Flow-induced calcium oscillations in rat osteoblasts are age, loading frequency, and shear stress dependent.

Bone adaptation to mechanical loading is dependent on age and the frequency and magnitude of loading. It is believed that load-induced fluid flow in the porous spaces of bone is an important signal that influences bone cell metabolism and bone adaptation. We used fluid flow-induced shear stress as a mechanical stimulus to study intracellular calcium (Ca) signaling in rat osteoblastic cells (ROB) isolated from young, mature, and old animals. Fluid flow produced higher magnitude and more abundant [Ca(2+)](i) oscillations than spontaneous oscillations, suggesting that flow-induced Ca signaling encodes a different cellular message than spontaneous oscillations. ROB from old rats showed less basal [Ca(2+)](i) activity and were less responsive to fluid flow. Cells were more responsive to 0.2 Hz than to 1 or 2 Hz and to 2 Pa than to 1 Pa. These data suggest that the frequency and magnitude of mechanical loading may be encoded by the percentage of cells displaying [Ca(2+)](i) oscillations but that the ability to transduce this information may be altered with age.

Contributions of active and passive toe flexion to forefoot loading.

Toe flexion during terminal stance has an active component contributed by the muscles that flex the toes and a passive component contributed by the plantar fascia. This study examined the relative importance of these two mechanisms in maintaining proper force sharing between the toes and forefoot. Thirteen nonpaired cadaver feet were tested in a dynamic gait stimulator, which reproduces the kinematics and kinetics of the foot, ankle, and tibia by applying physiologic muscle forces and proximal tibial kinematics. The distribution of plantar pressure beneath the foot was measured at the terminal stance phase of gait under normal extrinsic muscle activity with an intact plantar fascia, in the absence of extrinsic toe flexor activity (no flexor hallucis longus or flexor digitorum longus) with an intact plantar fascia, and after complete fasciotomy with normal extrinsic toe flexor activity. In the absence of the toe flexor muscles or after plantar fasciotomy the contact area decreased beneath the toes and contact force shifted from the toes to the metatarsal heads. In addition, pressure distribution beneath the metatarsal heads after fasciotomy shifted laterally and posteriorly, indicating that the plantar fascia enables more efficient force transmission through the high gear axis during locomotion. The plantar fascia enables the toes to provide plantar-directed force and bear high loads during push-off.

Bone strain and microcracks at stress fracture sites in human metatarsals.

Microcracks in bone have been implicated in the development of stress fractures. The goal of this study was to evaluate bone strain and microcracks at locations where stress fractures are common (second metatarsal diaphysis) and rare (fifth metatarsal diaphysis) in an attempt to increase our understanding of the pathogenesis of stress fractures. A dynamic gait simulator was used to simulate normal walking with cadaver feet. The feet were loaded over the entire stance phase of gait and diaphyseal strains were recorded in second and fifth metatarsals. Microcrack density (Cr.Dn) and surface density (Cr.S.Dn) were determined in metatarsal cross sections from the contralateral feet. Bone strain was significantly higher in second metatarsals (-1897 +/- 613 microstrain) than in fifth metatarsals (-908 +/- 503 microstrain). However, second metatarsal Cr.Dn (0.23 +/- 0.15 #/mm(2)) was not significantly different from fifth metatarsal Cr.Dn (0.35 +/- 0.19 #/mm(2)). There was also no significant difference between Cr.S.Dn in second (17.64 +/- 10.99 microm/mm(2)) and fifth (26.70 +/- 15.53 microm/mm(2)) metatarsals. There were no significant relationships between the microcrack parameters and peak strain in either metatarsal. Cracks that occurred in trabecular struts (92 +/- 33 microm) were significantly longer than those found ending at cement lines (71 +/- 15 microm) and within osteons (57 +/- 16 microm). There were no significant relationships between the microcrack parameters and age in either metatarsal. Peak strain was more than twofold greater in second metatarsals than in fifth metatarsals for simulations of normal walking; however, microcrack parameters were unable to explain the greater incidence of second metatarsal stress fractures.

Strains in the metatarsals during the stance phase of gait: implications for stress fractures.

BACKGROUND: Stress fractures of the metatarsals are common overuse injuries in athletes and military cadets, yet their etiology remains unclear. In vitro, high bone strains have been associated with the accumulation of microdamage and shortened fatigue life. It is therefore postulated that stress fractures in vivo are caused by elevated strains, which lead to the accumulation of excessive damage. We used a cadaver model to test the hypothesis that strains in the metatarsals increase with simulated muscle fatigue and plantar fasciotomy. METHODS: A dynamic gait simulator was used to load fifteen cadaveric feet during the entire stance phase of gait under conditions simulating normal walking, walking with fatigue of the auxiliary plantar flexors, and walking after a plantar fasciotomy. Strains were measured, with use of axial strain-gauges, in the dorsal, medial, and lateral aspects of the diaphysis of the second and fifth metatarsals as well as in the proximal metaphysis of the fifth metatarsal. RESULTS: When the feet were loaded under normal walking conditions, the mean peak strain in the dorsal aspect of the second metatarsal (-1897 microstrain) was more than twice that in the medial aspect of the fifth metatarsal (-908 microstrain). Simulated muscle fatigue significantly increased peak strain in the second metatarsal and decreased peak strain in the fifth metatarsal. Release of the plantar fascia caused significant alterations in strain in both metatarsal bones; these alterations were greater than those caused by muscle fatigue. After the plantar fasciotomy, the mean peak strain in the dorsal aspect of the second metatarsal (-3797 microstrain) was twice that under normal walking conditions. CONCLUSIONS: The peak axial strain in the diaphysis of the second metatarsal is significantly (p < 0.0001) higher than that in the diaphysis of the fifth metatarsal during normal gait. The plantar fascia and the auxiliary plantar flexors are important for maintaining normal strains in the metatarsals during gait.

Biomechanical consequences of plantar fascial release or rupture during gait. Part II: alterations in forefoot loading.

With a model using feet from cadavers, we tested the hypothesis that plantar fascial release or rupture alters the loading environment of the forefoot during the latter half of the stance phase of gait. The model simulated the position and loading environment of the foot at two instants: early in terminal stance immediately after heel-off and late in terminal stance just preceding contralateral heel strike. Eight feet were loaded at both positions by simulated plantar flexor contraction, and the distribution of plantar pressure was measured before and after progressive release of the plantar fascia. Strain in the diaphysis of the second metatarsal was also measured, from which the bending moments and axial force imposed on the metatarsal were calculated. Cutting the medial half of the central plantar fascial band significantly increased peak pressure under the metatarsal heads but had little effect on pressures in other regions of the forefoot or on second metatarsal strain and loading. Dividing the entire central band or completely releasing the plantar fascia from the calcaneus had a much greater effect and caused significant shifts in plantar pressure and force from the toes to beneath the metatarsal heads. These shifts were accompanied by significantly increased strain and bending in the second metatarsal. Complete fasciotomy increased the magnitude of strain in the dorsal aspect of the second metatarsal by more than 80%, suggesting that plantar fascial release or rupture accelerates the accumulation of fatigue damage in these bones. Altered forefoot loading may be a potential complication of plantar fasciotomy.

Biomechanical consequences of plantar fascial release or rupture during gait: part I--disruptions in longitudinal arch conformation.

To examine whether conformational changes induced by plantar fascial division may progress during gait, we loaded the feet of seven cadavers using an apparatus that simulates the actions of the extrinsic plantarflexors. We measured the effects of plantar fasciotomy at two instants in the terminal-stance phase of gait. Radiographic measurements of height of the arch, base length of the arch, and talo first-metatarsal angle were used to assess contributions to arch support made by the plantar fascia, tibialis posterior, peroneus longus and brevis, and digital flexor muscles. Complete fasciotomy caused significant collapse of the arch in the sagittal plane. Early in terminal stance, at the instant after heel-off, mean height of the arch decreased from 47 to 45 mm. Late in terminal stance, at the instant preceding contralateral heel strike, mean height of the arch decreased from 46 to 43. Effects of division of the central band, though significant, were mild. Medial base length of the arch increased from 163 to 167 mm in the absence of tibialis posterior contraction at late terminal stance. Arch-supporting abilities of the other extrinsic muscles were insignificant.

Patellar strain and patellofemoral contact after bone-patellar tendon-bone harvest for anterior cruciate ligament reconstruction.

OBJECTIVE: To characterize the morbific consequences of harvesting a patellar tendon graft for use in reconstructing the anterior cruciate ligament (ACL) of the knee, specifically, (1) to measure changes in patellar strain and patellofemoral contact due to graft harvest, (2) to evaluate the ability of bone-grafting the patellar defect to mitigate these effects, and (3) to characterize failure of the extensor mechanism after harvest of a patellar tendon graft. DESIGN: Twenty-two cadaver knee joints were tested before and after harvest of a patellar tendon graft and after filling the patellar defect with polymethylmethacrylate to simulate a healed bone graft, Knees were positioned in 30 degrees, 60 degrees, and 90 degrees flexion and loaded while measuring axial strain in the anterior patella and patellofemoral contact. Knees were then loaded to failure. RESULTS: Harvest of the graft produced increases in axial strain at all flexion angles. Filling the defect restored axial strain to normal values. Patellofemoral contact in the presence of a defect, either filled or empty, was not different from contact for intact patellae. Most knees failed by transpatellar fracture; mean extension moment at failure was 112.8Nm. The best predictors of failure were age and gender. CONCLUSION: Patients undergoing ACL reconstruction with a patellar tendon graft are at increased risk of anterior knee pain and disruption of the extensor mechanism. Bone-grafting the patellar defect created by graft harvest can reduce these risks. Our findings underscore the importance of carefully controlled rehabilitation and suggest that if an accelerated program of rehabilitation is anticipated, the patellar defect should be bone-grafted. Older patients, particularly women, are at increased risk of catastrophic failure of the knee extensor mechanism after ACL reconstruction using patellar tendon graft.