Osteopenic bone disease

Osteoporosis, osteomalacia, and hyperparathyroidism are the common causes of skeletal osteopenia. Radiograms of the skeleton are a basic part of the clinical evaluation of these osteopenic processes. Accurate interpretation of these radiograms is difficult; the presence and degree of osteopenia is often a subjective estimate. This article discusses radiographic features of the common deossifying disorders, including objective criteria that may be useful in routine clinical practice.     

Posttransplant bone disease

Even after a successful kidney transplantation with good kidney function, many renal transplant patients have disabling skeletal symptoms. Approximately 7% to 10% of renal transplant patients may experience a fracture, mainly of the cancellous bones but also of the vertebrae. The fracture frequency is even higher in female renal transplant patients and much higher still in diabetic renal transplant patients. Furthermore, approximately 60% of renal transplant patients have a significant reduction of the bone mineral content and bone mineral density, which is mainly manifest in the vertebrae and the hips. The etiology of posttransplant bone disease is multifactorial, depending on the pretransplant skeletal condition of the patient, on the immunosuppressive therapy given after transplantation, on posttransplant hormonal disturbances, and on the glomerular filtration rate that is obtained after transplantation. Bone biopsy studies have revealed alterations of bone remodeling that reflect a decrease in bone formation despite a continuing bone resorption. Prophylaxis and treatment of the posttransplant bone disease should take into consideration the numerous pathogenetic factors involved, which might vary significantly from patient to patient. As such, a “simple” and easy-to-manage protocol to be provided to all posttransplant patients has yet to be created.     

Dialysis bone disease

The bone disease associated with end-stage renal failure (ESRD) and treatment are complex and multifactorial, and has changed in both clinical and imaging features over the past three decades. Whereas previously features of vitamin D deficiency (rickets/osteomalacia) and intense, and prolonged, secondary hyperparathyroidism (bone resorption, osteosclerosis, metastatic calcification) predominated, these features are now rarely evident radiologically. This has occurred through the better understanding of vitamin D metabolism and improvements in therapeutic management. However, metastatic calcification in soft tissues and 'adynamic" bone continue to be problematic. New complications have developed as a consequence of treatment (dialysis and transplantation), including amyloid deposition, noninfective sponyloarthropathy, osteonecrosis, and osteopenia/osteoporosis). Radiographs remain the most widely used imaging technique in examining for skeletal disease in patients with ESRD on maintenance dialysis. Occasionally, more sophisticated imaging (CT, MRI, nuclear medicine scanning) are helpful (parathyroid tumor localization, differentiation between infection and amyloid deposition). Developments in quantitative methods to assess bone density enable the effects of ESRD and treatment to be studied and monitored. Technical developments in computed tomography (rapid, multislice scanning) allow quantitation and monitoring of metastatic cardiac calcification in patients on hemodialysis, which has relevance to prognosis.     

Cancer-associated bone disease

Bone is commonly affected in cancer. Cancer-induced bone disease results from the primary disease, or from therapies against the primary condition, causing bone fragility. Bone-modifying agents, such as bisphosphonates and denosumab, are efficacious in preventing and delaying cancer-related bone disease. With evidence-based care pathways, guidelines assist physicians in clinical decision-making. Of the 57 million deaths in 2008 worldwide, almost two thirds were due to non-communicable diseases, led by cardiovascular diseases and cancers. Bone is a commonly affected organ in cancer, and although the incidence of metastatic bone disease is not well defined, it is estimated that around half of patients who die from cancer in the USA each year have bone involvement. Furthermore, cancer-induced bone disease can result from the primary disease itself, either due to circulating bone resorbing substances or metastatic bone disease, such as commonly occurs with breast, lung and prostate cancer, or from therapies administered to treat the primary condition thus causing bone loss and fractures. Treatment-induced osteoporosis may occur in the setting of glucocorticoid therapy or oestrogen deprivation therapy, chemotherapy-induced ovarian failure and androgen deprivation therapy. Tumour skeletal-related events include pathologic fractures, spinal cord compression, surgery and radiotherapy to bone and may or may not include hypercalcaemia of malignancy while skeletal complication refers to pain and other symptoms. Some evidence demonstrates the efficacy of various interventions including bone-modifying agents, such as bisphosphonates and denosumab, in preventing or delaying cancer-related bone disease. The latter includes treatment of patients with metastatic skeletal lesions in general, adjuvant treatment of breast and prostate cancer in particular, and the prevention of cancer-associated bone disease. This has led to the development of guidelines by several societies and working groups to assist physicians in clinical decision making, providing them with evidence-based care pathways to prevent skeletal-related events and bone loss. The goal of this paper is to put forth an IOF position paper addressing bone diseases and cancer and summarizing the position papers of other organizations.     

Posttransplant bone disease

Kidney transplantation reverses some of the disturbances of mineral and bone metabolism. However, the reversal or degree of improvement is often incomplete. The well-documented bone loss, especially in the early posttransplant period, contributes to an increased incidence of fractures in kidney transplant recipients. To better understand the mechanism of bone loss posttransplant, we need to take in consideration both bone quantity (density) and quality (bone microarchitecture, turnover rate). In addition to bone density, which is a measure of bone quantity, there are other invasive and noninvasive tools that provide information about the bone architecture and turnover and may be helpful in evaluating kidney transplant recipients at risk of fractures. There are several factors that contribute to the development of bone loss in the posttransplant period. Among these, the use of glucocorticoids, as part of the posttransplant immunosuppressive regimen, remains the single most important risk factor for bone loss post–kidney transplant. Interventions for evaluation and management of bone disease posttransplant are described and discussed. Some of these measures have been shown to increase bone density, but so far, none have demonstrated an ability to reduce the fracture incidence.     

Paget's disease of bone

Paget's disease of bone is defined as a process of increased bone remodeling; the primary event is increased resorption (osteoclastic activity) followed by subsequent reactive bone formation (osteoblastic activity). It is usually asymmetric and may be asymptomatic. The etiology is unknown, but recent evidence appears to support the theory that a virus is an important etiologic factor. It may present with a wide variation in the clinical and radiographic picture. The most frequent sites of involvement include the spine, femora, cranium, pelvis, and sternum. The most common complaints are pain, skeletal deformity, and change in skin temperature. Pathologic fractures may be the presenting manifestations or complications in a patient with known Paget's disease. They occur most frequently in the long weight-bearing bones of the lower extremities such as the femoral neck and subtrochanteric and tibial regions. The two major therapeutic agents available for treatment are calcitonins (porcine, salmon, or human) and diphosphonates. The aim of such therapy is to control the metabolic activity of the disease, to normalize the biochemical parameters, and to improve the symptoms. Fortunately, tumors are rare; early diagnosis may give rise to more effective palliation, if not a significant cure rate.     

Posttransplantation bone disease

Transplanted patients experience rapid loss of bone, high fracture rates, and increases in morbidity and mortality as a consequence of a posttransplant scenario that is highly deleterious to the skeleton. Immune suppressive drugs, especially glucocorticoids, are toxic to bone, often acting on a background of preexisting osteodystrophy resulting from long-standing renal, hepatic, cardiac, or pulmonary disease. Cyclosporin and tacrolimus lead to a severe osteopenic state in rats, but the skeletal toxicity of the calcineurin inhibitors in the clinical environment is less clear. Nor is it clear whether cyclosporin and tacrolimus differ in their skeletal actions. Mycophenolate mofetil and sirolimus do not appear to have important skeletal toxicity. Preventative strategies include minimizing glucocorticoid exposure and implementing therapies to counter the increase in bone resorption and decrease in bone formation that follows transplantation. Antiresorptive agents, especially bisphosphonates, appear capable of retarding or halting the early bone loss and possibly reduce fracture rates also. Vitamin D and calcium are ineffective, but calcitriol has utility in some reports. Bone anabolic agents, such as synthetic parathyroid hormone and growth hormone, have potential, but data are lacking.     

Cancer-associated bone disease

Patients with cancer are at risk for many events involving the skeleton, including metastatic disease of bone and treatment-related bone loss. Cancer-related therapies that can affect bone include hormonal therapy, chemotherapy, and the use of glucocorticoids. Screening for bone loss, with lifestyle modifications and the early use of anti-osteoporosis therapies such as bisphosphonates, may decrease bone loss and reduce the risk of fracture. This article reviews risk factors and mechanisms associated with cancer-related bone loss and metastases as well as strategies for the detection of bone-related complications of cancer and therapies to treat these complications. This article focuses on the more common cancers with adverse skeletal effects: breast cancer, prostate cancer, and multiple myeloma.     

Hydatid disease of bone

A case of primary hydatid disease of the right femur is reported that presented with pathological fracture and was diagnosed at the time of exploration for biopsy. The patient was treated by removal of all cysts, irrigation with scolicidal solution, bone grafting and immobilisation of the fracture followed by four cycles of oral Albendazole. Eosinophilia and serological tests reverted to normal but the patient died due to acute myocardial infarction six months later. This uncommon condition should be considered in the differential diagnosis of pathological fractures, bone pain or osteolytic lesions, especially in patients of rural and farmer background.