Exercise and Pregnancy

By Kim Christensen, DC, DACRB, CCSP, CSCS

Both exercise and pregnancy exert stresses on the body, and the cumulative effects must be considered when recommending a rehabilitative exercise program to pregnant women.¹Credible human research about the topic is sparse, and animal studies provide conflicting findings.

Chronic disorders such as diabetes, hypertension, and heart disease are clear reasons to discourage persons at risk from intense rehabilitative exercising while pregnant. Also, small or underweight women probably should be cautioned, since these women bear more premature and low birth weight infants than larger, normal-weight women.

Getting in Shape

Weight loss endeavors during pregnancy should be discouraged regardless of whether a decreased caloric intake or exercise is used, because neuropsychological abnormalities in infants have been associated with pregnancy. Adolescents are particularly prone to exercise during pregnancy, but a "get-in-shape" program should be deferred until after delivery if it is not undertaken before pregnancy. The existing level of aerobic fitness is an important factor in determining the eligibility of a pregnant woman for a rehabilitative exercise program. The effects of aerobic training are rapidly lost when activity ceases.

Walking is an excellent activity for the pregnant woman. Jogging should be discouraged, at least in the later stages of pregnancy, because of progressive lordosis and possible strain on the pelvic ligaments. A conservative approach to exercise seems wise because of its effects on the fetal heart rate and breathing movements. The maternal heart rate should not exceed 140 to 150 beats per minute for about 15 minutes, three to five times a week. Exercise at this level elicits an aerobic training effect in most women of childbearing age, while producing minimal fetal responses.

Gentle stretching and a warmup period before each exercise period are important measures. A cool down period of 10 to 15 minutes is also recommended. And because increased weight shifts anteriorly over the course of a pregnancy, it is also recommended that pregnant patients be fitted for custom made flexible orthotics. The ideal orthotic would be one which absorbs heel-strike shock, provides firm arch support and combats the high stress levels which commonly affect the lumbar spine of the mother-to-be.

Sedentary women should not begin vigorous rehabilitative exercise or try to get into shape during pregnancy. The time to get into good physical condition is before or after pregnancy. Once pregnant, a sedentary woman can begin a walking program or something similar. However, a woman who has been exercising can pursue a rehabilitative exercise program during pregnancy by adjusting the intensity of the program, according to how she feels, and keeping her heart rate in the 140 to 150 beats per minute range.

Fetal Heart Rates

Doppler monitoring of fetal heart rates, showing fetal bradycardia during vigorous maternal exercise, has given rise to concern for fetal safety. Because Doppler measurement of fetal heart rate during maternal exertion is difficult, two-dimensional ultrasonic imaging was used by Carpenter et al.² to record the fetal heart rate and determine the effect of submaximal and maximal maternal exertion and the incidence of fetal bradycardia.

Forty-five women with a mean gestation of 25 weeks performed exercise twice on separate days using a cycle ergometer. Resting measurements were taken with the women seated on the ergometer for 10 minutes. They underwent 85 submaximal and 79 maximal cycle ergometer tests.

Fetal cardiac activity was monitored continuously and videotaped during exercise and rest periods using a linear array two-dimensional ultrasound system. The average fetal heart rate did not change during maternal exertion, but 15 of 16 post-exercise episodes of bradycardia occurred within three minutes after maximal maternal exertion. There were 18 episodes of fetal bradycardia; one occurred during exercise.

Brief submaximal exercise up to 70% of maximal aerobic power seems to have no effect on fetal heart rate. Maximal exertion, on the other hand, is commonly followed by fetal bradycardia. The significance of this bradycardia is as yet unknown, but it seems prudent to recommend that pregnant women limit vigorous exercise to activities of no more than 150 beats per minute and conclude their exertion with a cool-down period.

Supine Exercise

Several investigators have monitored fetal hart rate (FHR) as a way to assess fetal hypoxia or distress in response to maternal exercise. An early study reported little effect on FHR, whereas later studies yielded conflicting results when using the FHR response to exercise as a screening test for uteroplacental insufficiency. Recent studies have reported a transient increase in baseline FHR. The effect of brief periods of mild, supine exercise on FHR in the late second trimester and mid-third trimester was studied by Nesler et al.³

Twenty-five healthy, regularly-exercising women were studied: 12 in the late second trimester, and 13 in mid third trimester. Although significant increases in maternal mean arterial pressure and pulse occurred, the exercise intensity was mild, with the average percent maximal pulse being 46 +/- 5% in the second trimester group and 49 +/- 5% in the third trimester group. Small increases in FHR were observed in both groups, which were insignificant statistically and physiologically. No patient experienced significant FHR abnormalities as a consequence of the exercise sequence.

These results indicate that pregnant women may continue submaximal supine exercise of short duration through the 36th week of gestation without harmful effects to the fetus. Thus, moderate exercising by pregnant women does not cause increases in the FHR. However, exercising while in a supine position instead of on a cycle ergometer may be a better choice. However, it appears from comparison of studies that the more vigorous exercise program used by Carpenter et al.² demonstrated no more danger to the fetus than did the more conservative program described by Nesler et al.³

Aerobic Exercise

The health and fitness of pregnant women at the onset of gestation affect the course and outcome of the pregnancy. Whether pregnancy reduces physical fitness as measured by maximal oxygen consumption between the second and third trimesters, and whether maintaining a regular exercise program during the second half of pregnancy influences fitness, were determined in 23 women by South-Paul et al.⁴ at the beginning of the second trimester.

Patients were randomly assigned to either a non-exercising or an exercising group. They completed a maximal progressive exercise test on a cycle ergometer at 20 weeks and 30 weeks, during which time pulmonary parameters or aerobic capacity were assessed.

The exercising women had greater improvement in aerobic capacity than the non-exercising women, manifested by increases in tidal volume and oxygen consumption and a stable ventilatory equivalent for oxygen. Pregnancy did not decrease the maximal oxygen consumption between the second and third trimesters, during which detraining could have been substantial.

This study points out the value of exercising during pregnancy. In fact, none of the women in this study was previously trained and the average baseline oxygen consumption was in the low range for both groups. Yet, when placed in a supervised exercise program, the exercise group improved their fitness, as demonstrated by an increased maximal oxygen consumption per kilogram of body weight.

The effects of exercise on the fetus are important in view of the increasing participation by women in rehabilitative exercise clinics. Dale et al.⁵ undertook a retrospective study of 21 women who had been pregnant in the past five years and who had participated in running during the course of pregnancy. A prospective sample of 12 women who were currently pregnant and running was also done with 11 controls matched with the runners for age, race, and parity. Electronic fetal monitoring was carried out in four subjects, all with favorable obstetric outcomes.

Subjects in the retrospective sample had a mean age of 30 years and had run for an average of four years; the mean prepregnancy weekly distance was 18.7 miles. Mean distances run in the three trimesters were 14.2, 10.9, and 6.6 miles a week, respectively. Eight of the 21 subjects competed in races while pregnant. Mean maternal weight gain was 24.4 pounds. In the prospective study, the only major obstetric complication in a runner was threatened abortion. There were no neonatal complications in the running group except for jaundice in an infant. Electronic fetal monitoring during treadmill running showed transient bradycardia, with a return of fetal heart rate to normal during continued exercise.

The course of pregnancy and complications appear to be similar in women who run during pregnancy and those who do not. Women who run exhibit a trend toward failure to progress during labor, resulting in an increased rate of cesarean section delivery. There is no evidence from Dale et al.⁵ of a compromised neonatal status in cases of women who run during pregnancy. Exercise appears not to seriously compromise uteroplacental function. Whether the fetal bradycardia observed during initial exercise is a response to transient hypoxia, a result of shunting of blood to the leg muscles, or an effect of other stress remains to be determined.

In the Dale⁵ study that evaluates 33 pregnant runners and 11 pregnant nonrunners, there is a more concerned note, perhaps, about potential major obstetrical complications in runners than controls, and the possibility of a higher Cesarean section rate in this group because of failure of progression during labor. More data would be necessary to confirm this, but this would be another argument for caution in prescribing running during pregnancy. There was no significant difference between runners and nonrunners with respect to weight gain, length of labor, and delivery, and the absolute incidence of obstetric complications. Dale5 did note fetal bradycardia, usually transient for a 2 1/2 to 3 1/2 minute interval, with spontaneous recovery during exercise. This is the point of concern. Again, pregnant women should limit exercise to activities requiring heart rates of no more than 150 beats per minute and conclude their exertion with a cool-down period.

References 

1. Snyder DK, Carruth BR. J Adolesc Health Care 1984; 5:34-36.
2. Carpenter MW, Sady SP et al. JAMA 1988; 259:3006-3009.
3. Nesler DL, Hassett SL, Brooke J. Am J Perinatol 1988; 5:159-163.
4. South-Paul JE, Rajagopo KR, Tenholder MF. Obstet Gynecol 1988; 71:175-179.
5. Dale E, Mullinax KM, Bryan DJ. Can J Appl Sports Sci 1982; 7:98-103.

Why Friction Massage Heals Tendinitis

Latest Information on Why Friction Massage Heals Tendinitis

By Warren Hammer, MS, DC, DABCO

In manual therapy, clinical results usually precede the scientific validation. Most techniques are used because "it works." Usually the author of the method hypothesizes why it works, but the reasoning although appearing logical may have nothing to do with the result. 
According to Frank and Hart¹: "Mechanical loading influences cell behavior in all soft tissues, but how it does so is not fully understood." The latest research on the effect of loading or deep pressure has been directed to the cellular level. In 1979, Meikle et al.² found that continuous stress to newborn rabbit cranial sutures led to an increase in collagen synthesis. Fibroblasts are responsible for increased collagen synthesis. Slack et al.,³ using a model of cyclic tensile loading of isolated embryonic chick tendons in vitro, showed increased synthesis of proteins, glycosaminoglycans and DNA by the fibroblasts.

Healing of tendons occurs in three stages. In the inflammatory stage, platelets and fibrin fill the wound and fibroblasts and phagocytic cells migrate to the injured area. Fibroblasts produce fibronectin, which acts as an adhesive molecule to bind collagen. As healing proceeds the fibroblastic production of fibronectin decreases. In the proliferative stage, the fibroblasts increase in number and synthesize collagen. Finally, in the third stage of remodeling or the maturation stage. there is a realignment of collagen fibers, and the collagen production shifts from the immature Type III to the mature Type I collagen.

Davidson et al.⁴ recently (1997) created a tendinitis in the rat tendon by injecting the enzyme collagenase. This method has also been used to trigger an inflammatory response in horses and ponies. While the collagenase did not cause the typical inflammatory response with the appearance of numerous mononuclear blood cells and lymphocytes at the injured site, the hallmark of tendon injury which is collagen fiber disruption and misalignment was exhibited in the rat tendons. They used augmented soft tissue mobilization (ASTM), which is an aluminum instrument used to apply "considerable pressure" to a tendon without breaking the overlying skin. The tendon was massaged longitudinally moving distal to proximal and proximal to distal along the length of the Achilles tendons of the rats.

There were four groups of rats: a) control; b) collagenase induced tendinitis; c) collagenase induced tendinitis plus ASTM; and d) ASTM alone to a normal tendon. After injecting the collagenase, the tendons were allowed to heal for three weeks. After the three weeks, ASTM was performed on group C and D for three minutes on postoperative days 21, 25, 29 and 33, i.e., four treatments. One week after the last treatment, the tendons were harvested and evaluated under light and electron microscopy and immunostaining for type I and type III collagen and fibronectin.

Light microscopy showed increased activated fibroblast proliferation in the tendons of group C and D. ASTM proved to initiate fibroblast activation which eventually leads to collagen synthesis. Group C also showed more fibronectin antibodies than group A. There was little fibronectin in Group B, but an increased amount in Group D. Gait analysis was also performed, and a significant improvement in stride length and stride frequency only occurred for Group C between post surgery day 21 and the final observation day.

ASTM promoted healing and earlier recovery of limb function following collagenase injury by the increased fibroblastic proliferation. The earlier recovery allowed increased limb function which also helped in the promotion of fiber realignment.

Of course, more studies are necessary especially to determine the effect of friction on chronic long-term scar tissue. It definitely appears that applying friction massage with increased pressure creates fibroblastic proliferation.

References 

1. Frank CB, Hart DA. Cellular response to loading. In: Leadbetter WB, Buckwalter JA, Gordon SL. Sports-Induced Inflammation, Amer Acad of Orthop Surgeons, Park Ridge, IL, 1989:555-563.
2. Meikle MC, Reynolds JJ, Sellers A, et al. Rabbit cranial sutures in vitro: A new experimental model for studying the response of fibrous joints to mechanical stress. Calcif Tissue Int 1979;28:137-144.
3. Slack C, Flint MH, Thompson BM. The effect of tensional load on isolated embryonic chick tendons in organ culture. Connect Tissue Res 1984;12:229-247.
4. Davidson CJ, Ganion LR, Gehlsen GM et al. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Medicine & Science in Sports & Exercise. American College of Sports Md, 1997:313-319.

Fibromyalgia Syndrome

By David BenEliyahu

Fibromyalgia syndrome (FS) is a diagnosis given to patients who present with chronic pain and stiffness. It is a complex syndrome, and although controversial, it is widely recognized by rheumatologists as a distinct diagnostic entity. 
It affects about six million people, four million of which are female. It is often accompanied by fatigue, sleep disturbances, morning stiffness, anxiety and decreased pain thresholds. Widespread pain and tenderness at many tender spots on the body are the hallmark findings. In 1990, the American College of Rheumatology (ACR) developed specific criteria for classifying FS:

I. History of widespread pain: pain present on the right and left side of the body, and both below and above the waist.

Axial skeletal pain must be present in one of these area: cervical spine, dorsal spine, anterior chest and lumbar spine.

II. Pain in at least 11 of 18 tender points:

right/left suboccipital area	second rib
cervical spine C5-C7	lateral epicondyle
trapezius	gluteals
supraspinatus	knee

greater trochanter

FS has been divided into two types. Primary FS occurs in a spontaneous idiopathic form; its cause is unknown. Secondary FS is found in association with a primary associated disorder such as trauma, rheumatoid arthritis, postsurgical, spinal disorders, etc.

FS predominantly affects women. The etiology of FS is poorly understood at this time, however, some studies have implicated neurohormonal, CNS, metabolic and/or biochemical dysfunction. In a study of middle-aged women with FS, SPECT studies were obtained to evaluate cerebral blood flow in the thalamus and caudate nucleus, as well as measuring pain thresholds with psychological assessments. As expected, all three were abnormal in the FS group. Other studies have shown that FS patients have elevated levels of substance P, low levels of serotonin and tryptophan and 5-hydroxytryptamine. As a result, deficient 5-hydroxytryptamine activity can cause altered sleep, substance P metabolism and allodynia. An interesting study on the role of glycolysis and FS revealed increased pyruvate and lactate production in FS patients and hypothyroid patients and decreased ATP and LDH in FS patients, suggesting glycolytic impairment.

Some studies have suggested an association between thyroid dysfunction and FS (myofascitis, also). In a study by Carette et al., symptomatic improvement was noted in 10 of 19 FS patients. In a paper by Lowe et al., it was theorized that there is failed transcription regulation by the thyroid hormone that leads to serotonin deficiency in FS patients. They tend to be euthyroid with normal thyroid blood test findings, due to low affinity thyroid hormone receptors coded by a mutated C-eba beta-1 gene, yielding resistance to thyroid hormone. This causes alpha-adrenergic dominance and an increase in cyclic ADP and inhibitory GI proteins.

It is important for the chiropractic clinician to recognize FS, because it is not uncommonly seen after trauma. In a study of 67 patients with FS that met the ACR criteria, 60% noted onset subsequent to MVA; 12% after a work injury; 7% after surgery; and 5% after sports injury. Posttraumatic FS patients have shown higher degrees of pain disability and life interference, and are more difficult to manage. Fifty-six of the 67 patients had pain in 11 or more of the tender points (averaging 13.5). Patients received medication, biofeedback, manipulation, massage therapy, physical therapy and injections.

There was a dramatic reduction in use of all the therapies after a two year follow-up, although 86% still had symptoms and had signs of FS. This implies that a significant percentage of patients coming to our office may have FS and can benefit from a trial of chiropractic care. It should be noted that the patient would benefit most from a holistic package of chiropractic care, including not only manipulative therapy/adjustments, but with physiotherapy, massage, nutritional supplementation and exercise.

In a study comparing relaxation technique and exercise, aerobic exercise, flexibility and strength training were shown to have a beneficial effect on FS patients, without any adverse effect. In a Norwegian study, FS patients who exercised reported less symptoms than sedentary patients. Similar findings were observed in a Scandinavian study. EMG biofeedback and electroacupuncture have also been demonstrated to help lower pain and EMG activity in FS patients. In a study in the BMJ, was shown to decrease use of analgesics, pain scores, sleep disturbance and morning stiffness. In a study of 90 patients with FS, the usage of complementary therapies/alternative medicine was evaluated. Seventy-one percent of the patients utilized complementary therapies; the most popular was nutritional oral supplementation.

A similar study by Pioro et al. found 91% of the FS patients used alternative therapies. Two thirds of FS patients used multiple interventions.

All of these studies show that FS patients want and need a viable alternative therapy in addition to their standard medical care. Chiropractic doctors who offer advice on nutrition, exercise, and behavioral modification, in addition to chiropractic care, provide these patients with a valuable service. It is imperative to make the patient an active participant in their care and to establish a good home exercise program with stretching, strengthening and aerobic exercise. This will empower the patient to return to a functional lifestyle. Nutritional supplements can include vitamins, mineral and herbal medicine.

It is important to emphasize that FS is not myofascial pain syndrome (MPS), and the tender points are not trigger points. A muscle study showed that there are no histological changes at the tender points. In a review article in JMPT, Schneider pointed out that FS and MPS are two distinct entities that require different treatment approaches. FS is a systemic problem that involves neuroendocrine dysfunction and requires multidisciplinary treatment. MPS is due to muscle dysfunction caused by trigger points which responds well to manual treatment, like myofascial release, ischemic compression, spray-stretch, etc. MPS and FS can be seen in the same patient and coexist, especially subsequent to trauma (MVA or whiplash injuries), so treatment must be individualized to the two different problems.

The doctor of chiropractic should be able to recognize fibromyalgia syndrome and participate in the care of this patient in conjunction with a rheumatologist and or psychotherapist. Kelli et al. in the July/August 1997 issue of JMPT documented the efficacy of chiropractic care in a random clinical trial on fibromyalgia patients. Twenty one rheumatoid patients with FS participated in the study. Four weeks of spinal manipulation, soft tissue therapy, and stretching were compared to control patients taking medication only. Chiropractic care resulted in increased cervical and lumbar ROM, straight leg raise, visual analog pain scores, Oswestry and neck pain disability index scores. The Kelli et al. pilot study suggests that DCs can help FS patients, albeit larger clinical trials are necessary to confirm their findings.

Manifestaciones clínicas de trastornos temporomandibulares en bruxópatas

Manifestaciones clínicas de trastornos temporomandibulares en bruxópatas

Clinical Manifestations of Temporomandibular Disorders in  Patients with Bruxism

Elia Julia González Estefano¹,  Mildred Gutiérrez Segura², Bárbara Pellitero Reyes ³

RESUMEN

Se realizó un estudio de serie de casos, desde enero de 2005 a enero de 2007, en la Consulta de Prótesis de la Clínica Estomatológica Docente Manuel Ángulo Farrán de Holguín. La muestra se conformó por 86 pacientes bruxópatas, de uno u otro sexo, que cumplieron con los criterios de selección. Se utilizó la anamnesis y el examen clínico y apoyado en el test de Maglione se identificó la presencia de trastornos temporomandibulares y se evaluó su grado de severidad, así como se determinaron los principales signos y síntomas articulares. El análisis y procesamiento de los datos mostró que el 73,3% de los pacientes tenían trastornos temporomandibulares y de ellos, 68,2% disfunción leve. El movimiento mandibular más afectado fue la apertura, en el 77,7% de los casos. El dolor muscular fue más frecuente en el músculo masetero con 61,9% con predominio de este síntoma en forma bilateral. Los síntomas articulares más evidentes fueron los ruidos  seguido del dolor (55,5%). Estos resultados evidenciaron la relación existente entre este hábito parafuncional y los trastornos temporomandibulares con predominio de la afectación muscular, dolor, ruido articular y  limitación de los movimientos.

Palabras clave: bruxismo, trastornos temporomandibulares, parafunción, aparato masticatorio

ABSTRACT

A study of series of cases from January 2005 to January 2007 at Manuel Angulo Farrán Dental Clinic in Holguín was carried out. The sample comprised  86 patients, males and females, who were selected according to some selection  criteria. Maglione test was applied to identify the temporomandibular disorders, the degree of dysfunction and  the most frequently signs and symptoms. The results showed 73.3% patients that suffered from temporomandibular disorders and 68.2% of them with mild dysfunction. Oral open was the most frequently affected mandibular movement in 77.7% of patients. The masseter muscle pain was the prevailing one in 61.9%. The sounds in the joint were present in 73.0% of them and joint pain in 55.5%. The  results showed a relation between joint dysfunction and bruxism, where muscle and joint pain, sounds and trismus were the most  significant clinical manifestations.

Key words: bruxism, temporomandibular disorders, parafunctional activity, masticatory system

INTRODUCCIÓN

Los trastornos temporomandibulares (TTM) forman un grupo de problemas clínicos que comprometen la musculatura masticatoria, las articulaciones temporomandibulares y otras  estructuras asociadas.

El enfoque que más adeptos tiene sobre la etiología de los TTM es de origen multifactorial y aparecen como las principales causas las interferencias oclusales, traumas, parafunciones e incompatibilidades estructurales de la alteraciones temporomandibulares y unido a todo esto, un factor psicológico-social desencadenante o agravante: el estrés, que, ocasiona una actividad muscular exagerada y  asincrónica ¹, y que desempeña un importante papel en la etiología, evolución y el tratamiento de los TTM².

La mala postura, la incapacidad para relajarse, una dieta deficiente y la falta de sueño pueden ser “puntos desencadenantes”  que remiten el dolor a otras áreas y causa dolor de cabeza, oído o de dientes¹. 

En la etiopatogenia de la disfunción temporomandibular, el hábito del bruxismo ocupa un papel importante. El bruxismo se considera un hábito no funcional de apretamiento o frotamiento de los dientes que puede ocurrir durante el sueño o menos frecuente por el día, entre el 5 y el 20% de los adultos ³. Se plantea que este se incrementa en estudios clínicos hasta cifras que oscilan entre el 50 y el 90%⁴.

El bruxismo de sueño se asocia con frecuencia a problemas nerviosos y al estrés. Su etiología aún no se conoce bien, pero se consideran el estrés y la ansiedad como factores de riesgo⁵. Las alteraciones oclusales y la anatomía de las estructuras óseas de la región orofacial  presentan un papel menor mientras que otros factores, como el hábito de fumar, alcohol, drogas, enfermedades sistémicas, el estrés, traumas y la herencia parecen poseer un importante papel en su etiología⁶.

Su importancia radica en el deterioro dental que produce de difícil tratamiento, y la exacerbación del dolor orofacial que genera^7. Su repercusión clínica puede ir más allá del desgaste del diente y afectar estructuras de soporte, la musculatura cervico-craneal y la articulación temporomandibular. No obstante, los mecanismos a través de los cuales una actividad parafuncional intensa determina un efecto patológico en las articulaciones temporomandibulares y sus estructuras relacionadas aún no se han esclarecidos definitivamente⁸.                                  

Considerando el papel que desempeña el bruxismo en el desarrollo de los trastornos temporomandibulares se hace necesario estudiar su repercusión en estas estructuras⁹.

A la consulta acuden con frecuencia pacientes bruxópatas que presentan signos y síntomas de trastornos temporomandibulares. Con el objetivo de identificar la presencia de estos trastornos en los pacientes bruxópatas, evaluar su grado de severidad y determinar los principales signos y síntomas presentes, se estudió una muestra compuesta por 86 individuos.

MÉTODOS

Se realizó un estudio de serie de casos en el periodo de enero de 2005 a enero de 2007 en la Consulta de Prótesis de la Clínica Estomatológica Docente Manuel Angulo Farrán del municipio Holguín. El universo de estudio estuvo compuesto por 146 pacientes bruxópatas de uno u otro sexo que acudieron a la clínica. La muestra se conformó por  86  pacientes mayores  de 18 años, dentados o con brechas cortas (hasta tres dientes), desdentados parciales correctamente rehabilitados y que aceptaron participar en la investigación mediante el consentimiento informado. Se excluyeron los pacientes con trastornos sistémicos que le imposibilitó brindar información clara y precisa, pacientes sin control muscular y  con pérdida de los incisivos centrales.

Se consideraron pacientes bruxópatas los que rechinaban o apretaban los dientes con signos y síntomas como: patrones no funcionales de desgaste oclusal, fracturas de dientes y restauraciones, movilidad dentaria especialmente en las primeras horas de la mañana, hipertrofia de los músculos masticatorios, exostosis óseas, dolor en la articulación temporomandibular y cansancio  muscular ¹⁰.

Para identificar los pacientes bruxópatas con trastornos temporomandibulares y evaluar el grado de  disfunción en leve, moderado y severo, se utilizó  el índice de Maglione y colaboradores¹¹. Se realizó la anamnesis y el examen clínico donde se emplearon la observación, palpación, auscultación y medición para determinar los signos y síntomas presentes.

Se realizó palpación bimanual de las articulaciones en busca de dolor y ruidos articulares. Se exploró la amplitud de los movimientos de apertura, lateralidad y propulsión y se consideró limitación cuando la apertura fue menor de  40 mm y  la lateralidad  y propulsión menor de  7mm. También se consideró la existencia de desviación mandibular, traba (bloqueo ocasional de corta duración) y luxación (dislocación del cóndilo con fijación fuera de la cavidad).

Se palparon los músculos masetero y temporal y pterigoideo medial  para identificar la presencia de dolor. Se exploraron  funcionalmente los músculos pterigoideos lateral superior  e inferior y el pterigoideo medial¹².

Los datos se recogieron en un formulario y para el procesamiento y análisis de la información se confeccionó una base de datos. Los resultados obtenidos se expresan en cifras absolutas y porcentaje y se muestran en cuadros.

RESULTADOS

Los resultados muestran que de los 86 pacientes bruxópatas examinados,  63

presentaron TTM para el 73,3% (tabla I).

Tabla I. Trastornos temporomandibulares en los bruxópatas estudiados

TTM	Bruxópatas
	No	%
Con TTM	63	73,3
Sin TTM	23	26,7
Total	86	100,0

Fuente: encuesta

El grado de disfunción que predominó fue el leve con 43 pacientes para 68,3% en orden descendente (tabla II).

Tabla II. Grado de severidad de los trastornos temporomandibulares en la muestra estudiada

Severidad del trastorno	No	%
Disfunción leve	43	68,3
Disfunción moderada	14	22,2
Disfunción severa	6	9,5
Total	63	100,0

Fuente: encuesta

El movimiento más afectado resultó ser la apertura, en 49 pacientes (77,7%), seguido de la propulsión en 34 (53,9%) (Tabla III).

Tabla III. Limitación del movimiento mandibular en pacientes con   trastornos temporomandibulares

Movimientos mandibulares	Limitación
	No	%(*)
Apertura	49	77,7
Lateralidad derecha	26	41,2
Lateralidad izquierda	30	47,6
Propulsión	34	57,9

Fuente: encuesta (*) n =63

El músculo masetero fue el más afectado con dolor en 61,9%, seguido del temporal en 55,5 % y el pterigoideo lateral en 44,4% de los casos examinados (tabla IV).

Tabla IV. Dolor muscular en pacientes con trastornos temporomandibulares

Dolor muscular
Músculos	Bilateral		Unilateral                   Total
	No	%(*)	No	%(*)	No	%(*)
Masetero	24	38,0	17	26,9	41	61,9
Temporal	22	34,9	11	17,1	33	55,5
Pterigoideo medial	12	19,0	10	15,8	22	34,9
Pterigoideo lateral	15	23,8	13	20,6	28	44,4

  Fuente: encuesta                          (*)  n= 63

Los ruidos articulares se manifestaron en 73% de los pacientes seguido del dolor articular en 55,5% (tabla V).

Tabla V. Síntomas articulares en los pacientes con trastornos temporomandibulares

Síntomas articulares	No	%
Dolor	35	55,5
Ruido articular	46	73,0
Desviación	11	17,4
Traba	8	12,6

Fuente: encuesta                       (*)  n= 63

DISCUSIÓN

Los resultados  muestran la presencia elevada de TTM en la muestra estudiada pues, más de la mitad de los pacientes estaban afectados. 

Castillo Hernández  y colaboradores¹³ de 35 pacientes con el hábito encontraron que 27 presentaban disfunción (77,1), resultados similares a los nuestros. La Dra. González Docando ¹⁴plantea que  58,9% de los  pacientes bruxópatas tienen TTM.  La Dra. Barbán y col. reportan que 57,3%) de los pacientes con bruxismo de su estudio, tenían dolor en la articulación temporomandibular¹⁵.

En varias partes del mundo se ha confirmado, por un gran número de investigaciones la asociación entre estos dos trastornos. Castillo y colaboradores¹³ exponen que en el rechinamiento intervienen contracciones musculares isotónicas mientras que en el apretamiento se presenta actividad muscular isométrica. La  pobre irrigación sanguínea existente a causa del aumento de los productos de desecho del metabolismo anaeróbico, que se acumulan y estimulan a los quimiorreceptores, provocan la aparición de la fatiga y el espasmo muscular.

Las pequeñas fuerzas aplicadas a las estructuras articulares de forma repetitiva durante un período prolongado (microtraumas) por el aumento de la actividad muscular y la hiperactividad del músculo pterigoideo lateral superior provocan un movimiento anteromedial del disco lo que ocasiona su desplazamiento funcional¹².

Estos elementos ayudan a comprender la relación de este hábito disfuncional con los TTM y el por qué resultó tan elevado el porcentaje de pacientes afectados en nuestra investigación, lo que de forma general coincide con lo reportado en la literatura especializada.

El grado de disfunción leve, fue el que predominó, seguido por el moderado y severo en orden descendente. La O Salazón  y colaboradores ¹⁶ en su estudio, utilizando el test de Maglione, encontraron predominio de la disfunción moderada (56,6%), seguida de la disfunción leve (28,1%).  Paredes Coz ¹⁷ reportó que prevalecía el grado leve de disfunción (44,74 %), seguido de la disfunción moderada (25%).

 Es importante resaltar que un mayor o menor grado de disfunción puede estar en relación con varios factores, como la severidad del bruxismo, el tiempo, la frecuencia e intensidad con que se practique el hábito.

Al analizar los resultados obtenidos sobre los movimientos mandibulares se observó que el movimiento más afectado resultó ser la apertura. Paredes Coz ¹⁷ reporta la limitación  del movimiento mandibular en  55,26% de los pacientes. Estos resultados sobrepasan el 50% de sus pacientes y es elevado como sucede en la presente investigación.

La apertura oral es quizás el movimiento mandibular a cuya limitación son  más sensibles los pacientes y puede estar en relación con el dolor muscular y articular, síntoma que está presente en numerosos pacientes en este estudio.

Al examinar los músculos, los resultados revelaron que el músculo masetero fue el más afectado seguido del temporal y el pterigoideo lateral. En todos los músculos predominó el dolor muscular bilateral sobre el unilateral.

Los estudios electromiográficos demuestran mayor actividad muscular en los maseteros y temporales en posición de reposo de los pacientes bruxópatas que en los no bruxópatas¹⁸.            

Los músculos duelen por el exceso de contracción muscular sin reposo suficiente. La contracción muscular sostenida compromete la circulación venosa de retorno y dificulta la rápida eliminación de los catabolitos que se acumulan y producen inflamación y exudado de las fibras (miositis). En el área isquémica se liberan sustancias algogénicas como la bradicidina y las prostaglandinas, responsables del dolor. Si el dolor pasa a ser constante puede producir efectos de excitación central creando un círculo vicioso con la producción de mayor dolor muscular ¹².

Las manifestaciones clínicas articulares más frecuentes fueron los ruidos articulares y el dolor seguido de la desviación. Rodríguez y colaboradores¹⁹ reportan en su trabajo como síntomas más comunes, el dolor muscular y articular con ruidos articulares, y ello coincide con nuestros hallazgos.

La artralgia se produce por los nociceptores situados en los tejidos blandos que circundan la articulación: ligamentos discales, ligamentos capsulares y tejidos retrodiscales; cuando los dos primeros sufren distensión y la última compresión, aparece el dolor ¹².

Generalmente el disco articular, producto del apretamiento dentario se deforma, cambia de posición y se luxa. Ésa es la causa más importante de los ruidos, dolores y bloqueos de los movimientos mandibulares.

CONCLUSIONES

• La presencia de trastornos temporomandibulares en los pacientes bruxópatas fue elevada.
• El grado de severidad leve predominó en los pacientes con bruxismo.
• El movimiento mandibular de apertura fue el más afectado, al igual que el músculo masetero, evidenciándose en general predominio del dolor muscular bilateral.  
• El ruido  fue el signo articular más frecuente seguido del dolor y la desviación mandibular.

REFERENCIAS BIBLIOGRÁFICAS

1        Johansson A, Unell L, Carlsson G, Soderfeldt B, Halling A, Wider F. Associations between social and general heath factors and symptoms related to temporomandibular disorders and bruxism in a population of 50 year-old subjects. Acta Odontol Scand. 2004; 62 (4): 231-7.

2        Kanehira H, Agariguchi A, Kato H, Yoshimine S, Inoue H. Association between stress and temporomandibular disorder. [Internet]. 2008.  [Consultado 14 jul 2010]. Disponible en:http://preview.ncbi.nlm.nihgov/pubmed/18678971.

3        Bedi S, Sharma A. Management of temporomandibular disorder associated with bruxism. J Indian Soc Pedod Prev Dent. [Internet]. 2009 [Consultado 14 jul 2010]. Disponible en:http://preview.ncbi.nlm.nih.gov/pubmed/19915278.

4        Nekora-Azak A, Yengin E, Evlioglu G, Ceyhan A, Ocak O, Issever H. Prevalence of    bruxism awareness in Istanbul, Turkey. Cranio [Internet] 2010. Disponible en:   http://preview.ncbi.nlm.nih.gov/pubmed/20491234.

5        Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K. Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil. [Internet] 2008. [consultado julio 2010].Disponible en: http://preview.ncbi.nlm.nih.gov/pubmed/18557915

6        Cuccia AM. Etiology of sleep bruxism: a review of the literature [Internet]. 2008. [consultado julio 2010]. Disponible en: http://preview.ncbi.nlm.nih.gov/pubmed/18710065.

7        El stress de la cavidad oral: Bruxismo [Internet].2005 [Consultado 20 abr 2009]. Disponible en: http/www.microsoft.com/Isasi/redir.dll?

8        Manfredini D, Contini E, Ramagnoli M, Basco M. Prevalence of bruxism in patients with different research diagnostic criterio for temporomandibular disorders  (RDC/TMD) diagnosis. Cranio. 2003; 21(4):279-85.

9        Ahlberg K, Ahlberg J, Konumen M, Partnen M, Hublin C, Savalainen A. bruxism and restless legs syndrome in media personnel with or without irregular shift work. Acta Odontol Scand. 2006; 63 (2): 94-8.

10   Especialidades bruxismo. [Internet]. 2006 [Consultado 20 abr 2006]. Disponible en:  http:/WWW.-odoncat.com/bruxismo.htm

11   Maglione H. Frecuencia y relación de los síntomas en el proceso de disfunción del sistema estomatognático. Rev Asoc Odont Arq.1982; 70 (6): 327-33.

12   Okeson JP. Etiología del bruxismo. En: Oclusión y afecciones temporomandibulares. 3 ed. España: Mosby / Doymar; 1995. p. 164-5.

13   Castillo Hernández R, Reyes Céspedes A, González M. Hábitos parafuncionales y ansiedad versus disfunción temporomandibular.  Rev Cub Ortod. 2002; 16(1):14-23.

14   González Docando JE, González Docando RM, Hermida Rojas M, Farrey Guzmán Y. Bruxismo, su comportamiento en una comunidad del área del Norte de Ciego de Ávila. Mediciego. 2007; (13):20-34.

15   Barbán Martínez DM,  Rodríguez González Y, Ureña Espinosa M, Portelles Morales T. Caracterización de una población bruxómana. [Internet]. 2008 [Consultado 6 sept 2010]. Disponible en: http://www.ltu.sld.cu//revista/index_files/articles /2008/julio-sept2008/julio-sept 08_1.html.

16   La O Salazón N, Corona Carpio MH, Rey Prada J, Arias Araña Z, Perdomo Mersilly X. Gravedad de la disfunción TM. MEDISAN [Internet] 2006; [Consultado 22 mayo 2007]; 10(2): [aprox. 5p.]. Disponible en: http:// bvs.sld.cu/revistas/sen/vollo2006.html.

17   Paredes Coz G. Epidemiología de disfunción craneomandibular en las áreas de influencia. Facultad de Odontología de la UNSMSM [Internet]. 2008 [Consultado 22 mayo 2007]. Disponible en:  http://sisbib.unmsm.cdu.pc/Bvrevistas/-odontología/20087.

18   Li XL, Lin XF, Teng W, Li SH. The characteristics of masticatory muscle activity in bruxers [Internet]. 2008 [Consultado 7 sept 2010]. Disponible en:http://preview.ncbi.nlm.nih.gov/pubmed/19186861.

19   Rodríguez L, Díaz Lemus JB, Tokura M,  Cerguerra Luz JG. Frecuencia de   Hábitos parafuncionales e sus manifestaciones clínicas en pacientes con disfuncaos da articulao temporomandibular. Rev Odontol.  2002; 13(2): 113-23.