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Biomedical subjects

J A Buckwalter

Publications and source records attributed to J A Buckwalter.

At least 37 records · Page 2Linked to original sources
PubMed2000

Total ankle replacement revisited.

The surgical treatment of painful, end-stage ankle arthritis includes ankle arthrodesis and total ankle replacement. In the past decade, total ankle replacement has become a viable alternative to ankle arthrodesis. Modern implant designs either involve a syndesmosis fusion and resurfacing of the medial and lateral recesses of the ankle joint or the use of a 3-component, mobile bearing implant. In limited clinical series, the early results of both these prosthetic design approaches are encouraging. In selected patients, ankle arthroplasty is an effective approach to relieving pain and improving function. The purposes of this paper are to review the clinical results from total ankle replacement and ankle arthrodesis; discuss indications, contraindications, design features, postoperative rehabilitation, and initial results for the major current total ankle designs; and present concepts for future total ankle development. In particular, this article explores the advantages and concerns with 2 prevalent but different design approaches. It also discusses future directions for total ankle replacement.

Ankle Joint↗
PubMed2000

Arthur Steindler. Orthopaedic scholar, teacher, and clinician.

Arthur Steindler, a native of Austria, immigrated to the United States in 1907 and during the next 50 years he became very influential in the development of orthopaedics during the twentieth century. His life is a compelling example of how an individual can make major contributions to the advancement of medical science and practice. His clinical interests spanned the entire range of musculoskeletal disorders including developmental, genetic, infectious, neoplastic and neuromuscular diseases, and their operative and nonoperative treatment. He founded the clinical and academic Orthopaedic Surgery programs at the University of Iowa in Iowa City and directed their growth for 34 years. During that time his clinical work, scholarship, and teaching helped the University of Iowa become a national and international orthopaedic center. He helped establish a statewide system to provide medical care for indigent patients and personally treated more than 70,000 patients, many of them children crippled by polio, tuberculosis, spastic paralysis, scoliosis, congenital deformities, and degenerative neuromuscular diseases. To improve the function of the weakened and deformed limbs of the children, he devised various innovative operations. He wrote more than 130 papers and nine books in several languages on the natural history, etiology, and treatment of musculoskeletal diseases and injuries, pioneered the application of biomechanics to evaluation and treatment of musculoskeletal disorders, and wrote the first comprehensive text on the mechanics of human movement. He taught more than 300 orthopaedists, and when Ruth Jackson, the individual recognized as the first woman orthopaedic surgeon in the United States, decided to pursue a career in orthopaedics, she sought out Arthur Steindler and received her formal orthopaedic education under his direction. That Steindler accomplished so much after moving to the small midwestern town of Iowa City at the age of 37 is impressive, and clearly documents his remarkable abilities and determination.

Academic Medical Centers↗
PubMed2000

Synovial joint degeneration and the syndrome of osteoarthritis.

The adverse effects of osteoarthritis on the quality of life for tens of millions of people and on the costs of health care and economic productivity make it a major health problem that will increase in incidence and impact with the aging of the population. Although in most patients the cause of osteoarthritis remains unknown and no cure has been identified, appropriate diagnosis and treatment, including education of the patients, can minimize symptoms and help patients maintain active and productive lives. Accomplishing this aim requires that physicians have an understanding of the pathophysiology of joint degeneration and the relationships between joint degeneration and the clinical syndrome of osteoarthritis. Although much remains to be learned about the development and progression of the joint degeneration responsible for osteoarthritis, it is clear that the loss of articular cartilage results from disruption of the structural integrity of the articular cartilage coupled with or caused by an imbalance in the anabolic and catabolic activity of the tissue. The progression of joint degeneration varies considerably among patients. In some individuals the joint degenerates rapidly; in others the degenerative changes progress slowly over decades and in others the disease may remain stable. In rare patients, the joint degenerative changes spontaneously improve. Although joint degeneration is the underlying cause of the symptoms of osteoarthritis, including joint pain and loss of joint function, not all patients with joint degeneration have symptoms of osteoarthritis. Future therapeutic approaches may include disease-modifying drugs and surgical procedures that correct mechanical abnormalities, debride joints, and replace degenerated articular cartilage with implants that stimulate restoration of a cartilaginous joint surface. Development of methods to detect and monitor subtle changes in cartilage metabolism and identify the joint changes that precede loss of articular cartilage may make it possible to detect the earliest signs of osteoarthritis, when therapeutic interventions have the greatest potential for preventing progression of the disease.

Humans↗
PubMed2000

The role of chondrocyte-matrix interactions in maintaining and repairing articular cartilage.

Throughout life chondrocytes maintain the articular cartilage matrix by replacing degraded macromolecules and respond to focal cartilage injury or degeneration by increasing local synthesis activity. These observations suggest that mechanisms exist within articular cartilage that stimulate chondrocyte anabolic activity in response to matrix degradation or damage. An important cartilage anabolic factor, insulin-like growth factor I (IGF-I), appears to have a role in stimulating chondrocyte anabolic activity. Although IGF-I is ubiquitous, its bioavailability is controlled by a class of secreted proteins, IGF binding proteins (IGFPBs). Of the six known IGFPBs, IGFBP-3 is the most abundant in human articular cartilage. We recently found that with increasing age, articular chondrocytes increase their expression of IGFBP-3. This observation led us to investigate the potential role of IGFBP-3 in chondrocyte-matrix interactions. Using immunofluorescent staining and confocal microscopy we found that IGFBP-3 accumulates with increasing age in the chondrocyte territorial matrix where it co-localizes with fibronectin, but not with tenascin-C or type VI collagen. Using purified proteins we demonstrated that IGFBP-3 binds to fibronectin in a dose dependent manner, but not to tenascin-C. In vitro studies showed that IGFBP-3 alone inhibited chondrocyte synthetic activity while intact fibronectin alone significantly stimulated activity. When fibronectin and IGFBP-3 were combined we found that the inhibitory activity of low concentrations of IGFPB-3 was enhanced. These observations indicate that in mature articular cartilage IGF-I is stored in the chondrocyte territorial matrix through binding to a complex of IGFPB-3 and intact fibronectin. Storage of IGF-I of the territorial matrix may help maintain a relatively constant level of available IGF-I and the local increase in matrix synthesis following matrix damage may result from release of IGF-I. This mechanism may have an important role in maintaining and repairing articular cartilage and failure of this mechanism may lead to progressive articular cartilage degeneration.

Adaptation, Physiological↗
PubMed2000

Damage control mechanisms in articular cartilage: the role of the insulin-like growth factor I axis.

Articular chondrocytes maintain cartilage throughout life by replacing lost or damaged matrix with freshly synthesized material. Synthesis activity is regulated, rapidly increasing to well above basal levels in response to cartilage injury. Such responses suggest that synthesis activity is linked to the rate of matrix loss by endogenous "damage control" mechanisms. As a major stimulator of matrix synthesis in cartilage, insulin-like growth factor I (IGF-I) is likely to play a role in such mechanisms. Although IGF-I is nearly ubiquitous, its bioavailability in cartilage is controlled by IGF-I binding proteins (IGFBPs) secreted by chondrocytes. IGFBPs are part of a complex system, termed the IGF-I axis, that tightly regulates IGF-I activities. For the most part, IGFBPs block IGF-I activity by sequestering IGF-I from its cell surface receptor. We recently found that the expression of one binding protein, IGFBP-3, increases with chondrocyte age, paralleling an age-related decline in synthesis activity. In addition, IGFBP-3 is overexpressed in osteoarthritic cartilage, leading to metabolic disturbances that contribute to cartilage degeneration. These observations indicate that IGFBP-3 plays a crucial role in regulating matrix synthesis in cartilage, and suggest that cartilage damage control mechanisms may fail due to age-related changes in IGFBP-3 expression or distribution. Our investigation of this hypothesis began with immunolocalization studies to determine the tissue distribution of IGFBP-3 in human cartilage. We found that IGFBP-3 accumulated around chondrocytes in the pericellular/territorial matrix, where it co-localized with fibronectin, but not with the other matrix proteins tenascin-C and type VI collagen. This result suggested that the IGFBP-3 distribution is determined by binding to fibronectin. Binding studies using purified proteins demonstrated that IGFBP-3 does in fact bind to fibronectin, but not to tenascin-C or type VI collagen. Finally, we investigated the metabolic effects of fibronectin and IGFBP-3 in a chondrocyte culture system. These experiments showed that fibronectin enhanced the inhibitory effect that low concentrations of IGFBP-3 had on matrix synthesis. Taken together, these observations confirm that IGFBP-3-fibronectin interactions affect the IGF-I axis, and they indicate that IGF-I is stored in the chondrocyte territorial matrix through binding to a complex of IGFBP-3 and intact fibronectin. This arrangement may play an important role in cartilage damage control mechanisms. The local increase in matrix synthesis following injury could result from damage-induced IGF-I release from such pools. An age-related failure to organize this system may contribute to degenerative disease.

Adult↗
PubMed2000

Diabetic muscle infarction.

Diabetic muscle infarction is a rare complication of diabetes mellitus that is not clearly defined in the orthopaedic literature. This study is a descriptive case series of 7 new cases of diabetic muscle infarction and 55 previously reported cases in the literature. In the majority of patients, diabetic muscle infarction presents as a localized, exquisitely painful swelling and limited range of motion of the lower extremity. No cases affecting the muscles of the upper extremity have been observed. The onset is usually acute, persists for several weeks, and resolves spontaneously over several weeks to months without the need for intervention. Diabetic muscle infarction is a condition that should be considered in the differential diagnosis of any diabetic patient with lower extremity pain and swelling without systemic signs of infection. Magnetic resonance imaging is sensitive and specific enough to make the diagnosis. Muscle biopsy and surgical irrigation and debridement are not recommended since they are associated with complications. Pain management and activity restriction in the acute phase followed by gentle physical therapy is the treatment of choice. Recurrences in the same or opposite limb are common. Although the short-term prognosis is very good and the majority of cases resolve spontaneously, the long-term survival is uncertain in this patient population.

Adult↗
PubMed1999

Prevalence of articular cartilage degeneration in the ankle and knee joints of human organ donors.

The prevalence of osteoarthritis (OA) is higher in some joints than in others. Fibrillation and full-thickness cartilage defects in the knee have been considered to be evidence of developing OA (pre-OA). While similar changes have been reported in the ankle (talocrural joint), the frequency of these changes is much higher than expected if the degeneration represents pre-OA. These observations suggest that in the ankle degenerative changes do not proceed to OA. The current study was to determine the prevalence of articular cartilage degeneration in ankles in a population of 470 bone donors with no history of joint disease. Knees from 50 donors were also available. Our data suggest that degeneration in the ankle cartilage does not appear to be a normal part of aging, was more frequent in men than women, increased with age, and occurred most often in both limbs with the same severity. In those donors with degeneration in the ankle, the knee also showed degenerative changes with an equal or higher grade. These data suggest that factors (such as altered mechanics) responsible for degeneration in one limb also cause changes in the contralateral limb and that factors affecting the ankle joints also appear to influence the knee joints.

Adult↗
PubMed1999

Exercise and osteoarthritis.

The relation of exercise to osteoarthritis is one of great interest and importance. In this paper, we review two recent studies. One reported that older individuals with normal knee and hip joints who jog for recreational activities do not have an increased risk for the development of osteoarthritis in weight-bearing joints. However, in another case-control study of women with hip osteoarthritis, the risk of hip osteoarthritis increased twofold with high levels of participation in recreational activities before the age of 50 years and fourfold for women with high levels of sporting activities and occupational physical loads. Therefore, participation in certain types of sporting activities and occupations that increase loading to the hip joint before the age of 50 years may be associated with an increased risk of hip osteoarthritis. However, recreational jogging in individuals 60 or more years of age with normal knee and hip joints does not increase the risk for the development of osteoarthritis. These studies add to our knowledge base regarding lifetime and current risk factors for the development of knee and hip osteoarthritis from exercise.

Exercise↗
PubMed1999

Evaluating methods of restoring cartilaginous articular surfaces.

Surgeons and scientists have developed various approaches to restoring cartilaginous articular surfaces with the intention of relieving pain and improving mobility for people with traumatic or degenerative damage to their synovial joints. These approaches can be divided into two categories: methods intended to stimulate formation of new cartilaginous tissue and transplantation of osteochondral allografts or autografts. Experimental studies have shown that multiple variations of these approaches can restore some form of cartilaginous articular surface, but formation or transplantation of cartilaginous tissue in an animal model does not prove that a given method has the potential to relieve joint symptoms or improve joint function in humans. The effort to restore cartilaginous articular surfaces has reached the point that investigators should now evaluate the experimental results of methods intended to restore cartilaginous articular surfaces in ways that will identify the most promising approaches to the solution of clinical problems. Important issues concerning the experimental models include the types of articular surface defects studied, the age of the animal, and differences in articular cartilage among species. Important considerations in assessing the outcome of procedures designed to restore an articular surface include the overall function of the animal or patient, the function of the joint, the structure of the joint, and the structure, composition, and mechanical properties of the new tissue. This approach to evaluating methods of restoring a cartilaginous articular surface assumes that the goal of any of these methods is to provide sustained improved joint function and decreased joint symptoms in people with traumatic or degenerative joint damage, and that tissues that differ from normal articular cartilage may achieve this goal.

Aging↗
PubMed1999

Reg Cooper.

Explore the source record for details and available documents.

History, 20th Century↗
PubMed1999

The variable presentation and natural history of Langerhans cell histiocytosis.

Langerhans cell histiocytosis is not a well defined or predictable disease. Instead, it is a spectrum of disorders of unknown etiology that vary widely in presentation and natural history, but have in common the proliferation of histiocytic cells and infiltration of these cells into normal tissues. Although the lesions of Langerhans cell histiocytosis consist primarily of histiocytes, eosinophils are a prominent feature in some lesions. Lesions may develop in any tissue, but bone, skin and lymph nodes are the most commonly affected, and more than 75% of patients have skeletal lesions. Bone lesions caused by Langerhans cell histiocytosis vary from focal sharply defined areas of bone lysis to diffuse osteopenia and can resemble lesions caused by a wide variety of metabolic, infectious and neoplastic diseases. The natural history varies from a benign disorder that resolves spontaneously to a progressive fatal disease. In general, the younger the individual at the time of onset of the disease, the poorer the prognosis and the more extensive the disease. Treatment may include surgery, chemotherapy and radiation therapy, depending on the extent and severity of the disease.

Disease Progression↗