Patterns of weight distribution under the metatarsal heads. (1/165)

The longitudinal arch between the heel and the forefoot and the transverse arch between the first and fifth metatarsal heads, absorb shock, energy and force. A device to measure plantar pressure was used in 66 normal healthy subjects and in 294 patients with various types of foot disorder. Only 22 (3%) of a total of 720 feet, had a dynamic metatarsal arch during the stance phase of walking, and all had known abnormality. Our findings show that there is no distal transverse metatarsal arch during the stance phase. This is important for the classification and description of disorders of the foot.  (+info)

Fractures of the proximal fifth metatarsal. (2/165)

Fractures of the proximal portion of the fifth metatarsal may be classified as avulsions of the tuberosity or fractures of the shaft within 1.5 cm of the tuberosity. Tuberosity avulsion fractures cause pain and tenderness at the base of the fifth metatarsal and follow forced inversion during plantar flexion of the foot and ankle. Local bruising, swelling and other injuries may be present. Nondisplaced tuberosity fractures are usually treated conservatively, but orthopedic referral is indicated for fractures that are comminuted or displaced, fractures that involve more than 30 percent of the cubo-metatarsal articulation surface and fractures with delayed union. Management and prognosis of both acute (Jones fracture) and stress fracture of the fifth metatarsal within 1.5 cm of the tuberosity depend on the type of fracture, based on Torg's classification. Type I fractures are generally treated conservatively with a nonweight-bearing short leg cast for six to eight weeks. Type II fractures may also be treated conservatively or may be managed surgically, depending on patient preference and other factors. All displaced fractures and type III fractures should be managed surgically. Although most fractures of the proximal portion of the fifth metatarsal respond well to appropriate management, delayed union, muscle atrophy and chronic pain may be long-term complications.  (+info)

Parathyroid hormone-related peptide (PTHrP)-dependent and -independent effects of transforming growth factor beta (TGF-beta) on endochondral bone formation. (3/165)

Previously, we showed that expression of a dominant-negative form of the transforming growth factor beta (TGF-beta) type II receptor in skeletal tissue resulted in increased hypertrophic differentiation in growth plate and articular chondrocytes, suggesting a role for TGF-beta in limiting terminal differentiation in vivo. Parathyroid hormone-related peptide (PTHrP) has also been demonstrated to regulate chondrocyte differentiation in vivo. Mice with targeted deletion of the PTHrP gene demonstrate increased endochondral bone formation, and misexpression of PTHrP in cartilage results in delayed bone formation due to slowed conversion of proliferative chondrocytes into hypertrophic chondrocytes. Since the development of skeletal elements requires the coordination of signals from several sources, this report tests the hypothesis that TGF-beta and PTHrP act in a common signal cascade to regulate endochondral bone formation. Mouse embryonic metatarsal bone rudiments grown in organ culture were used to demonstrate that TGF-beta inhibits several stages of endochondral bone formation, including chondrocyte proliferation, hypertrophic differentiation, and matrix mineralization. Treatment with TGF-beta1 also stimulated the expression of PTHrP mRNA. PTHrP added to cultures inhibited hypertrophic differentiation and matrix mineralization but did not affect cell proliferation. Furthermore, terminal differentiation was not inhibited by TGF-beta in metatarsal rudiments from PTHrP-null embryos; however, growth and matrix mineralization were still inhibited. The data support the model that TGF-beta acts upstream of PTHrP to regulate the rate of hypertrophic differentiation and suggest that TGF-beta has both PTHrP-dependent and PTHrP-independent effects on endochondral bone formation.  (+info)

FGF signaling inhibits chondrocyte proliferation and regulates bone development through the STAT-1 pathway. (4/165)

Several genetic forms of human dwarfism have been linked to activating mutations in FGF receptor 3, indicating that FGF signaling has a critical role in chondrocyte maturation and skeletal development. However, the mechanisms through which FGFs affect chondrocyte proliferation and differentiation remain poorly understood. We show here that activation of FGF signaling inhibits chondrocyte proliferation both in a rat chondrosarcoma (RCS) cell line and in primary murine chondrocytes. FGF treatment of RCS cells induces phosphorylation of STAT-1, its translocation to the nucleus, and an increase in the expression of the cell-cycle inhibitor p21WAF1/CIP1. We have used primary chondrocytes from STAT-1 knock-out mice to provide genetic evidence that STAT-1 function is required for the FGF mediated growth inhibition. Furthermore, FGF treatment of metatarsal rudiments from wild-type and STAT-1(-/-) murine embryos produces a drastic impairment of chondrocyte proliferation and bone development in wild-type, but not in STAT-1(-/-) rudiments. We propose that STAT-1 mediated down regulation of chondrocyte proliferation by FGF signaling is an homeostatic mechanism which ensures harmonious bone development and morphogenesis.  (+info)

Intermediate-term outcome of primary digit amputations in patients with diabetes mellitus who have forefoot sepsis requiring hospitalization and presumed adequate circulatory status. (5/165)

PURPOSE: The intermediate success and outcome of primary forefoot amputations in patients with diabetes mellitus who have sepsis limited to the forefoot and presumed adequate forefoot perfusion, as determined by means of noninvasive methods, was studied. METHODS: Cases of a university hospital-based practice from January 1984 to April 1998 were retrospectively reviewed. Patients included had diabetes mellitus with forefoot sepsis requiring immediate hospitalization for digit amputations who had adequate arterial circulation for healing based on noninvasive and clinical assessment: palpable pedal pulses (29%), "compressible" ankle pressure of 70 mm Hg or higher (48%), pulsatile metatarsal waveforms (67%), and/or toe pressure higher than 55 mm Hg (36%). All patients underwent a primary single- or multiple-digit amputation (through the interphalangeal joint, metatarsal head, or metatarsal shaft). Additional forefoot procedures (debridement, digit amputation) were performed during the follow-up period as needed for persistent or recurrent infection. The main outcome variables were recurrent or persistent foot infection (defined as requiring rehospitalization for antibiotics, wound care, and/or reoperation), the number of repeat operations and hospitalizations for salvage of limbs with recurrent or persistent infections, and time to complete forefoot healing or foot amputation. RESULTS: Ninety-two patients who had diabetes mellitus with 97 forefoot infections comprised the study group. Ninety-seven primary digit amputations (34 through interphalangeal joints, 28 through metatarsal heads, 35 through metatarsal shafts) were performed. The median length of hospital stay was 10 days. There were no operative deaths. The mean follow-up period was 21 months (range, 3 days to 105 months). The primary amputation healed (without persistent infection) in only 38 limbs (39%), at a mean time of 13 +/- 10 weeks. Twenty-three limbs (24%) had not healed the primary amputation without evidence of persistent infection at last follow-up (mean, 12 weeks). Infection persisted in 35 limbs (36%), and infection recurred in 15 of 38 (40%) healed limbs. An average of 1.0 reoperations (range, 0 to 3) and 1.6 rehospitalizations (range, 1 to 4) were involved in salvage attempts in these recurrent/persistent infections. Five persistent and five recurrent infections ultimately healed (mean, 53 weeks). Complete healing was achieved in only 33 of 97 limbs (34%). Twenty-two foot amputations (20 transtibial, two Syme's) were performed (mean, 49 +/- 74 weeks; 20 for persistent infection). Eighteen persistent/recurrent infections remained unhealed at the last follow-up examination (mean, 105 weeks). CONCLUSION: Patients with diabetes mellitus who have sepsis limited to the forefoot requiring acute hospitalization and undergoing primary digit amputations have a high incidence of intermediate-term, persistent, and recurrent infection, leading to a modest rate of limb loss, despite having apparently salvageable lesions and noninvasive evidence of presumed adequate forefoot perfusion.  (+info)

A densitometric analysis of the human first metatarsal bone. (6/165)

Bone responds to the stresses placed on it by remodeling its structure, which includes shape, trabecular distribution and density distribution. We studied 49 pairs of cadaveric human 1st metatarsal bones in an attempt to establish the pattern of density distribution and to correlate it with the biomechanical function of the bone. We found that the head is denser than the base, the dorsal portion of the whole metatarsal is denser than the plantar portion and the lateral portion of the whole metatarsal is denser than the medial aspect. The same pattern of density with respect to dorsal vs plantar and lateral vs medial was also seen in the head when it was examined alone. When we compared the 4 portions of the head with the same portion of the metatarsal as a whole we found that only the medial portion of the head was less dense than its respective portion of the whole metatarsal. All of these patterns of density distribution are consistent with respect to age, sex and laterality. We have also hypothesised as to the relationship between density distribution seen both in the whole metatarsal and in the metatarsal head and their biomechanical function in the gait cycle.  (+info)

Total dislocations of the navicular: are they ever isolated injuries? (7/165)

Isolated dislocations of the navicular are rare injuries; we present our experience of six cases in which the navicular was dislocated without fracture. All patients had complex injuries, with considerable disruption of the midfoot. Five patients had open reduction and stabilisation with Kirschner wires. One developed subluxation and deformity of the midfoot because of inadequate stabilisation of the lateral column, and there was one patient with ischaemic necrosis. We believe that the navicular cannot dislocate in isolation because of the rigid bony supports around it; there has to be significant disruption of both longitudinal columns of the foot. Most commonly, an abduction/pronation injury causes a midtarsal dislocation, and on spontaneous reduction the navicular may dislocate medially. This mechanism is similar to a perilunate dislocation. Stabilisation of both medial and lateral columns of the foot may sometimes be essential for isolated dislocations. In spite of our low incidence of ischaemic necrosis, there is always a likelihood of this complication.  (+info)

Autologous morsellised bone grafting restores uncontained femoral bone defects in knee arthroplasty. An in vivo study in horses. (8/165)

The properties of impacted morsellised bone graft (MBG) in revision total knee arthroplasty (TKA) were studied in 12 horses. The left hind metatarsophalangeal joint was replaced by a human TKA. The horses were then randomly divided into graft and control groups. In the graft group, a unicondylar, lateral uncontained defect was created in the third metatarsal bone and reconstructed using autologous MBG before cementing the TKA. In the control group, a cemented TKA was implanted without the bone resection and grafting procedure. After four to eight months, the animals were killed and a biomechanical loading test was performed with a cyclic load equivalent to the horse's body-weight to study mechanical stability. After removal of the prosthesis, the distal third metatarsal bone was studied radiologically, histologically and by quantitative and micro CT. Biomechanical testing showed that the differences in deformation between the graft and the control condyles were not significant for either elastic or time-dependent deformations. The differences in bone mineral density (BMD) between the graft and the control condyles were not significant. The BMD of the MBG was significantly lower than that in the other regions in the same limb. Micro CT showed a significant difference in the degree of anisotropy between the graft and host bone, even although the structure of the area of the MBG had trabecular orientation in the direction of the axial load. Histological analysis revealed that all the grafts were revascularised and completely incorporated into a new trabecular structure with few or no remnants of graft. Our study provides a basis for the clinical application of this technique with MBG in revision TKA.  (+info)