This document summarizes bone and joint diseases as seen on radiographs. It describes generalized decreased and increased bone density caused by conditions like osteoporosis, osteomalacia, hyperparathyroidism and Paget's disease. Specific findings of osteoporosis, rickets, osteomalacia and hyperparathyroidism are outlined. Joint diseases discussed include osteoarthritis and its features of joint space narrowing and soft tissue swelling. Diagnosis of arthritis depends on the number and location of involved joints and presence of underlying diseases.
Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.
Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.
Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications.
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Book: Mayo Clinic Family Health Book, 5th Edition
Symptoms
Signs and symptoms of rickets can include:
Delayed growth
Delayed motor skills
Pain in the spine, pelvis and legs
Muscle weakness
Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as:
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.
Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.
Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications.
Products & Services
Book: Mayo Clinic Family Health Book, 5th Edition
Symptoms
Signs and symptoms of rickets can include:
Delayed growth
Delayed motor skills
Pain in the spine, pelvis and legs
Muscle weakness
Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as:
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Rickets is a metabolic disease of growing bone that is unique to children.
It caused by a failure of mineralization of osteoid tissue in a developing skeleton, particularly at the growth plate.
Imperfect calcification typically resulting in soft bones and skeleton deformities.
Rickets is a metabolic disease of growing bone that is unique to children.
It caused by a failure of mineralization of osteoid tissue in a developing skeleton, particularly at the growth plate.
Imperfect calcification typically resulting in soft bones and skeleton deformities.
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Metabolic bone diseases encompass a spectrum of disorders characterized by abnormalities in bone metabolism, structure, and mineralization. These conditions often result from disturbances in the intricate balance between bone formation and resorption, leading to weakened bones prone to fractures, deformities, and other complications. This comprehensive exploration will delve into the pathophysiology, clinical manifestations, diagnostic approaches, and management strategies for various metabolic bone diseases, shedding light on these complex yet fascinating conditions.
Introduction to Metabolic Bone Diseases
The skeleton serves as the structural framework of the body, providing support, protection, and mobility. Maintaining the integrity and strength of bones relies on a delicate equilibrium between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Disruptions in this equilibrium can give rise to metabolic bone diseases, which can be classified broadly into two categories: disorders of bone remodeling and mineralization.
Disorders of Bone Remodeling
Osteoporosis
Osteoporosis stands as the most prevalent metabolic bone disease, characterized by decreased bone mass and microarchitectural deterioration, predisposing individuals to increased fracture risk, particularly in the hip, spine, and wrist. Postmenopausal women and elderly individuals are at heightened risk due to hormonal changes and age-related bone loss. Contributing factors include inadequate calcium and vitamin D intake, sedentary lifestyle, smoking, and excessive alcohol consumption. Dual-energy X-ray absorptiometry (DXA) is the gold standard for diagnosing osteoporosis, and management strategies focus on lifestyle modifications, calcium and vitamin D supplementation, and pharmacological interventions to mitigate fracture risk.
Osteogenesis Imperfecta (OI)
OI, often referred to as brittle bone disease, encompasses a group of genetic disorders characterized by fragile bones prone to fractures, skeletal deformities, and short stature. Mutations affecting the synthesis or structure of type I collagen, the primary protein component of bone, underlie this condition. OI exhibits considerable clinical heterogeneity, ranging from mild forms with few fractures to severe cases associated with significant morbidity and mortality. Management involves a multidisciplinary approach, encompassing supportive measures, physical therapy, and surgical interventions to optimize bone health and function.
Paget's Disease of Bone
Paget's disease represents a disorder of excessive bone remodeling, marked by focal areas of increased bone resorption and disorganized bone formation, resulting in enlarged and weakened bones. Though the exact etiology remains elusive, environmental and genetic factors likely contribute to its pathogenesis. Affected individuals may present with bone pain, deformities, and complications such as fractures, nerve compression, and secondary osteoarthritis.
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Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
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3. Radiographic density of the bone depend on the amount of calcium present in the bone. decrease in bone calcium lead to decrease in bone density.
4. Main causes of generalized decrease in bone density; Osteoporosis. Osteomalacia. Hyperparathyroidism. Multiple myeloma.
5. osteoporosis Osteoporosis is the consequence of a deficiency of protein matrix(osteoid) & decrease amount of the normal bone (i.e. loss of bone mass) while remaining bone is normally mineralized (microstructure of the bone remain normal & histologically also normal)
7. Main Causes of osteoporosis 1-Idiopathic; according to the age, subdivided to; Juvenile Senile Postmenopausal; up to 50% of female over 60 years of age have osteoporosis. 2-Cushing’s disease & steroid therapy. 3-disuse
8. Radiological features Change in bone density usually unapparent until 30-50% of the bone mass has been lost. Decreased cortical thickness. Decreased no. of the trabeculae present in the bone.
9. Changes best seen in the spine. Resorption of the horizontal trabeculae. Empty box ; apparent increased end plate density due to Resorption of the spongy bone. VB compression fracture; wedged or biconcave types with apparent widening of the disc spaces
10. Generalized decrease in bone density Prminent vertical trabicuale Empty box VB compression fracture
11. Local decreased bone density caused by localized pain or immobilization of a fracture Disuse osteoporosis
12. Indistinctness of the cortex of the right femoral head and osteopenia of the entire femoral head
13. Rickets & osteomalacia There is poor mineralization of osteoid. If occur before epiphyseal closure, it known as rickets. If occur in adult ,it known as osteomalacia.
14. Radiological finding of rickets The changes are maximal where bone growth is occur, so they best seen in the knees, wrists & ankles Loss of provisional zone of calcification. Indistinct metaphyses& metaphyses become irregular and cupped. Wide growth plate. decreased bone density. Deformities of the bones occur because of bone softening. Greenstick fractures are common
15. This patient shows abnormal bone density, with coarsened abnormal trabeculae in a generalized pattern. Even more prominently, we see widened and irregular metaphyses Rickets
16. The anterior ends of the ribs are quite abnormal in this patient, with splaying at the costochondral junction (rachitic rosary)
17. Radiological findings; Decreased bone density. Looser’s zones; are short lucent band running through the cortex at the Rt angles & may have sclerotic margin, commonest site are scapula, medial aspect of femurs,& pubic rami & ribs Bone deformity due to bone softening e.g. biconcave vertebra bodies osteomalacia
18. This patient has generalized osteopenia. In addition, several of the right lower ribs demonstrate transverse fractures with a wide lucency at the fracture site (arrow). Your diagnosis? Osteomalacia with looser’s zone
19. Hyperparathyroidism Cause mobilization of the calcium from the bone, resulting in a decreased bone density. Hyperparathyroidism could be primary hyperparathyroidism (90 percent due to an adenoma) or secondary hyperparathyroidism due to renal dysfunction.
20. Many patients with primary hyperparathyroidism present with renal stone & minority present with radiologically detected bone changes.
21. Radiological features of hyperparathyroidism Generalized decrease in bone density. The hallmark of hyperparathyroidism is subperiosteal bone Resorption. Soft tissue calcification; vascular & chondrocalcification sometime occur. Brown tumor are occasionally present which are small lytic lesion which could be single or multiple
22. Extensive subperiostealresorption is seen on both the radial and ulnar side of the middle phalanges (white arrows, left hand). brown tumor in the left distal ulna as well as the left trapezoid (black arrows, left hand). as well as in the right head of the third metacarpal and the base of the proximal phalanx of the fifth digit (black arrows, right hand).
23. Features of both primary & secondary hyperparathyroidism are similar except that brown tumors are much rarer & vascular calcification is commoner in secondary hyperparathyroidism
26. Causes; Sclerotic metastases, commonest cause. Osteopetrosis (marble bone disease); congenital, bone sclerotic & brittle leading to multiple fractures. Myelosclerosis; there is replacement of the bone marrow by fibrous tissue & lay down of the bone which is usually appear as patchy areas of sclerosis
27. This child has extremely dense bones throughout the body. There is abnormal modeling at the metaphyses with flaring. Your diagnosis? Osteopetrosis
28. Alteration in trabecular pattern & changes in the shape1-Paget’s disease2-Hemolytic anemia3-Radiation induced bone diseases
29. Usually is the chance finding in elderly. One or more bones may be affected, the usual sites are pelvis, spine , skull & long bones 1-Paget’s disease
30.
31. this patient gives a classic appearance of advanced mixed lytic and sclerotic Paget's disease , bone expansion,loss of corticomedullary differentiation and anterior bowing of the tibia Paget’s disease
33. There are many types of hemolytic anemia , but radiological changes are seen in main two types; thalassaemia & sickle cell disease. Both causes bone marrow hyperplasia, but sickle cell disease also may show evidence of bone infarction & infection 2-Hemolytic anemia
34. dense striations in a very widened diploic space of the cranium (hair-on-end appearance). Additionally, note that the paranasal sinuses are obliterated Thalassemia
35. The metacarpals and phalanges are squared and show a very thinned endosteal cortex with abnormal density. Resorption of some trabeculae & remaining trabeculae become thick & prominent. Thalassemia
36. Radiological features of marrow hyperplasia Thinning of the cortex & bone expansion. Resorption of some trabeculae & remaining trabeculae become thick & prominent. In the skull; it cause widening of the deploe & perpendicular striation occur which is known as ‘ Hair-on-end’. The ribs may enlarged & phalanges may become rectangular.
38. Mixed lytic and sclerotic density is seen involving most of the right upper ribs, the right clavicle, scapula, and proximal humerus. Multiple healed rib fractures are seen in this area. Radiation osteonecrosis
39. Radiotherapy may cause local damage of the bone in the radiation field. Early change may be limited to osteoporosis. In severe case it may cause osteonecrosis; bone thinning & patchy increase in bone density with small lytic areas. Pathological feature may occur Occasionally radiation induce sarcomatous changes , usually osteosarcoma, which occur several years after the radiation therapy.
41. Is congenital disorder. There are multiple bony projections known as osteochondromas or exostoses. They have cartilaginous cup which may contain calcification. When exostoses occur in the long bone , they occur near metaphyses & are directed away form the joint Diaphyseal aclasia (multiple exostoses)
52. 2-Soft tissue swelling; Periarticular soft tissue swelling is a feature of inflammatory & infective arthritis. Discrete asymmetrical periarticular soft tissue swelling can be seen in gout due to gouty tophi
53. 3-Osteoporosis; Occur in many type of painful conditions & under use of the bones is an important cause.
55. To Dx arthritis, it is important to have the following information; 1-Is more than one joint involved? RA, typically involve several joint while infection & synovial tumors usually involve single joint.
59. OA when seen in the hands ,it almost always involves DIP& often affect the CM joint of the thumb & in the large joints, it commonly involve hip& knee, but relatively rare in the ankle , shoulders & elbow joints unless there is some underlying causes.
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61.
62. Degenerative arthritis (OA) Is the commonest form of arthritis. Changes occur secondary to wear & tear of the articular cartilage.