RESUMEN
An impeded blood flow through the femoral head is incriminated in the etiopathogenesis of osteonecrosis of the femoral head. The disorder is either primary (idiopathic avascular osteonecrosis) or secondary to one condition or another, say, corticosteroid medication, fracture of the neck, coagulation defects, physical or thermal damage, storage disorders, alcoholism, and infectious, autoimmune as also marrow infiltrating diseases. In the wake of the necrosis, several mediators are released in increased amounts, prime among which is the vascular endothelial growth factor. The intermediates recruit endothelial progenitor cells, macrophages, osteoclasts, fibroblasts, and osteoblasts, which, pervading throughout the necrotic areas, initiate the reparative processes. The dead, soft and hard tissular debris is substituted by fibrous - later on by hematopoietic-fatty tissue - and bone. The newly formed, appositional and intramembranous bone is deficient in its mechanical properties. The ordinary load-carrying functions suffice to deform these weakened femoral heads so that osteoarthritic changes develop. Considering contemporary assumptions of the causes of osteonecrosis, oxygenation, revascularization, and core decompression are the realistic therapeutic interventions. Necrosis of rats' femoral heads is studied as a model of osteonecrosis in both adults and children. In view of rodents' lifelong persisting physeal cartilage, vascular deprivation-induced osteonecrosis in rats mimics children's Perthes disease. The experimental model, which is well suited to test treatment modalities, has been used to investigate the effects of exposure to hyperbaric oxygen with and without non-weight bearing, medication of enoxaparin, and creation of an intraosseous conduit on the remodeling of the avascular necrotic femoral head. Intriguingly, the shape of treated rats' femoral heads is disfigured to a greater degree than that of untreated animals. This is most likely due to the reduced yield strength and elastic modulus as well as the raised strain-to-failure of the recently formed bone making up the post-necrotic femoral heads. It follows that expedited osteogenesis is, counter intuition, detrimental to maintaining the hemispherical shape of the femoral head, and thus to an articulation with congruent load-bearing surfaces. If this is indeed the case, the remodeling of the necrotic femoral head should be delayed, rather than sped up, as the present day paradigm would have it. Bearing in mind that the dead osseous structures keep their mechanical attributes for quite a while, a slowed down new bone formation would favor the gradual replacement of the necrotic by living bone. Therefore, management of the adult patients with osteonecrosis and children with Perthes disease should focus on a slowly progressive substitution so that the decline of the bone's mechanical properties is kept to a minimum. One viable therapeutic mode is a medication of inhibitors of the vascular endothelial growth factor.
Asunto(s)
Cabeza Femoral/patología , Osteonecrosis/patología , Animales , Cartílago/anatomía & histología , Cartílago/patología , Cabeza Femoral/anatomía & histología , Humanos , Modelos Biológicos , Modelos Teóricos , Necrosis , Neovascularización Patológica , Osteonecrosis/terapia , RatasRESUMEN
The femoral heads of 15 rats were studied histologically 3 months after the induction of ischaemic necrosis by incising the cervical periosteum and cutting the ligamentum teres. The epiphyses consisted of immature disorganized subchondral and trabecular bone. The inter-trabecular spaces contained fibrous or haematopoietic tissue. Residual necrotic bone was rare. There was marked osteoblastic and osteoclastic activity. The articular aspect of the heads showed a spectrum of changes, ranging from cartilaginous degeneration with fibrillation and loss of glycosaminoglycans to an eburnated and polished bony surface. In seven rats, transphyseal bridges connected the epiphyseal and metaphyseal bony trabeculae to each other. It is suggested that the postnecrotic reparative processes, including the resorption of the necrotic debris and its replacement by newly formed, weak bone, led to an osteoarthritis-like disorder. This healing pattern of the necrotic femoral head was reminiscent of the progressive remodelling that occurs in rings in femoral capital osteonecrosis of adult human patients and in Perthes's disease of children.
Asunto(s)
Remodelación Ósea , Modelos Animales de Enfermedad , Necrosis de la Cabeza Femoral/patología , Osteoartritis de la Cadera/patología , Animales , Epífisis/patología , Necrosis de la Cabeza Femoral/complicaciones , Enfermedad de Legg-Calve-Perthes/patología , Ligamentos Articulares/lesiones , Ligamentos Articulares/cirugía , Masculino , Osteoartritis de la Cadera/etiología , Ratas , Ratas Sprague-Dawley , Cicatrización de HeridasRESUMEN
Osteonecrosis of rat femoral heads was induced by stripping the periosteum of the neck and cutting the ligamentum teres. The epiphyseal marrow and bone were necrotic on the 5th postoperative day. Specimens obtained 18 and 36 days postoperatively showed fibrous and hematopoietic-fatty tissue in the intertrabecular spaces, osteoclastic bone resorption, osteogenesis, and degeneration of the joint cartilage. Morphometrically, the means of the height-to-length ratios of the control, 6-day, 18-day, and 36-day femoral heads were 0.26, 0.28, 0.48, and 0.29, respectively. The shape factor of the femoral heads of the control rats was higher than 0.81 in 80% of the cases, while those of rats killed on the 6th, 18th, and 36th postoperative day were higher than 0.81 in 65, 60, and 50% of cases, respectively. Statistically, the means of the height-to-length ratios and the values of the shape factors of the femoral heads of the rats killed 18 days postoperatively differed significantly from those of the other three groups of rats. The quantitatively gauged data of the remodeled epiphyses negate the authors' subjective impression concerning early flattening of the femoral heads after surgically produced osteonecrosis.
Asunto(s)
Cabeza Femoral/patología , Osteonecrosis/patología , Animales , Remodelación Ósea , Modelos Animales de Enfermedad , Cabeza Femoral/cirugía , Estudios de Seguimiento , Procesamiento de Imagen Asistido por Computador , Masculino , Osteonecrosis/cirugía , Ratas , Ratas Sprague-DawleyRESUMEN
In view of the lifelong persistence of the physis, the femoral head of rats may serve to model Perthes disease and slipped capital femoral epiphysis. To produce osteonecrosis, the blood supply of one femoral head of 133, 6-month-old animals was severed by circumferentially incising the periosteum of the neck and cutting the ligamentum teres. The rats were killed 7 days to 90 days postoperatively. Associated with resorption of the necrotic bone and marrow, remodeling of the epiphysis was characterized by an ingrowth of vascularized fibrous tissue, formation of new bone and some cartilage, architectural deformation and flattening of the head. In 22 of 83 rats killed 30 days or more postoperatively, gaps in the continuity of the physeal cartilage were occupied by osseous bridges, connecting newly formed epiphyseal bony trabeculae with either the preexisting or newly formed metaphyseal osseous trabeculae. This healing mode may follow ischemic death of physeal chondrocytes or be owing to another mechanism, e.g., release of mediatory substances of inflammation. These findings raise the possibility that fixation of the healing epiphysis of a child's previously necrotic femoral head to the metaphysis occurs by transphyseal osseous growth in cases in which the physis is involved in the necrotic process.
Asunto(s)
Remodelación Ósea , Cartílago/patología , Modelos Animales de Enfermedad , Epífisis Desprendida/patología , Epífisis/patología , Necrosis de la Cabeza Femoral/patología , Enfermedad de Legg-Calve-Perthes/patología , Factores de Edad , Animales , Cartílago/fisiopatología , Niño , Condrocitos/patología , Condrocitos/fisiología , Epífisis/fisiopatología , Epífisis Desprendida/fisiopatología , Epífisis Desprendida/terapia , Femenino , Necrosis de la Cabeza Femoral/fisiopatología , Necrosis de la Cabeza Femoral/terapia , Humanos , Inflamación , Enfermedad de Legg-Calve-Perthes/fisiopatología , Enfermedad de Legg-Calve-Perthes/terapia , Masculino , Osteoblastos/patología , Osteoblastos/fisiología , Ratas , Ratas Sprague-Dawley , Factores de TiempoRESUMEN
We examined the role of hyperbaric oxygenation (HBO2) combined with non-weight bearing (NWB) in the treatment of vascular deprivation-induced osteonecrosis of the femoral head in the rat. Group 1 included 16 rats treated by a combination of NWB and HBO2. Twenty animals treated by NWB alone (group 2), and 18 rats which received no treatment (group 3), served as the control groups. Maximal benefit of HBO2 was observed on Day 30 of the study. The femoral heads were less deformed in group 1 animals (P = 0.07). Preservation of the femoral heads was observed in a larger proportion of the HBO2-treated animals (P = 0.06). A smaller proportion of high-grade new bone formation was observed, and more animals demonstrated well-regenerated hematopoietic tissue (P = 0.08). The tendency for less deformation of the femoral head in the HBO2-treated group might be a predictor of better function of the hipjoint.
Asunto(s)
Necrosis de la Cabeza Femoral/terapia , Oxigenoterapia Hiperbárica , Animales , Terapia Combinada , Fémur/irrigación sanguínea , Necrosis de la Cabeza Femoral/etiología , Necrosis de la Cabeza Femoral/patología , Masculino , Ratas , Ratas Sprague-Dawley , Soporte de PesoAsunto(s)
Artroplastia de Reemplazo de Cadera/efectos adversos , Artroplastia de Reemplazo de Cadera/instrumentación , Luxación de la Cadera/etiología , Luxación de la Cadera/cirugía , Enfermedad de Legg-Calve-Perthes/complicaciones , Falla de Prótesis , Trastornos Urinarios/etiología , Adulto , Artroplastia de Reemplazo de Cadera/métodos , Fenómenos Biomecánicos , Tirantes , Cistoscopía , Luxación de la Cadera/diagnóstico por imagen , Humanos , Masculino , Recurrencia , Reoperación , Trastornos Urinarios/diagnóstico , Trastornos Urinarios/fisiopatología , Urodinámica , UrografíaRESUMEN
The reparative processes following vascular deprivation-induced necrosis of the femoral head were studied histologically in rats sacrificed 2, 7, 14, 21, 42 and 92 days postoperatively. The blood supply was severed by incision of the periosteum at the neck of the femoral head and transection of the ligamentum teres. Granulation tissue and a well-vascularized fibrous tissue originating from the joint capsule invaded the necrotic marrow spaces. With progressive resorption of the necrotic tissues and osteoneogenesis, both appositional and intramembranous, within the fibrotic intertrabecular spaces, the remodeling process led to a shift of the normal spongy architecture of the femoral head to a compacta-like one. In a few cases, osseous bridges bisected a necrotic physeal cartilage at the latest time intervals. The remodeling was associated with flattening of the femoral heads as well as with degenerative, regenerative and reparative alterations of the articular cartilage. In one of the two femoral heads obtained three months postoperatively, cystic spaces developed in the fibrous subchondral zone. Our findings are consistent with the view that ineffective attempts at restoring the prenecrotic state of the femoral head by replacing the necrotic with viable tissue triggers the collapse of the femoral head. Thickening and condensation of the subchondral bone, leading to increased stiffness of the subchondral zone, result in the osteoarthritis-like disorder. Mimicking the well-known phases of human osteonecrosis, the model readily allows for preclinical studies of therapeutic regimens.
Asunto(s)
Cabeza Femoral/irrigación sanguínea , Enfermedad de Legg-Calve-Perthes/etiología , Osteoartritis/etiología , Animales , Remodelación Ósea , Cartílago Articular/patología , Modelos Animales de Enfermedad , Femenino , Enfermedad de Legg-Calve-Perthes/patología , Ligamentos Articulares/cirugía , Osteoartritis/patología , Ratas , Flujo Sanguíneo Regional , Procedimientos Quirúrgicos VascularesRESUMEN
Acute compartment syndrome (ACS) is a devastating complication of rhabdomyolysis caused by muscle tamponade secondary to increased intracompartmental pressure (Pi). ACS requires emergency surgical decompression when Pi greater than 30 mmHg (normal less than 4.0 mmHg) and clinical signs exist. The present study was undertaken to examine whether mannitol which has been used extensively for prevention of acute renal failure in rhabdomyiolysis may also improve muscular hemodynamics in ACS. ACS was produced in dogs by injecting dog plasma into the anterolateral compartment of the hind limb. The Pi was directly monitored. Control dogs received saline, whereas experimental dogs received intravenously 20% mannitol (0.15 ml/min/kg) over a period of 1 h. The initial Pi was set arbitrarily at 100 mm Hg. Following the establishment of ACS, the spontaneous mean decrease in Pi in the control group was 40% of initial value over 60 min (n = 5) versus a decrease of 65%/60 min in the experimental (mannitol) group (n = 7, p less than 0.01). The net mean decompressive effect of mannitol treatments was approximately 28 mm Hg (mean control Pi minus mean experimental Pi at time 60 min). Extrapolated to man with ACS, such a decrease in Pi induced by mannitol theoretically could relieve compartmental tamponade noninvasively.
Asunto(s)
Síndromes Compartimentales/tratamiento farmacológico , Manitol/farmacología , Músculos/irrigación sanguínea , Angiografía , Animales , Síndromes Compartimentales/fisiopatología , Modelos Animales de Enfermedad , Perros , Femenino , Hemodinámica/efectos de los fármacos , Hemodinámica/fisiología , Soluciones Hipertónicas , Inyecciones Intravenosas , Masculino , Manitol/uso terapéutico , Músculos/efectos de los fármacos , Músculos/fisiopatologíaRESUMEN
A case report of identical male twins with the clinical and radiological features of the rare Ale - Calo or M.E.M.R. (Multiple Exostoses - Mental Retardation) or Langer-Giedion's syndrome - is presented. The additional finding of bilateral cryptorchidism in our case is also very rare in twins, and has hitherto not been described in association with the Ale - Calo syndrome. Differential diagnosis is reviewed briefly.