Rickets or osteomalacia

Vitamin D deficiency Hypophosphatemia

Hyperparathyroidism
Primary hyperparathyroidism Secondary hyperparathyroidism Renal osteodystrophy

Pagets Disease

Osteomalacia
is caused by deficient calcification of an otherwise normal protein bone matrix Due to failure of calcium and phosphorus deposition in bone matrix

X-ray Findings:
Involvement of the pelvis and long bones, with demineralization and bowing Less often, the spine and skull are involved as well. Fractures are rare except for "pseudo fractures."

lucent band of decreased cortical density perpendicular to bone surface often multiple, +/- symmetrical +/- callus formation "pathognomonic" of osteomalacia
seen on compressive (concave) side (eg, prox femur)

also seen in Paget disease on tensile (convex) side

AP view loosers zone

frogleg view loosers zone

This is a classic pseudofracture and is pathognomonic for osteomalacia.

The skeletal effects are due to lack of calcification of osteoid. The most obvious change are at 'metaphysis'where rapid growth is occurring. First change to appear is a 'loss of normal zone of provisional calcification' adjacent to metaphysis. This begins as an indistinctness of the metaphyseal margin, progressing to a 'frayed' appearance with widening of the growth plate, due to lack of calcification of metaphyseal bone. Weight bearing & stress on uncalcified bone gives rise to 'splaying' & 'cupping' of metaphysis.

A similar but less marked effect occurs in subperiosteal layer , which may cause lack of distinctness of cortical margin. Eventually a generalized reduction in bone density is seen. In the epiphysis - there may be some haziness of cortical margin. Thus all findings in Rickets occur due to failure of calcification & abnormal demineralization

The first changes of rickets appear in rapidly growing distal ends of ulna & radius (wrist & knee are commonly involved due to more use). Rarefaction of provisional zone of calcification with widening of epiphysisdiaphysis distance is first to appear. Following treatment there is ossification of provisional zone of calcification.

Splaying, fraying, cupping, widening of growth plates of bilateral distal radius and ulna.

Closer view of a knee showing thick growth plates that appear fuzzy, and widened knee joints

This x-ray shows a widened growth plate with an irregular pattern on the metaphyseal side.

This is an x-ray of the same patient taken after treatment with calcium and vitamin D. The growth plate has been reduced to its normal width as the cartilage has begun to calcify. The margin is smooth and clean on the end of the ulna. The calcification bands are visible on both radius and ulna.

This is an x-ray of a child with bowed legs due to rickets

Xrays:
sub-periosteal resorption pepper pot skull/salt & pepper skull

rugger jersey spine

cystic brown tumours

Subperiosteal resorption of cortical bone is virtually diagnostic of hyperparathyroid bone disease. In this form, a lacelike appearance of the phalangeal bone may progress to a spiculated contour and, eventually, to complete resorption of the entire cortex. Other sites of subperiosteal resorption include the phalangeal tufts; medial aspect of the proximal ends of the tibia, humerus and femur; superior and inferior margins of the ribs; and lamina dura. Subperiosteal resorption of bone may also be apparent at the margins of certain joints, especially those in the hand, wrist and foot

-The plain x-ray of the hand shows typical changes of hyperparathyroidism, with resorption of subperiosteal bone on the radial side of proximal and middle phalanges of the 2nd and 3rd digits. -This is most obvious in the proximal phalanx of the middle finger.

X-ray Wrist shows marked subperiosteal bone resorption in the radial aspect of the middle phalanges of the 2nd and 3rd digits.

X-ray Skull (Lateral) shows diffuse trabecular resorption, giving a granular 'salt and pepper' appearance. Loss of distinction between the outer and inner tables of the skull is seen

Xrays:

sub-periosteal resorption
pepper pot skull/salt & pepper skull

rugger jersey spine

cystic brown tumours

Xrays:
sub-periosteal resorption pepper pot skull/salt & pepper skull rugger jersey spine

cystic brown tumours

Xrays:

sub-periosteal resorption
pepper pot skull/salt & pepper skull

rugger jersey spine

cystic brown tumours

Xrays:

sub-periosteal resorption
pepper pot skull/salt & pepper skull rugger jersey spine cystic brown tumours

Xray appearance

holes in bone without sclerotic reaction

no reaction of the host bone to the lesions Bone scan may be negative

Radiology

cortical thickening
osteolytic, osteosclerotic and mixed lesions osteoporosis circumscripta

bone scan

In the skull, the initial osteolytic phase of pagets is called "osteoporosis circumscripta" due to the presence of geographic lucent regions primarily within the frontal bone. This is followed by excessive new bone formation leading to cortical thickening and osteosclerotic changes in the inner table, diploe, and subsequently the inner surface of the outer table. In this phase, plain radiographs manifest a characteristic "cotton wool" appearance of sclerotic lesions surrounded by areas of demineralization.

typical appearance of the skull in advanced pagets

Characteristic x-ray findings include the following:

Increased bone sclerosis Abnormal architecture with coarse cortical trabeculation or cortical thickening Bowing Bony enlargement There may be stress microfractures of the tibia or femur.

This lateral skull view shows the typical "cotton-wool" appearance.

Lateral radiograph of the skull shows a diffuse lucency affecting the frontal and temporal bones. The margin between lucent and normal bone is well defined.

Paget's disease of the lumbar spine. Typical features include expansion of bone, the picture frame appearance, obvious softening of bone, plasticity, and posterior element involvement.

Osteoporosis is caused by a deficiency of organic bone matrix. Osteoporosis is a disease characterized by low bone mass and loss of bone tissue that may lead to weak and fragile bones. Has an increased risk for fractured bones (broken bones).

The serum calcuim, phosphorus, and alkaline phosphatase are normal. Common causes of generalized osteoporosis:
Senility Cushings disease Hyperparathyroidism Severe childhood anemias Osteogenesis imperfecta Multiple myeloma

Local osteoporosis can result from:

Disuse Neurovascular disturbances (Sudecks atrophy) Local joint disease

* Osteoporosis is most marked in the spine and pelvis.

The earliest feature of spinal osteoporosis is prominent vertical striations due to loss of secondary horizontal trabecula

General osteoporosis. There is reduced radiographic density (osteopenia), with reduction in the number of trabeculae, which may be destroyed completely, and the bone cortex becomes thinned, as evident in the lateral radiograph of the calcaneus.

General osteoporosis. There is reduced radiographic density (osteopenia), with reduction in the number of trabeculae, which may be destroyed completely, and the bone cortex becomes thinned, as evident in the radiograph of the phalanx.

Sudecks Atrophy Demineralization of bone with intact but very thin cortices.

Radiographic distinction of osteomalacia from osteoporosis is often difficult. Frequently, the two conditions coexist.

Osteonecrosis is a disease of impaired osseous blood flow. Neither the etiology nor the natural history has been definitively determined. Many of the patients are young when they are diagnosed.

TRAUMATIC CONDITIONS : A displaced fracture of the femoral neck or a hip dislocation are wellknown etiologies of ONH; they lead to a mechanical interruption of the circulation to the femoral head. NONTRAUMATIC CONDITIONS : - Corticosteroid administration (respiratory and rheumatod deseases, organ transplantation as well as Cushing disease) have a somewhat higher prevalence of osteonecrosis. - Excessive alcohol intake has been identified as an etiologic factor. - Many other pathologies has been associated with Osteonecrosis : hemoglobinopathies, Dysbaric osteonecrosis, Gaucher desease, lupus, high-dose radiation, chemotherapy, hyperlipidemia...

The Xray findings : Early on are completely normal, but with ongoing problem, one sees progressively :
Osteopenia Central radiolucency with a sclerotic border A Subchondral lucency - making up the crescent sign Fattening of the head. Collapse of the head. Secondary changes of Osteoarthritis. Joint space narrowing Progressive joint destruction

Since the X-Rays may be completely normal - it is essential to be able to see the problem early. Suggest an MRI if highly-suspected

These x-rays of the hip show the different stages of the disease. - At first (stage I), there are no detectable changes on x-ray (fig A). - In stage II, there are some changes but the surface is still intact (fig B). -As the disease progresses, the surace begins to collapse (fig C) until, -finally, the integrity of the joint is destroyed (fig D).