metabolic bone disorders radiology

• Rickets • occur in children

• Causes Malabsorption Long term

anticonvulsant therapy

Toxins like alumininium hydroxide which cause tubular damage

• The skeletal effests are due to lack of calcification of osteoid

• Consequently the most obvious cahnges are at the metaphysis where the most rapid growth is occuring.

• Initial abnormality is a loss of the normal zone of provisional calcification adjacent to metaphysis.

• Begins as indistinctness of metaphyseal margin progressing to a frayed appearance with a widening of the growth plate due to lack of calcification of metaphyseal bone.

• Anteroposterior and lateral radiographs of the wrist of an 8-year-old boy with rickets demonstrates cupping and fraying of the metaphyseal region.

• Radiograph in a 4-year-old girl with rickets depicts bowing of the legs caused by loading.

• Metaphyseal cupping and fraying in the

• distal radius and ulna in rickets

• Fraying examples

fraying

fraying

• Weight bearing and stress on the uncalcified bone give rise to splaying and cupping of the metaphysis and distortion of bone architecture.

• Rickets of the knees demonstrates bowing of the femurs, metaphyseal cupping and fraying,

• coarsening of the trabecular pattern, increase in distance between end of shaft and epiphyseal center,

• poorly ossified epiphyseal centers. - See more at: http://www.learningradiology.com/archives2012/COW%20501-Rickets/ricketscorrect.html#sthash.5fnW8M7T.dpuf

• Radiograph of a two-year old rickets sufferer, with a marked genu varum (bowing of the femurs) and decreased bone opacity, suggesting poor bone mineralization.

• Wrist X ray showing changes in rickets, mainly cupping is seen here.

widening of the wrist

• A similar but less marked effect occurs in the subperiosteal layer which may cause lack of distinctness of the cortical margin.

• Eventualy a generalized decrease in bone density is seen and in long standing cases fracture may occur.

• with treatment mineralization occurs,giving rise to dense white line at the zone of provisional calcification adjacent to the metaphysis,but becoming contiguous with the metaphysis during the healing process.

• In cases of intermittent dietary vitamin deficiency,or inadequate treatment,the metaphysis will show patchy sclerosis.

• In severe cases of rickets additional deformities of bones occur with bowing of the long bones,thoracic kyphosis with a pigeon chest,enlargement of anterior ribs,causing the ricketic rosary and bossing of skull.

• Rickets may be seen in low birthweight and premature infants,and may be severe causing spontaneous fractures and respiratory difficulty.affected infants are usually below 1000gm in weight or less than 28weeks gestation.

Richetic rosary

• Enlarged costochondral junctions of ribs resembling string of rosary beads

• Chest X ray showing changes consistent with rickets, this changed is usually referred to as Rosary beads of rickets.The chest radiograph in this child shows nodular prominence of the costochondral junctions, consistent with rickets..

• Skeletal deformity• Toddlers: Bowed legs (genu varum)• Older children: Knock-knees (genu valgum) or

"windswept knees"• Cranial deformity (such as skull bossing or delayed

fontanelle closure)• Pelvic deformity• Spinal deformity (such as kyphoscoliosis or lumbar

lordosis)

• Growth disturbance

genu varum

• Chest X ray showing changes consistent with rickets, this changed is usually referred to as Rosary beads of rickets

• Hypocalcemia (low level of calcium in the blood)• Tetany (uncontrolled muscle spasms all over the body)• Craniotabes (soft skull)• Costochondral swelling (aka "rickety rosary" or "rachitic

rosary")• Harrison's groove[4]• Double malleoli sign due to metaphyseal hyperplasia• Widening of wrist raises early suspicion, it is due to

metaphyseal cartilage hyperplasia.

• Harrison's groove, also known as Harrison's sulcus, is a horizontal groove along the lower border of the thorax corresponding to the costal insertion of the diaphragm; It is usually caused by chronic asthma or obstructive respiratory disease. It may also appear in rickets because the patients lack the mineralized calcium in their bones necessary to harden them; thus the diaphragm, which is always in tension, pulls the softened bone inward. During rickets it is due to the indentation of lower ribs at the point of attachment of diaphragm.

• An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance (Caput Quadratum). These deformities persist into adult life if not treated. Long-term consequences include permanent bends or disfiguration of the long bones, and a curved back

• Osteomalacia Bone pain is frequent

complaint Occur in adults Serum alkaline

phosphatase is elevated and serum phosphorus is low

• The hall mark is the pseudofracture or Looser;s zone.This is a narrow zone of lucency usually running perpendicular or nearly perpendicular to the bone cortex.

• initially poorly defined these zones become progressively more prominent with sclerotic margins.

• They are frequently bilateral and symmetrical occur at regular sites such as pubic rami,proximal femur,scapula ,lower ribs and ulna.

• Looser's zones in the inferior femoral neck

These lesions are composed of poorly mineralized osteoid matrix and are not true fractures or stress fractures. They are oriented perpendicular to the long axis of the bone, and do not cross the entire bone. Common sites include axillary margins of the scapulae, ribs, pubic rami, proximal femurs, proximal ulnae.

• Osteomalacia with "Looser's zones" or Milkman's pseudofractures.

• ostepenia develops with pencilling- in of vertebral bodies and loss of vertebral height in characteristic cod fish vertebra pattern.

• Bowing of long bones may occur.• Compression wedge fracture of vertebra a

re less common than in osteoporosis.

• ScurvyScurvy is caused by a lack of vitamin C and manifests as collagen defects, hemorrhagic diathesis, abnormalities in bone maturation, epiphyseal disease, lifting of the periosteum, hemarthroses, irritability, decreased appetite, delayed development, and pseudoparalysis related to bone pain

• Radiographic signs1.Wimberger sign2.Frankel's line3.Trumerfeld zone4.pelkan's spur

• Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia. Transverse metaphyseal lines of increased and decreased opacity (Trummerfeld zone) are associated with lateral growth of the metaphyseal calcification zone and periosteal elevation, which produces the characteristic metaphyseal beaks known as Pelkan spurs.

• Osteoporosis• Most frequent

metabolic bone disease

Decrease in bone mass

• Causes

• Radiological features• Fractures particularly

in femoral neck,spine,distal radius and pubic symphysis

• Osteopenia• Pencilling- in of

vertebra• Biconcave vertebral

bodies(cod fish vertebra)

colle's fracture

spine

Compression fracture of spineAnterior wedgingKyphosis

• Anteroposterior and lateral radiographs of an L1 osteoporotic wedge compression fracture.

• Anterior wedge compression fracture with an intact posterior vertebral cortex.

• A vertebral burst fracture

• Osteoporotic spine. Note the considerable reduction in overall bone density and the lateral wedge fracture of L2.

• overall reduction in the bone density and moderate kyphosis of the dorsal spine.

• lateral wedge fracture of L3 and a central burst fracture of L5. The patient had a recent fall.

• considerable reduction in the overall bone density and lateral wedge fracture of L2.

codfish vertebra

• Recent fractures of the 8th and 10th thoracic vertebrae with low signal on T1 and high signal on STIR. Deformities of Th12 (fish vertebra) and L1 through L5 (biconcave deformities or endplate impressions) from earlier fractures. Epidural lipomatosis L2-L5.

• Insufficiency fractures of the sacrum and the pubic rami are seen on an isotopic bone scan as a characteristic H, or Honda, sign (arrows), which appears as intense radiopharmaceutical uptake at the fracture sites.

T2W

• This radiograph of the spine shows a lateral wedge fracture of L3 (yellow asterisk) and compression fracture of L5 (red asterisk) in an osteoporotic patient who suffered a recent fall. More detailed imaging, usually with computed tomography (CT) scanning, is often needed to better evaluate compression fractures and to determine the urgency of surgical interventions.

• Lateral spine radiograph depicting osteoporotic wedge fractures of L1-L2. Source: Wikimedia Commons.

types

Postmenopausal and senileidiopathic juvenileSteroid induced osteoporosis

• Weight-bearing exercises positively affect bone marrow density by increasing cortical bone mass and load-bearing strength; 45 minutes 4 times per week is the recommended schedule. Specialty training regimens, such as the tai chi chuan exercises shown, are also helpful in improving agility and balance, thereby reducing the risk for falls and subsequent fractures.

• Primary hyperparathyroidism

• Overproduction of parathyroid hormone (PTH) with associated hypercalcemia

• Most frequent cause: single adenoma in 85% of cases• Clinical: Bones (osteopenia, brown tumors), stones (renal calculi) and

abdominal groans (ulcer disease)• Laboratory: increased parathormone level with hypercalcemia is

diagnostic of primary hyperparathyroidism• Imaging of the parathyroid glands: radiolabeled technetium 99m

sestamibi persists in adenomas on nuclear scans• Brown tumors are more common than in secondary form• Treatment: Symptomatic patients are usually treated by surgically

removing abnormal gland(s)

• the most common radiologic finding in primary hyperparathyroidism is osteopenia, which may be generalized or asymmetric.

• Additional findings include bone resorption, which may occur at many different anatomic sites. Bone resorption may be classified as subperiosteal, intracortical, trabecular, endosteal, subchondral, subligamentous, or subtendinous.

Subperiosteal bone resorption is an early and virtually pathognomonic sign of hyperparathyroidism, and this finding is marked by marginal erosions with adjacent resorption of bone and sclerosis. An unusual lacelike appearance may be seen beneath the periosteum with an occasional spiculated external cortex. The underlying resorptive process may progress to complete cortical disappearance.

• Although subperiosteal bone resorption can affect many sites, the most common site in hyperparathyroidism is the middle phalanges of the index and middle fingers, primarily on the radial aspect

• Bilateral anteroposterior (AP) radiographic views of the hands in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and primary hyperparathyroidism. These images show subperiosteal bone resorption along the radial aspects of the middle phalanges.

• Anteroposterior radiographic view of the right hand in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and primary hyperparathyroidism (same patient as in the previous image). This image shows subperiosteal bone resorption along the radial aspects of the middle phalanges (arrows).

• Radiograph of the middle phalanges in a patient with primary hyperparathyroidism. This image demonstrates subperiosteal resorption that has resulted in severe tuftal resorption (white arrows). Also, note the subperiosteal and intracortical resorption of the middle phalanges (black arrows).

• Anteroposterior radiographic view of the left shoulder in external rotation in a patient with primary hyperparathyroidism. This image shows the healing stage of marked subperiosteal resorption (arrow) of the medial aspect of the proximal humerus.

• Radiograph of the shoulder in a patient with primary hyperparathyroidism. This image demonstrates distal clavicular resorption.

• This image shows scalloped defects along the inner margin of the cortex, which denote endosteal resorption.

• . This image depicts a brown tumor. Note the osseous expansion and lucency of the proximal humerus. Brown tumors can have varied appearances.

• This image depicts brown tumors. Note the eccentric (arrowheads) and central positions (arrow) of the lesions.

• presence of brown tumors in the pelvis.

• medullary nephrocalcinosis.

• Technetium-99m sestamibi (99mTc MIBI) images in a patient with primary hyperparathyroidism. The initial (A) and 3.5-hour delayed (B) images demonstrate a 6-cm parathyroid adenoma (arrows).

• Sagittal (left image) and coronal (right image) T1-weighted magnetic resonance images of the brain in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) (same patient as in the previous image). These images show a pituitary macroadenoma (arrows).

• image demonstrates subperiosteal resorption that has resulted in severe tuftal resorption (arrows).

• Secondary Hyperparathyroidism. White arrows point to subperiosteal resorption along the radial (lateral) aspects of the middle phalanges of the index, middle and ring fingers, a finding virtually pathognomonic for hyperparathyroidism. The cortex appears spiculated. There is acro-osteolysis (yellow arrows) of several of the terminal phalanges. A small, lytic lucency in the head of the metacarpal of the middle finger represents a brown tumor.

• Bilateral hand radiographs in a 50 year old woman demonstrate generalised osteopenia, erosion of the terminal phalyngeal tufts (acro-osteolysis) and sub-periosteal resorption of bone particularly the radial aspects of the 2nd and 3rd middle phalanges.

• Subperiosteal resorption as well as acroosteolysis

• : Subperiosteal resorption in a child

• Acroosteolysis (also subperiosteal resorption)

ruger jersey spine

pepper pot

• Salt and pepper skull

• Normal skull in the same patient following treatment of hyperparathyroidism

•

• Brown Tumor• Brown tumors are more common in patients with

primary hyperparathyroidism, however, due to the increased prevalence of secondary hyperparathyroidism, there are more brown tumors from secondary hyperparathyroidism than form primary hyperparathyroidism. It is difficult to differentiate a Brown Tumor from a giant cell tumor or fibrous dysplasia; however, other signs of hyperparathyroidism should be present.

• Brown tumor in the phalanx (also subperiosteal resorption, tuft resorption, and osteopenia)

• Brown tumor in the inferior obturator ramus