The physis, or growth plate, is a cartilaginous region at the end of children's long bones that serves as the primary center for longitudinal growth and characterizes the immature skeleton. Musculoskeletal injury, including fracture, infection, malignancy, or iatrogenic damage, has risk of physeal damage. Physeal injuries account for 30% of pediatric fractures and may result in impaired bone growth. Once damaged, cartilage tissue within the physis is often replaced by unwanted bony tissue, forming a "bony bar" that can lead to complications such as complete growth arrest, angular or rotational deformities, and altered joint mechanics. Children with a bony bar occupying <50% of the physis usually undergo bony bar resection and insertion of an interpositional material, such as a fat graft, to prevent recurrence and allow the surrounding uninjured physeal tissue to restore longitudinal bone growth. Clinical success for this procedure is <35% and often the bony bar and associated growth impairments return. Children who are not candidates for bony bar resection due to a physeal bar occupying >50% of their physis undergo corrective osteotomy or bone lengthening procedures. These approaches are complex and have variable success rates. As such, there is a critical need for regenerative approaches to not only prevent initial bony bar formation but also regenerate healthy physeal cartilage following injury. This review describes physeal anatomy, mechanisms of physeal injury, and current treatment options with associated limitations. Furthermore, we provide an overview of the current research using cell-based therapies, growth factors, and biomaterials in the different animal models of injury along with strategic directions for modulating intrinsic injury pathways to inhibit bony bar formation and/or promote physeal tissue formation. Pediatric physeal injuries constitute a unique niche within regenerative medicine for which there is a critical need for research to decrease child morbidity related to this injurious process.
A third of all pediatric fractures involve the growth plate and can result in impaired bone growth. The growth plate (or physis) is cartilage tissue found at the end of all long bones in children that is responsible for longitudinal bone growth. Once damaged, cartilage tissue within the growth plate can undergo premature ossification and lead to unwanted bony repair tissue, which forms a "bony bar." In some cases, this bony bar can result in bone growth deformities, such as angular deformities, or it can completely halt longitudinal bone growth. There is currently no clinical treatment that can fully repair an injured growth plate. Using an animal model of growth plate injury to better understand the mechanisms underlying bony bar formation and to identify ways to inhibit it is a great opportunity to develop better treatments for growth plate injuries. This protocol describes how to disrupt the rat proximal tibial growth plate using a drill-hole defect. This small animal model reliably produces a bony bar and can result in growth deformities similar to those seen in children. This model allows for investigation into the molecular mechanisms of bony bar formation and serves as a means to test potential treatment options for growth plate injuries.
1. Because of the controversy over the clinical effects of corticosteroids on joint tissues a series of experiments on the knee joints of rabbits was undertaken. 2. The articular cartilage of the distal femoral epiphyses of normalcontrols has been compared with that of rabbits treated daily either with cortisone or with methyl prednisolone systemically or by intra-articular injections. 3. The changes caused by intravenous papain and their subsequent recovery have been described, and the adverse effect of corticosteroids on recovery has been assessed. 4. The biological mechanisms involved are discussed, and as a result caution is urged in the administration of corticosteroids in the presence of progressive degenerative joint disease.
Evaluations of the conservative treatment of spinal tuberculosis have shown how disappointing the results can be. The inefficiency of posterior spinal fusion is acknowledged and is accepted as a hindrance to anterior bony fusion. The exclusion of antibiotics from established tuberculous abscesses prevents their influence in such cases (Florey, 1954), and they are ineffective when their use is not supported by operation (Stevenson, 1954; Wilkinson, 1954 Distribution (Fig. 1).-The distribution of lesions is similar to that in other reported series (Fraser, 1929 Radiology.-Radiological findings were studied in all cases. Lateral tomograms were of great value, particularly in the thoracic region, in assessing the extent of cavities pre-operatively, and in deciding whether bony fusion had occurred afterwards. Post-operative x-ray films were taken, and repeated after two and four months and thereafter at six-month intervals until fusion occurred. TreatmentThe niceties of antibiotic therapy, such as duration and dosage, and the period of recumbency and ambulant spinal support were studied. Especial attention has been paid to the time between the operation and the patient's return to work.The criteria of Swett, Bennett, and Street (1940) were accepted for "cure ": true healing was diagnosed only when bony fusion could be demonstrated between the vertebral bodies.Pre-operative Management
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