Normal Weight Bearing Research Articles

Skeletal unloading decreases production of 1,25-dihydroxyvitamin D.

The plasma concentration of 1,25-dihydroxyvitamin D [1,25(OH)2D] decreases during skeletal unloading and increases when normal weight bearing is restored. To determine whether these changes in plasma 1,25(OH)2D reflect changes in production, metabolic clearance, or both we measured the kinetics of 1,25(OH)2D metabolism in rats whose skeletons were normally loaded, unloaded, or reloaded after a period of nonweight bearing. Skeletal unloading produced a transient but striking fall in the production (-73%) and plasma concentration (-72%) of 1,25(OH)2D without having a significant effect (< 20%) on metabolic clearance. Skeletal reloading returned production to normal. Bone formation predictably decreased during unloading and returned to normal after return to weight bearing. No consistent changes in blood ionized calcium, plasma immunoreactive parathyroid hormone (irPTH), or plasma phosphorus occurred. These data suggest that the changes in plasma 1,25-(OH)2D associated with changes in skeletal weight bearing primarily reflect changes in 1,25(OH)2D production. The data provide no evidence that the changes in 1,25(OH)2D production are a consequence of changes in blood ionized calcium, plasma irPTH, or phosphorus.

Histomorphometric assessment of the mechanisms for rapid ingrowth of bone to HA/TCP coated implants

The purpose of this work is to use dynamic histomorphometry to evaluate the basic biological mechanisms by which hydroxyapatite/tricalcium phosphate (HA/TCP) implant coatings accelerate bone formation rates. Twenty-five rabbits had an HA/TCP coated cylindrical titanium fiber metal mesh implant surgically placed in the subchondral bone of the proximal tibia and a noncoated implant placed in the contralateral tibia. Twenty-two of these animals had HA/TCP coated cylindrical solid titanium implants placed in the distal femur and an uncoated implant placed in the contralateral femur. The animals were double labeled with vital stains, and sacrificed at 3, 6, 16, or 26 weeks after surgery. Histomorphometric analyses were done of the bone implant interfaces. Both static and dynamic histomorphometric parameters indicate that HA/TCP coatings stimulate faster bone ingrowth to coated fiber metal implants through the early production of woven bone and by subsequent rapid lamellar bone formation rates. Coated fiber metal implants demonstrated significantly more bone ingrowth than noncoated implants through 16 weeks postimplantation, but not by 26 weeks. In solid implants, the differences between coated and noncoated implants are less pronounced and not statistically significant, although there is a trend toward increased bone apposition to the surface of the implants over the first 16 weeks following implantation. The clinical significance of these results is that coated implants may allow earlier return to normal weightbearing.

Effect of axial load and ankle position on ankle stability.

The range of motion of 10 fresh cadaveric ankle specimens was measured for flexion, anterior-posterior drawer, inversion-eversion, and internal-external rotation under conditions that simulated normal weight-bearing. At a 70 kg load, range of motion significantly diminished in all directions (p < 0.005). Plantar flexion was diminished to a greater degree than dorsiflexion. For anterior-posterior drawer in the loaded state, ankle flexion did not play a significant role in determining stability. Factors such as ligamentous attachments may be more critical than mortise geometry in determining anterior-posterior translation. For torsion and version, stability was greatest in dorsiflexion. That ankle stability is related to articular congruity with increased load-bearing emphasizes the importance of anatomical restoration of the ankle mortise in the injury state.

Distinguishing unloading- versus reloading-induced changes in rat soleus muscle.

Previously, solei from rats orbited 12.5 days aboard Cosmos 1887 biosatellite were biopsied 48-56 hours postflight. These atrophic muscles showed severe pathology. Designing a ground-based model of that space flight, we tested the hypothesis that 48 hours of postflight muscle reloading induced pathological changes. Rats were subjected to 12.5 days of hindlimb suspension unloading and biopsied immediately after suspension or after returning to normal weightbearing 12, 24, or 48 hours. Soleus morphological changes were quantitated on histochemically and immunohistochemically stained cross-sections. Solei from 0-hour reloaded rats showed significantly decreased wet weights, diminished myofiber cross-sectional area, angular myofibers, myofibril disruption, and more myofibers expressing fast myosin. Compared with suspension alone (0-hour reloading), reloading 12-48 hours induced slightly increased soleus wet weights, myofiber swelling, significant interstitial tissue edema, macrophage activation, and monocyte infiltration. These results suggest the degree and type of muscle degenerative changes observed postflight depend on the duration of gravity readaptation before biopsy and not solely on exposure to microgravity.

Mechanical effects of function on bone healing: Nonweight bearing and exercise in osteotomized rats

The effects of different degrees of function and weight bearing on the healing of femoral osteotomies were studied in rats. A transverse osteotomy of the left femur was stabilized by intramedullary pinning. The rats were allocated to three groups: (1) tenotomy of the left achilles tendon to avoid weight bearing, (2) unrestricted weight bearing, and (3) a 4-week training programme 4 weeks after the osteotomy. After 8 weeks, the rats were killed; and callus production, bending moment, bending rigidity, and fracture energy at the osteotomy site were evaluated. There were no differences in the area of external callus. The bending moment was less in the nonweight-bearing rats. Bending rigidity and fracture energy were marginally less in the nonweight-bearing rats. There were no significant differences between the weight bearing and exercised rats. The results indicate that normal weight bearing stimulates bone healing, whereas activity above normal neither accelerates nor impairs this process.

The measurement of fracture site movement during normal weightbearing in patients treated with external fixation

The measurement of fracture site movement during normal weightbearing in patients treated with external fixation

Effects of movement and weightbearing on the glycosaminoglycan content of sheep articular cartilage

Immobilised non-weightbearing joints show significant loss of proteoglycan. It is unclear whether this is due to a lack of compression, a lack of movement, or both. Evidence suggests that movement alone is insufficient to maintain proteoglycan levels. To investigate this problem, 20 sheep were divided into four groups and the right forelegs subjected to (1) normal weightbearing and movement, (2) movement without weightbearing, (3) weightbearing without movement and (4) non-weightbearing without movement. After one month, full thickness core samples of cartilage taken from the radio-carpal joints of both forelegs were analysed for glycosaminoglycan (GAG) content. Immobilised non-weightbearing joints showed a significant loss of GAG compared with the other groups. More importantly, movement alone without weightbearing was sufficient to maintain GAG content, as was weightbearing without movement.

Bone response to normal weight bearing after a period of skeletal unloading

Skeletal unloading in the growing rat induces a temporary inhibition of bone formation and thereby a deficit in bone calcium compared with age-matched, normally loaded animals. To determine whether this deficit can be restored by skeletal reloading we measured bone formation rate at the tibiofibular junction and total bone calcium in the tibia and lumbar vertebra in rats whose hindlimbs were unloaded for 2 wk and then reloaded by return to normal weight bearing. Continuously loaded or unloaded animals were also studied. Skeletal unloading reduced bone formation by 34% and tibial and vertebral calcium by 12 and 22%, respectively. Reloading significantly increased the rates of bone formation and calcium accretion 30-34% above normally loaded animals, and by 2 wk had decreased the deficit in tibial and vertebral calcium by 36 and 23%, respectively. These data indicate that the deficit in bone calcium induced by skeletal unloading in the growing rat can be restored in part by return to normal weight bearing. However, the time required to restore bone calcium exceeds the time required to produce the original calcium deficit.

Glucocorticoids and inhibition of bone formation induced by skeletal unloading.

Skeletal unloading or loss of normal weight bearing in the growing animal inhibits bone formation and reduces bone calcium. To determine whether the inhibition of bone formation induced by skeletal unloading is a consequence of an increase in plasma glucocorticoids and/or an increase in bone sensitivity to glucocorticoids, we measured plasma corticosterone throughout the day in unloaded and normally loaded rats (hindlimb elevation model) and examined the effect of adrenalectomy on the response of bone to skeletal unloading. Plasma corticosterone levels were similar in normally loaded and unloaded rats at all times. Skeletal unloading in sham-adrenalectomized animals reduced tibial and vertebral calcium by 11.5 and 11.1%, respectively, and in adrenalectomized animals by 15.3 and 20.3%, respectively. Uptake of 45Ca and [3H]proline in the tibia was reduced by 8 and 14%, respectively, in the sham-adrenalectomized animals and by 13 and 19% in the adrenalectomized animals. Bone formation and apposition rates were reduced to the same level in sham- and adrenalectomized animals. These results suggest that the inhibition of bone formation induced by skeletal unloading is not a consequence of increased plasma glucocorticoids or an increase in bone sensitivity to the glucocorticoids but, rather, point to a local mediator in bone that senses mechanical load and transmits that information to the bone-forming cells directly.

Mechanical, morphological and biochemical adaptations of bone and muscle to hindlimb suspension and exercise

The influences of weightbearing forces on the structural remodeling, matrix biochemistry, and mechanical characteristics of the rat tibia and femur and surrounding musculature were examined by means of a hindlimb suspension protocol and highly intensive treadmil running. Female, young adult, Sprague-Dawley rats were designated as either normal control, sedentary suspended, or exercise suspended rats. For 4 weeks, sedentary suspended rats were deprived of hindlimb-to-ground contact forces, while the exercise suspended rats experienced hindlimb ground reaction forces only during daily intensive treadmill training sessions. The suspension produced generalized atrophy of hindlimb skeletal muscles, with greater atrophy occurring in predominantly slow-twitch extensors and adductors, as compared with the mixed fiber-type extensors and flexors. Region-specific cortical thinning and endosteal resorption in tibial and femoral diaphyses occurred in conjunction with decrements in bone mechanical properties. Tibial and femoral regional remodeling was related to both the absence of cyclic bending strains due to normal weightbearing forces and the decrease in forces applied to bone by antigravity muscles. To a moderate extent, the superimposed strenuous running counteracted muscular atrophy during the suspension, particularly in the predominantly slow-twitch extensor and adductor muscles. The exercise did not, however, mitigate changes in bone mechanical properties and cross-sectional morphologies, and in some cases exacerbated the changes. Suspension with or without exercise did not alter the normal concentrations of collagen, phosphorus, and calcium in either tibia or femur.

The Influence of Hallux Extension on the Foot During Ambulation

A review of the literature, focusing on functional anatomy of components of the foot/ ankle complex, provides the rationale for normal hallux extension being a rehabilitation goal when treating patients with foot dysfunction. Hallux extension of 60 to 65 has been found to assist in transforming the foot into the rigid lever necessary for gait, allow the hallux and first metatarsal head to support normal weightbearing loads, and facilitate flexor hallicus longus action during gait. J Orthop Sports Phys Ther 1984;5(5):240-242.

Effect of weight-bearing on the appearance and development of the secondary calcaneal epiphysis.

The calcaneus ossifies from a primary center for the main body of the bone and from a secondary center for the posterior extremity (4). The secondary center has received considerable medical attention because in normal children it is strikingly dense when compared to the calcaneal body and it shows considerable irregularity of ossification (Fig. 1). Sever (11) related this roentgen appearance with pain and tenderness in the heel and termed it apophysitis of the os calcis. “Sever's disease” became and remained a popular diagnosis (1, 3, 7–9) until 1948 when Hughes (6) concluded that the changes termed Sever's disease were normal and “there is insufficient proof that osteochondrosis is ever the underlying cause of adolescent painful heels.” Caffey (2) re-emphasized mistaking the normality of the roentgen findings for apophysitis, and the condition is receiving less and less attention. Albeit the sclerosis of the calcaneal secondary epiphysis has been recognized as normal, no explanation has been given for the increased density. A preliminary observation that the sclerosis and development of the epiphysis might be related to weight-bearing prompted a roentgenological study of the calcaneus in children with and without normal weight-bearing. The purposes of the study are to determine if the secondary epiphysis is sclerotic in all normal weight-bearing children and to evaluate the relationship of weight-bearing to the sclerosis and developmental ossification of the epiphysis. Material and Method Calcaneal roentgenograms of 289 children were studied: 130 boys and 159 girls, aged four to seventeen years. One hundred and three were examined primarily for this study; the remaining 186 were patients referred to the Department of Radiology for recent trauma to the lower leg, ankle, or foot, but not primarily to the calcaneus. No child had symptoms referable to the calcaneus. Studies were also made of an additional 74 children who did not have normal weight-bearing either unilaterally or bilaterally. Forty-two were boys; 32, girls, with an age distribution ranging from seven to fifteen years. The cause of the non-weight-bearing was neurological in 15 boys and 24 girls and fracture in 27 boys and 8 girls. In the neurogenic disease group were 20 patients with poliomyehtis, 12 with spinal meningocele, and 7 with cerebral palsy. All fractures were of the lower tibial shaft, tibial malleoli, or metatarsals. Each calcaneus was evaluated in respect to (a) the presence of sclerosis of the secondary epiphysis and (b) the appearance and development of the epiphyseal ossification. Presence of Sclerosis The calcaneal epiphysis is not sclerotic when ossification commences in it. Ossification begins in several irregular foci which fuse together within a few months after their appearance. All patients with normal weight-bearing in this study showed sclerosis of the epiphysis by the time the foci fused.