scanning session consisting of three different scanning sites along the muscle in two directions, longitudinally and transversely, to characterize the tissue composition of the muscle, a high day-to-day reproducibility was obtained. CONCLUSION: The described scanning session is a relatively sensitive and reproducible method for studying the muscle tissue composition. RelevanceQuantitative ultrasonography seems to be a potential clinical and occupational examination method to detect tissue composition of myalgic muscles compared to healthy muscles.

Occlusal harmony and disharmony: frauds in clinical dentistry?

In defining the principles of occlusal function it is possible to demonstrate how firmly the number, the placement and the distribution of occlusal contacts control muscle activity and joint function during biting and chewing. This control implies that the intercuspal position is determined by positive feedback, that is by afferent activity that varies with occlusal stability. Conventional dental treatment involving occlusal surfaces alters this input and consequently alters the coordination of the muscles of mastication and the function of the temporomandibular joints. To assess and direct this input properly, quantitative parameters of electromyography and kinesiography are needed. Terms such as harmony and disharmony are irrelevant and must be abandoned.