Metabolic Bone Disease
Dr Prassan Tripathi
MS ORTHO
Asst Prof
Four Groups
1. Inadequate Osteoid synthesis - Osteopenia
2.Inadequate Mineralisation of Osteoid
Osteomalacia & Rickets – a.Dietary b. Disuse
3.Decreased Osteoid synthesis and increased Osteolysis
Osteoporosis – a.Senile b.Post Menopausal
4.Increase in Bone Mass – Osteosclerosis
a.Paget”s disease, b.Osteopetrosis
Characterized by abnormalities in calcium metabolism and/or bone cell physiology.
Metabolic Bone Disease
Introduction
• Metabolic bone disease (MBD)
• • Encompasses a diverse group of disorders
• associated with altered calcium and
• phosphorus homeostasis.
• • To orthopedic surgeons; MBD is often silent
• until the patient presents with fracture.
OSTEOPOROSIS
• Most common metabolic bone disease.
• One of the most prevalent conditions
associated with aging.
• Definition : Systemic skeletal disease
characterized by low bone mass and micro
architectural deterioration of bone tissue ,
with a consequent increase in bone fragility
and susceptibility to bone fracture.
"Microarchitectural deterioration" refers to the thinning of the trabeculae and the
loss of intertrabecular connections in bone
RISK FACTORS
Major risk factors
• Age > 65 years
• Systemic glucocorticoid therapy
of >3 months duration
• Mal-absorption syndrome
• Primary hyper parathyroidism
• Propensity to fall
• Osteopenia apparent on X-ray
film
• Hypo-gonadism
• Early menopause (before age 45)
• Family history of osteoporotic
fracture (especially maternal hip
fracture)
Minor risk factors
• Rheumatoid arthritis
• Past history of clinical
hyperthyroidism
• Chronic anticonvulsant therapy
• Low dietary calcium intake
• Smoker
• Excessive alcohol intake
• Excessive caffeine intake
• Weight <57 kg
• Weight loss >10% of weight at
age 25
• Chronic heparin therapy
• Clinical definition: requires the presence of a
nontraumatic fracture.
• Histologic definition: requires normally
mineralized bone to be present in reduced
quantity.
Diagnosis Osteoporosis
• Bone densitometry; gold standard
• 1. Detection osteoporosis before fractures.
• 2. Determination disease severity.
• 3. Estimation risk of fracture.
• Serial BMD measurements enabl determination
of rate of bone loss or gain and thereby help in
monitoring therapy.
• Plain film; loss of 30% to 50% of bone is required
• before it is detected on conventional radiographs.
Ostoporosis Classification
• Ostoporosis Classification
• • Primary osteoporosis. (idiopathic) : more common
• – Type 1 (postmenopausal)
• – Type 2 (age-related or senile)
• • Secondary osteoporosis.
• – Metabolic (acromegaly, hypercorticism, hyperthyroidism,
• hyperparathyroidism, hypogonadism, pregnancy, diabetes
• mellitus)
• – Congenital (osteogenesis imperfecta, Ehlers-Danlos syndrome,
• homocystinuria, mastocytosis, ochronosis, Gaucher's disease)
• – Nutritional (alcoholism, malnutrition, calcium deficiency, scurvy)
• – Drug-related (steroids, heparin).
PROXIMAL PORTION OF THE FEMUR:
• Analysis of the trabecular pattern of the upper end of the femur has
• been used as an index of osteoporosis.
• In this region, five anatomic groups of trabeculae can be identified.
• 1. Principal compressive group.
• 2. Secondary compressive group.
• 3. Greater trochanter group.
• 4. Principal tensile group.
• 5 .Secondary tensile group.
• Patterns of trabecular loss may correlate with increasing severity of
• osteoporosis. This trabecular analysis is termed as SINGH INDEX.
ANATOMIC GROUPS OF TRABECULA
• Principle compressive
group
• Principal tensile group
• Secondary compressive
group
• Secondary tensile group
• Greater trochanter
group
• Wards triangle
NORMAL TRABECULAR PATTERNS. Proximal Femur. A. Three major patterns exist: principal
compressive group (1), secondary compressive group (2), and principal tensile group (3). The
confluence of these trabeculae leaves an area relatively void of structure, Ward’s triangle (W).
B. Specimen Radiograph- the arrangement of the trabecular bundles can be discerned,
defining Ward’s triangle, which is relatively devoid of bony struts.
C. Specimen Radiograph. The corresponding plain film confirms the trabecular orientation and
arrangement within the proximal femur and Ward’s triangle.
Radiological finding (1)
• The m/c radiologic finding is generalized
osteopenia.
• – Cortical thinning and accentuation of Weight
bearing trabeculae.
• – The bone surfaces are well defined, with
sharp margins.
Radiological finding (2)
• Fractures - vertebral deformities, which are
also common, include biconcave end plates
(fish vertebrae) and anterior wedging.
Lateral radiograph of the lumbar spine in a 55-year-old woman with postmenopausal
osteoporosis shows generalized osteopenia,
compression fractures, and biconcave vertebral endplates ("fish vertebra"). Notice thin,
well-defined vertebral cortices ( arrows).
Radiological finding (3)
• Patients with osteoporosis secondary to
excess steroids.
• – Generalized osteopenia.
• – Fractures with exuberant callus
• – Steroid-related complications;
• Intravertebral vacuum (nitrogen gas);
• Avascular necrosis.
• Osteomyelitis.
Differential considerations for
diffuse osteopenia
• 1. Osteomalacia.
• – indistinct trabeculae and poorly defined
interfaces between cortical and trabecular bone.
• – Presence of Looser's zones.
• 2. Hyperparathyroidism.
• – bone resorption at characteristic sites.
• 3. Multiple myeloma.
• – MR imaging may show areas of marrow
replacement.
Regional or localized
osteoporosis
1. Immobilization and disuse
2. Reflex sympathetic dystrophy syndrome (RSDS)
3. Transient regional osteoporosis
– Transient osteoporosis of the hip.
– Regional migratory osteoporosis.
4. Inflammatory arthritis.
5. Tumors
6. Infection.
Radiologic findings in regional
osteoporosis (1)
• RSDS : mediated by the sympathetic nervous
system and is characterized by – aggressive
osteoporosis, – soft tissue swelling.
• The cause is usually traumatic, but the disease
may also be idiopathic.
AP radiograph of the hand in a patient with reflex sympathetic dystrophy syndrome shows
soft-tissue swelling and periarticular osteopenia.
RICKETS AND
OSTEOMALACIA
• Rickets and osteomalacia
• Rickets and osteomalacia are similar histologically.
• Abnormality in vitamin D metabolism.
• Incomplete mineralization of normal osteoid tissue.
• Rickets
• Occurs in children
• Affects immature bone
• Osteomalacia
• Occurs in adult
• Affects mature bone
Pathology
• Rickets is associated with the inability to calcify
the intercellular matrix in the growth plate,
causing chondrocytes to pile up irregularly,
increase in the width of the growth plate, poor
mineralization of the zone of calcification and
sparse bone formation in the zone of ossification.
The new trabeculae are thin and weak, and the
metaphysis becomes broad and cup shaped.
Osteomalacia is characterized by widened osteoid
seams and thinner cortices.
Maintain calcium and phosphate
homeostasis.
Clinical findings of
Rickets and Osteomalacia
• Depend in part on the aetiology and severity of the
disorder, as well as the age of the patient at
presentation
• Rickets: stunted skeletal growth.
• Apathetic, Irritable, Hypokinetic.
• Frontal bossing, softening of the skull, dental
caries, rachitic rosary, kyphosis, joint enlargement,
or bowing of long bones.
• Fractures and slipped capital femoral epiphyses.
• Osteomalacia: Insidious course.
• Non specific Symptoms such as fatigue,
malaise, or widespread bone pain.
• Proximal muscle weakness and abnormal gait
(Waddling) may be present.
Radiologic findings of
Osteomalacia
• The M/C radiologic sign is generalized osteopenia.
• Coarsened and indistinct bony trabeculae.
• Poorly defined interfaces between cortical and trabecular
bone.
• Looser's zone, or pseudofracture. (more specific but less
common)
• End plate deformities and fractures of vertebral bodies,
bowing and fractures of long bones, and basilar
invagination of skull.
• Vertebral fractures may show either a characterstic
biconcave appearance or wedge shaped deformities
indistinguishable from osteoporotic fractures.
• Looser's zone. a thin transverse band of
rarefaction in an otherwise normal looking bone
that occur in a bilateral and symmetric
distribution.
• These zones are due to incomplete stress
fractures which heal with callus lacking in
calcium.
• Characteristic sites; medial proximal femur, inner
margins of femoral neck, proximal ulna, axillary
margin of the scapula, pubic rami, and ribs.
• DDx; Paget's disease or fibrous dysplasia.
AP radiograph of the hip in a 50-year-old man with osteomalacia shows coarsened
trabecular pattern with indistinct trabeculae.
AP radiograph of the hip in a patient with osteomalacia shows multiple Looser zones (
arrows) in the superior pubic ramus.
Osteomalacia. AP radiograph of the pelvis showing osteopenia with bilateral femoral
neck pseudofractures (arrows).
Radiologic findings of
Rickets
• The M/C radiologic sign is generalized osteopenia.
• In active rickets there is thickening and widening of growth plate,
cupping of the metaphysis and, and sometimes, bowing of the
diaphysis.
• The metaphysis may remain abnormally wide even after healing has
occurred.
• Increased lucency, widening, elongation, irregularity, and cupping of
the metaphysis.
• – Earliest; Slight axial widening of the physis
• – Next; Increased lucency of the zone of provisional calcification.
• – More advance; The physis widens and its contour becomes
irregular.
• Occasionally, in patients with rickets caused by chronic renal
disease, increased sclerosis may be seen.
• The regions of highest yield on radiologic evaluation of
rickets are those that are undergoing rapid growth and
remodelling.
• – Costochondral junctions of middle ribs (rachitic rosary)
• Radial aspects of the proximal and middle phalanges of the
middle and index fingers
• Medial borders of
• - Proximal humerus.
• - Femoral neck
• - Distal femur
• - Proximal Tibia
• The complication of rickets.
• – Skeletal deformities.
• – In neonates; posterior flattening and squaring of the
skull, or craniotabes, may be seen.
• – In early childhood; bowing deformities of arms and
legs are common.
• – Older children: scoliosis, vertebral end plate
deformities, basilar invagination of the skull may be
seen.
• Advance disease: Slipped capital femoral epiphysis.
A, AP radiograph of the knee in a 2-year-old girl with rickets shows generalized osteopenia
and widening of the metaphysis of the proximal tibia and fibula. B, AP radiograph of
the wrist in another child with rickets shows generalized osteopenia, as well as widening and
irregularity of the metaphysis of the distal radius and ulna.
Rickets in a young child with growth plate widening and irregularity in the wrist (A) and knees
(B). Note the small epiphyses in the knees.
Rachitic rosary. (A) and lateral (B) radiographs of the chest showing prominence of the
costochondral junctions (arrows).
Vitamin D-resistant rickets in a 1-year-old child. (A) AP radiograph of the knees showing
irregularity and widening of the growth plates. The epiphyses are
small and irregular as well. (B) Three years after high-dose vitamin D therapy, the knees
appear normal. There is residual femoral bowing.
HYPERPARATHYROIDISM
• Primary
• – Parathyroid adenoma(80%)
• Secondary
• – chronic renal insufficiency.
• Hyperparathyroidism may result in either
diffuse bone resorption or bone formation,
bone resorption usually dominates.
Radiologic findings of
HYPERPARATHYROIDISM
• The M/C radiologic abnormality is generalized osteopenia.
• Bone resorption, bone sclerosis, brown tumors,
chondrocalcinosis, soft tissue calcification, and vascular
calcification.
• Brown tumors appear as well-defined lytic lesions.
• – After resection of parathyroid adenomas, the lesions may
become sclerotic and may mimic blastic metastasis.
• Bone resorption, the most characteristic finding, is usually
classified as
• – subchondral, trabecular, endosteal, intracortical,
subperiosteal, subligamentous, and subtendinous.
Radiologic findings of
HYPERPARATHYROIDISM
• Subperiosteal resorption - M/C
• – Usually occurs in the hands and feet.
• – M/C affected site: radial aspects of the middle phalanges.
• – Acro-osteolysis or phalangeal tufts resoption may also be present.
• • Trabecular resorption
• – Often seen in the diploic space of the skull, where it has a characteristic
salt and pepper appearance.
• The skull displays a diffuse osteoporosis described as “ pinhead stippling”
• • Subchondral resorption
• – May be seen in the sacroiliac joints, sternoclavicular joints,
acromioclavicular joints, symphysis pubis, and discovertebral junction .
• Vertebrae are porotic and deeply indented by ballooned discs.Collapse of
the bodies is frequent
AP radiograph of the hand in a 66-year-old woman with primary hyperparathyroidism
owing to parathyroid adenoma shows subperiosteal bone resorption ( arrows) along the
radial aspect of 2nd, 3rd, and 4th middle phalanges.
AP radiograph of the knee in a child with hyperparathyroidism shows subperiosteal bone
resorption ( arrow) along the proximal medial tibia.
Lateral radiograph of the skull in a 23-year-old man with secondary hyperparathyroidism
shows trabecular resorption of the diploic space ("salt and pepper" appearance).
Dental radiograph in another child with hyperparathyroidism shows resorption ( arrow) of
the lamina dura of the mandible.
Radiologic findings of
HYPERPARATHYROIDISM
Primary
• Chondrocalcinosis
• usually seen in the menisci
of the knee, the Triangular
fibrocartilage of the wrist,
and the pubic symphysis
Secondary
• Bony sclerosis; focal or
generalized.
• Rugger-jersey appearance
of spine.
• Soft tissue and vascular
calcification.
AP radiograph of the wrist in an 83-year-old woman with primary hyperparathyroidism
shows chondrocalcinosis ( arrow) of the triangular fibrocartilage.
Secondary HPT. Radiograph of the pelvis an d hips showing diffuse osteosclerosis.
A, AP radiograph of the spine in a patient with secondary hyperparathyroidism shows
generalized bone sclerosis, small kidneys, and left renal calculi. B, Lateral radiograph of
the lumbar spine in another patient with secondary hyperparathyroidism shows
horizontal, bandlike ("rugger jersey") sclerosis of the vertebral bodies ( arrows).
AP radiograph of the hand in a 50-year-old man with renal osteodystrophy shows acro-
osteolysis ( short arrows), subperiosteal bone resorption ( long arrows), and vascular
calcifications.
Secondary HPT. Radiograph of the hand showing resorption of the first to third tufts with
soft tissue calcification (1). There is articular calcification (2), and subperiosteal and
subligamentous resorption (3).
Laboratory Findings
• Hypercalcemia
• Hypophosphatemia
• High Alkaline Phosphatase
• Hypercalciuria
• Hyperphosphaturia.
The differential diagnosis of
HYPERPARATHYROIDISM
• Focal subperiosteal resorption involving a single bone
• – Neoplasms or osteomyelitis.
• • Bone sclerosis in patients with secondary
hyperparathyroidism.
• – Metastatic disease, radiation-induced bone disease,
hypoparathyroidism, myelofibrosis, mastocytosis, sickle-cell
disease, and Paget's disease.
• • Chondrocalcinosis
• – Pyrophosphate arthropathy (CPPD) or hemochromatosis.
• • Brown tumors
• – includes other focal lytic lesions, such as giant cell tumor
• and fibrous dysplasia.
HYPOPARATHYROIDISM
• The M/C cause is excision of or trauma to the
parathyroid glands during thyroidectomy.
• – may not be recognized for years after
surgery.
• Characterized by low serum calcium and high
serum phosphorus levels.
Clinical presentation:
• Neuromuscular dysfunction – twitching,
carpopedal spasm and laryngeal spasms,
positive Chvostek’s and Trousseau signs and
convulsions.
• Short stature.
• Delay or failure of tooth eruption.
• Gastrointestinal complaints.
Radiologic findings of
HYPOPARATHYROIDISM
• Radiologic findings are varied.
• Bony sclerosis. = M/C finding
• Focal or generalized
• Subcutaneous calcification.
• Calvarial thickening
• Basal ganglia calcification
• Hypoplastic dentition
• Premature physeal fusion
• Spinal ossification.
• Occasionally : Osteoporosis, Enthesopathy, Dense
metaphyseal bands.
Lateral radiograph of the skull in a 5-year-old girl with pseudohypoparathyroidism shows
thickening ( arrows) of the calvarium.
differential diagnosis of
HYPOPARATHYROIDISM
• Widespread bony sclerosis.
• – Blastic metastasis, myelofibrosis, renal osteodystrophy,
sickle-cell disease, and fluorosis.
• • Dense metaphyseal bands.
• – Leukemia therapy, heavy-metal poisoning, or
hypothyroidism.
• • Calcifications of the basal ganglia
• – Toxoplasmosis or cytomegalovirus infections, after
radiation therapy, and after carbon monoxide exposure.
• • Subcutaneous calcifications.
• – Collagen-vascular diseases, hypervitaminosis D, and renal
osteodystrophy.
Pseudohypoparathyroidism
• Rare Inherited disorder first described by
Albright that is caused by congenital lack of
adenyl cyclase.
• End-organ resistance to parathyroid hormone.
• X-linked dominant trait
• More common in women.
• Shares many features with hypoparathyroidism.
Radiologic findings of
Pseudohypoparathyroidism
• Similar to those of hypoparathyroidism
• Bony sclerosis, Soft tissue calcification, Dense
metaphyseal bands, Calvarial thickening and Basal
ganglia calcification.
• In addition
• Short metacarpals, metatarsals, and phalanges;
diaphyseal exostoses; and cone-shaped epiphyses.
• Typically, the first, fourth, and fifth rays are shortened.
• Growth deformities
• Bowing of long bones.
Ps eudohypoparathyroidism. (A,B) AP radiographs of the h ands showing shortening of
the fourth and fifth metacarpals.
AP radiograph of the hand in another child with pseudohypoparathyroidism shows
short 3rd , 4th , and 5th metacarpals.
Pseudopseudohypoparathyroidism
• Incomplete genetic manifestation of PHP.
• End-organ resistance to parathyroid hormone.
• Share most of their clinical and radiologic
features of pseudohypoparathyroidism.
RENAL
OSTEODYSTROPHY
• Bone disease in patients with chronic renal
insufficiency.
• It combines features of rickets, osteomalacia,
secondary hyperparathyroidism, and
osteoporosis.
• Aluminum toxicity is an additional component
that may be seen in patients undergoing dialysis.
• In children with chronic renal failure, the findings
of rickets dominate, whereas in adults the
findings of secondary hyperparathyroidism are
more prominent.
Radiologic findings in
RENAL OSTEODYSTROPHY
• Combination of the findings of rickets,
osteomalacia, secondary
hyperparathyroidism, and osteoporosis
• Periosteal neostosis (lucency between the
periosteum and subjacent bone) may be
present.
• It is usually seen in asymmetric distribution in
the metatarsals, femur, and pubic rami.
The differential diagnosis of
RENAL OSTEODYSTROPHY
• Periosteal neostosis
• – hypertrophic osteoarthropathy, osteomyelitis,
or neoplasm.
• Soft tissue calcification
• – Collagen-vascular diseases, idiopathic tumoral
calcinosis, hydroxyapatite crystal deposition
disease, and hypervitaminosis D.
• The most common complications in patients
with renal osteodystrophy are insufficiency
fractures.
• In patients who have had renal transplantation,
osteonecrosis, insufficiency fractures,
tendinitis, and tendon ruptures are common.
Frog-lateral radiograph of the hip in a patient with osteonecrosis of the femoral head
shows a characteristic subchondral lucency ( arrow) and collapse of the femoral head.
PAGET'S DISEASE
• A common disorder of unknown aetiology
that is characterized by excessive and
abnormal remodelling of bone.
• Men > women
• Age > 40 years.
• Polyostotic > monostotic.
PAGET'S DISEASE
• Asymptomatic.
• • Bone pain, progressive bony enlargement, bowing of
long bones, or fractures at presentation.
• • Deafness
• – from cranial-nerve compression at the skull base or
from middle-ear ossicle involvement.
• • The spinal cord compressed
• – basilar invagination of the skull or enlargement of
• the vertebrae.
Radiologic findings of
PAGET'S DISEASE
• Epiphyseal involvement with sharply demarcated lysis
that advances down the diaphysis is quite specific.
• Three sequential stages may be seen:
• 1. Lytic - most common in skull and long bones.
• 2. Mixed
• 3. Sclerotic - typically involves the axial skeleton.
• The hallmarks of advanced Paget's disease are bone
enlargement and increased bone sclerosis.
• Cortical and trabecular thickening and distortion are also
frequently present.
Radiologic findings of
PAGET'S DISEASE
• Spine
• – M/C in lumbar region: picture-frame vertebra, ivory vertebra, or
compression fractures.
• • Skull
• – Lytic phase, or osteoporosis circumscripta, usually begins in the
frontal or occipital bones.
• – More advanced disease in the skull manifests a cotton wool
appearance of mixed sclerosis and lysis.
• • Pelvis
• – The earliest finding = thickening of the iliopectineal line.
• – Occasionally, patchy areas of lucency and sclerosis.
• – Protrusion deformity of the acetabula is a well-recognized
complication of advanced disease of the pelvis.
Radiologic findings of
PAGET'S DISEASE
• Long bones
• – Lysis of subarticular bone is seen initially.
• – A wedge of lucency down the diaphysis: flame-
shaped or blade-of-grass.
• – In the tibia, the lytic phase occasionally begins in
the diaphysis.
• – Advanced disease of the long bones is
characterized by coarsened trabecula , bony
sclerosis, bony enlargement, and deformity.
A, Frontal radiograph of the pelvis in a patient with advanced Paget's disease shows bony
enlargement, bone sclerosis, and trabecular disorganization involving the right femur, right
hemipelvis, and sacrum. B, Frontal radiograph of humerus in another patient with advanced
Paget's disease shows bony enlargement, cortical and trabecular thickening, and trabecular
disorganization.
Frontal radiograph of the femur in a patient with advanced Paget's disease shows bowing
deformity of the femur along with bony enlargement, bone sclerosis, cortical
thickening, and trabecular disorganization.
Complications of
PAGET'S DISEASE
• Basilar invagination
• Spinal stenosis
• Premature osteoarthritis
• Insufficiency fractures
• Osteomyelitis
• Neoplasms: osteosarcomas.
• Sarcomatous degeneration: common in
patients with widespread disease
Frontal radiograph of the pelvis in a patient with widespread Paget's disease shows
enlargement and cortical thickening of the pelvis. Additionally, there is an expansile lytic
lesion ( arrows) in the ischium, representing malignant degeneration of Paget's disease
into fibrosarcoma.
Metabolic Bone Disease By Dr Prassan Tripathi

Metabolic Bone Disease By Dr Prassan Tripathi

  • 1.
    Metabolic Bone Disease DrPrassan Tripathi MS ORTHO Asst Prof
  • 2.
    Four Groups 1. InadequateOsteoid synthesis - Osteopenia 2.Inadequate Mineralisation of Osteoid Osteomalacia & Rickets – a.Dietary b. Disuse 3.Decreased Osteoid synthesis and increased Osteolysis Osteoporosis – a.Senile b.Post Menopausal 4.Increase in Bone Mass – Osteosclerosis a.Paget”s disease, b.Osteopetrosis Characterized by abnormalities in calcium metabolism and/or bone cell physiology. Metabolic Bone Disease
  • 3.
    Introduction • Metabolic bonedisease (MBD) • • Encompasses a diverse group of disorders • associated with altered calcium and • phosphorus homeostasis. • • To orthopedic surgeons; MBD is often silent • until the patient presents with fracture.
  • 4.
    OSTEOPOROSIS • Most commonmetabolic bone disease. • One of the most prevalent conditions associated with aging. • Definition : Systemic skeletal disease characterized by low bone mass and micro architectural deterioration of bone tissue , with a consequent increase in bone fragility and susceptibility to bone fracture.
  • 6.
    "Microarchitectural deterioration" refersto the thinning of the trabeculae and the loss of intertrabecular connections in bone
  • 7.
    RISK FACTORS Major riskfactors • Age > 65 years • Systemic glucocorticoid therapy of >3 months duration • Mal-absorption syndrome • Primary hyper parathyroidism • Propensity to fall • Osteopenia apparent on X-ray film • Hypo-gonadism • Early menopause (before age 45) • Family history of osteoporotic fracture (especially maternal hip fracture) Minor risk factors • Rheumatoid arthritis • Past history of clinical hyperthyroidism • Chronic anticonvulsant therapy • Low dietary calcium intake • Smoker • Excessive alcohol intake • Excessive caffeine intake • Weight <57 kg • Weight loss >10% of weight at age 25 • Chronic heparin therapy
  • 8.
    • Clinical definition:requires the presence of a nontraumatic fracture. • Histologic definition: requires normally mineralized bone to be present in reduced quantity.
  • 10.
    Diagnosis Osteoporosis • Bonedensitometry; gold standard • 1. Detection osteoporosis before fractures. • 2. Determination disease severity. • 3. Estimation risk of fracture. • Serial BMD measurements enabl determination of rate of bone loss or gain and thereby help in monitoring therapy. • Plain film; loss of 30% to 50% of bone is required • before it is detected on conventional radiographs.
  • 12.
    Ostoporosis Classification • OstoporosisClassification • • Primary osteoporosis. (idiopathic) : more common • – Type 1 (postmenopausal) • – Type 2 (age-related or senile) • • Secondary osteoporosis. • – Metabolic (acromegaly, hypercorticism, hyperthyroidism, • hyperparathyroidism, hypogonadism, pregnancy, diabetes • mellitus) • – Congenital (osteogenesis imperfecta, Ehlers-Danlos syndrome, • homocystinuria, mastocytosis, ochronosis, Gaucher's disease) • – Nutritional (alcoholism, malnutrition, calcium deficiency, scurvy) • – Drug-related (steroids, heparin).
  • 13.
    PROXIMAL PORTION OFTHE FEMUR: • Analysis of the trabecular pattern of the upper end of the femur has • been used as an index of osteoporosis. • In this region, five anatomic groups of trabeculae can be identified. • 1. Principal compressive group. • 2. Secondary compressive group. • 3. Greater trochanter group. • 4. Principal tensile group. • 5 .Secondary tensile group. • Patterns of trabecular loss may correlate with increasing severity of • osteoporosis. This trabecular analysis is termed as SINGH INDEX.
  • 14.
    ANATOMIC GROUPS OFTRABECULA • Principle compressive group • Principal tensile group • Secondary compressive group • Secondary tensile group • Greater trochanter group • Wards triangle
  • 15.
    NORMAL TRABECULAR PATTERNS.Proximal Femur. A. Three major patterns exist: principal compressive group (1), secondary compressive group (2), and principal tensile group (3). The confluence of these trabeculae leaves an area relatively void of structure, Ward’s triangle (W). B. Specimen Radiograph- the arrangement of the trabecular bundles can be discerned, defining Ward’s triangle, which is relatively devoid of bony struts. C. Specimen Radiograph. The corresponding plain film confirms the trabecular orientation and arrangement within the proximal femur and Ward’s triangle.
  • 17.
    Radiological finding (1) •The m/c radiologic finding is generalized osteopenia. • – Cortical thinning and accentuation of Weight bearing trabeculae. • – The bone surfaces are well defined, with sharp margins.
  • 18.
    Radiological finding (2) •Fractures - vertebral deformities, which are also common, include biconcave end plates (fish vertebrae) and anterior wedging.
  • 19.
    Lateral radiograph ofthe lumbar spine in a 55-year-old woman with postmenopausal osteoporosis shows generalized osteopenia, compression fractures, and biconcave vertebral endplates ("fish vertebra"). Notice thin, well-defined vertebral cortices ( arrows).
  • 21.
    Radiological finding (3) •Patients with osteoporosis secondary to excess steroids. • – Generalized osteopenia. • – Fractures with exuberant callus • – Steroid-related complications; • Intravertebral vacuum (nitrogen gas); • Avascular necrosis. • Osteomyelitis.
  • 22.
    Differential considerations for diffuseosteopenia • 1. Osteomalacia. • – indistinct trabeculae and poorly defined interfaces between cortical and trabecular bone. • – Presence of Looser's zones. • 2. Hyperparathyroidism. • – bone resorption at characteristic sites. • 3. Multiple myeloma. • – MR imaging may show areas of marrow replacement.
  • 23.
    Regional or localized osteoporosis 1.Immobilization and disuse 2. Reflex sympathetic dystrophy syndrome (RSDS) 3. Transient regional osteoporosis – Transient osteoporosis of the hip. – Regional migratory osteoporosis. 4. Inflammatory arthritis. 5. Tumors 6. Infection.
  • 24.
    Radiologic findings inregional osteoporosis (1) • RSDS : mediated by the sympathetic nervous system and is characterized by – aggressive osteoporosis, – soft tissue swelling. • The cause is usually traumatic, but the disease may also be idiopathic.
  • 25.
    AP radiograph ofthe hand in a patient with reflex sympathetic dystrophy syndrome shows soft-tissue swelling and periarticular osteopenia.
  • 27.
    RICKETS AND OSTEOMALACIA • Ricketsand osteomalacia • Rickets and osteomalacia are similar histologically. • Abnormality in vitamin D metabolism. • Incomplete mineralization of normal osteoid tissue. • Rickets • Occurs in children • Affects immature bone • Osteomalacia • Occurs in adult • Affects mature bone
  • 28.
    Pathology • Rickets isassociated with the inability to calcify the intercellular matrix in the growth plate, causing chondrocytes to pile up irregularly, increase in the width of the growth plate, poor mineralization of the zone of calcification and sparse bone formation in the zone of ossification. The new trabeculae are thin and weak, and the metaphysis becomes broad and cup shaped. Osteomalacia is characterized by widened osteoid seams and thinner cortices.
  • 29.
    Maintain calcium andphosphate homeostasis.
  • 30.
    Clinical findings of Ricketsand Osteomalacia • Depend in part on the aetiology and severity of the disorder, as well as the age of the patient at presentation • Rickets: stunted skeletal growth. • Apathetic, Irritable, Hypokinetic. • Frontal bossing, softening of the skull, dental caries, rachitic rosary, kyphosis, joint enlargement, or bowing of long bones. • Fractures and slipped capital femoral epiphyses.
  • 32.
    • Osteomalacia: Insidiouscourse. • Non specific Symptoms such as fatigue, malaise, or widespread bone pain. • Proximal muscle weakness and abnormal gait (Waddling) may be present.
  • 33.
    Radiologic findings of Osteomalacia •The M/C radiologic sign is generalized osteopenia. • Coarsened and indistinct bony trabeculae. • Poorly defined interfaces between cortical and trabecular bone. • Looser's zone, or pseudofracture. (more specific but less common) • End plate deformities and fractures of vertebral bodies, bowing and fractures of long bones, and basilar invagination of skull. • Vertebral fractures may show either a characterstic biconcave appearance or wedge shaped deformities indistinguishable from osteoporotic fractures.
  • 34.
    • Looser's zone.a thin transverse band of rarefaction in an otherwise normal looking bone that occur in a bilateral and symmetric distribution. • These zones are due to incomplete stress fractures which heal with callus lacking in calcium. • Characteristic sites; medial proximal femur, inner margins of femoral neck, proximal ulna, axillary margin of the scapula, pubic rami, and ribs. • DDx; Paget's disease or fibrous dysplasia.
  • 35.
    AP radiograph ofthe hip in a 50-year-old man with osteomalacia shows coarsened trabecular pattern with indistinct trabeculae.
  • 36.
    AP radiograph ofthe hip in a patient with osteomalacia shows multiple Looser zones ( arrows) in the superior pubic ramus.
  • 38.
    Osteomalacia. AP radiographof the pelvis showing osteopenia with bilateral femoral neck pseudofractures (arrows).
  • 39.
    Radiologic findings of Rickets •The M/C radiologic sign is generalized osteopenia. • In active rickets there is thickening and widening of growth plate, cupping of the metaphysis and, and sometimes, bowing of the diaphysis. • The metaphysis may remain abnormally wide even after healing has occurred. • Increased lucency, widening, elongation, irregularity, and cupping of the metaphysis. • – Earliest; Slight axial widening of the physis • – Next; Increased lucency of the zone of provisional calcification. • – More advance; The physis widens and its contour becomes irregular. • Occasionally, in patients with rickets caused by chronic renal disease, increased sclerosis may be seen.
  • 40.
    • The regionsof highest yield on radiologic evaluation of rickets are those that are undergoing rapid growth and remodelling. • – Costochondral junctions of middle ribs (rachitic rosary) • Radial aspects of the proximal and middle phalanges of the middle and index fingers • Medial borders of • - Proximal humerus. • - Femoral neck • - Distal femur • - Proximal Tibia
  • 41.
    • The complicationof rickets. • – Skeletal deformities. • – In neonates; posterior flattening and squaring of the skull, or craniotabes, may be seen. • – In early childhood; bowing deformities of arms and legs are common. • – Older children: scoliosis, vertebral end plate deformities, basilar invagination of the skull may be seen. • Advance disease: Slipped capital femoral epiphysis.
  • 42.
    A, AP radiographof the knee in a 2-year-old girl with rickets shows generalized osteopenia and widening of the metaphysis of the proximal tibia and fibula. B, AP radiograph of the wrist in another child with rickets shows generalized osteopenia, as well as widening and irregularity of the metaphysis of the distal radius and ulna.
  • 43.
    Rickets in ayoung child with growth plate widening and irregularity in the wrist (A) and knees (B). Note the small epiphyses in the knees.
  • 44.
    Rachitic rosary. (A)and lateral (B) radiographs of the chest showing prominence of the costochondral junctions (arrows).
  • 45.
    Vitamin D-resistant ricketsin a 1-year-old child. (A) AP radiograph of the knees showing irregularity and widening of the growth plates. The epiphyses are small and irregular as well. (B) Three years after high-dose vitamin D therapy, the knees appear normal. There is residual femoral bowing.
  • 46.
    HYPERPARATHYROIDISM • Primary • –Parathyroid adenoma(80%) • Secondary • – chronic renal insufficiency. • Hyperparathyroidism may result in either diffuse bone resorption or bone formation, bone resorption usually dominates.
  • 48.
    Radiologic findings of HYPERPARATHYROIDISM •The M/C radiologic abnormality is generalized osteopenia. • Bone resorption, bone sclerosis, brown tumors, chondrocalcinosis, soft tissue calcification, and vascular calcification. • Brown tumors appear as well-defined lytic lesions. • – After resection of parathyroid adenomas, the lesions may become sclerotic and may mimic blastic metastasis. • Bone resorption, the most characteristic finding, is usually classified as • – subchondral, trabecular, endosteal, intracortical, subperiosteal, subligamentous, and subtendinous.
  • 50.
    Radiologic findings of HYPERPARATHYROIDISM •Subperiosteal resorption - M/C • – Usually occurs in the hands and feet. • – M/C affected site: radial aspects of the middle phalanges. • – Acro-osteolysis or phalangeal tufts resoption may also be present. • • Trabecular resorption • – Often seen in the diploic space of the skull, where it has a characteristic salt and pepper appearance. • The skull displays a diffuse osteoporosis described as “ pinhead stippling” • • Subchondral resorption • – May be seen in the sacroiliac joints, sternoclavicular joints, acromioclavicular joints, symphysis pubis, and discovertebral junction . • Vertebrae are porotic and deeply indented by ballooned discs.Collapse of the bodies is frequent
  • 51.
    AP radiograph ofthe hand in a 66-year-old woman with primary hyperparathyroidism owing to parathyroid adenoma shows subperiosteal bone resorption ( arrows) along the radial aspect of 2nd, 3rd, and 4th middle phalanges.
  • 53.
    AP radiograph ofthe knee in a child with hyperparathyroidism shows subperiosteal bone resorption ( arrow) along the proximal medial tibia.
  • 54.
    Lateral radiograph ofthe skull in a 23-year-old man with secondary hyperparathyroidism shows trabecular resorption of the diploic space ("salt and pepper" appearance).
  • 56.
    Dental radiograph inanother child with hyperparathyroidism shows resorption ( arrow) of the lamina dura of the mandible.
  • 57.
    Radiologic findings of HYPERPARATHYROIDISM Primary •Chondrocalcinosis • usually seen in the menisci of the knee, the Triangular fibrocartilage of the wrist, and the pubic symphysis Secondary • Bony sclerosis; focal or generalized. • Rugger-jersey appearance of spine. • Soft tissue and vascular calcification.
  • 58.
    AP radiograph ofthe wrist in an 83-year-old woman with primary hyperparathyroidism shows chondrocalcinosis ( arrow) of the triangular fibrocartilage.
  • 60.
    Secondary HPT. Radiographof the pelvis an d hips showing diffuse osteosclerosis.
  • 61.
    A, AP radiographof the spine in a patient with secondary hyperparathyroidism shows generalized bone sclerosis, small kidneys, and left renal calculi. B, Lateral radiograph of the lumbar spine in another patient with secondary hyperparathyroidism shows horizontal, bandlike ("rugger jersey") sclerosis of the vertebral bodies ( arrows).
  • 63.
    AP radiograph ofthe hand in a 50-year-old man with renal osteodystrophy shows acro- osteolysis ( short arrows), subperiosteal bone resorption ( long arrows), and vascular calcifications.
  • 64.
    Secondary HPT. Radiographof the hand showing resorption of the first to third tufts with soft tissue calcification (1). There is articular calcification (2), and subperiosteal and subligamentous resorption (3).
  • 65.
    Laboratory Findings • Hypercalcemia •Hypophosphatemia • High Alkaline Phosphatase • Hypercalciuria • Hyperphosphaturia.
  • 66.
    The differential diagnosisof HYPERPARATHYROIDISM • Focal subperiosteal resorption involving a single bone • – Neoplasms or osteomyelitis. • • Bone sclerosis in patients with secondary hyperparathyroidism. • – Metastatic disease, radiation-induced bone disease, hypoparathyroidism, myelofibrosis, mastocytosis, sickle-cell disease, and Paget's disease. • • Chondrocalcinosis • – Pyrophosphate arthropathy (CPPD) or hemochromatosis. • • Brown tumors • – includes other focal lytic lesions, such as giant cell tumor • and fibrous dysplasia.
  • 67.
    HYPOPARATHYROIDISM • The M/Ccause is excision of or trauma to the parathyroid glands during thyroidectomy. • – may not be recognized for years after surgery. • Characterized by low serum calcium and high serum phosphorus levels.
  • 68.
    Clinical presentation: • Neuromusculardysfunction – twitching, carpopedal spasm and laryngeal spasms, positive Chvostek’s and Trousseau signs and convulsions. • Short stature. • Delay or failure of tooth eruption. • Gastrointestinal complaints.
  • 69.
    Radiologic findings of HYPOPARATHYROIDISM •Radiologic findings are varied. • Bony sclerosis. = M/C finding • Focal or generalized • Subcutaneous calcification. • Calvarial thickening • Basal ganglia calcification • Hypoplastic dentition • Premature physeal fusion • Spinal ossification. • Occasionally : Osteoporosis, Enthesopathy, Dense metaphyseal bands.
  • 70.
    Lateral radiograph ofthe skull in a 5-year-old girl with pseudohypoparathyroidism shows thickening ( arrows) of the calvarium.
  • 71.
    differential diagnosis of HYPOPARATHYROIDISM •Widespread bony sclerosis. • – Blastic metastasis, myelofibrosis, renal osteodystrophy, sickle-cell disease, and fluorosis. • • Dense metaphyseal bands. • – Leukemia therapy, heavy-metal poisoning, or hypothyroidism. • • Calcifications of the basal ganglia • – Toxoplasmosis or cytomegalovirus infections, after radiation therapy, and after carbon monoxide exposure. • • Subcutaneous calcifications. • – Collagen-vascular diseases, hypervitaminosis D, and renal osteodystrophy.
  • 72.
    Pseudohypoparathyroidism • Rare Inheriteddisorder first described by Albright that is caused by congenital lack of adenyl cyclase. • End-organ resistance to parathyroid hormone. • X-linked dominant trait • More common in women. • Shares many features with hypoparathyroidism.
  • 73.
    Radiologic findings of Pseudohypoparathyroidism •Similar to those of hypoparathyroidism • Bony sclerosis, Soft tissue calcification, Dense metaphyseal bands, Calvarial thickening and Basal ganglia calcification. • In addition • Short metacarpals, metatarsals, and phalanges; diaphyseal exostoses; and cone-shaped epiphyses. • Typically, the first, fourth, and fifth rays are shortened. • Growth deformities • Bowing of long bones.
  • 74.
    Ps eudohypoparathyroidism. (A,B)AP radiographs of the h ands showing shortening of the fourth and fifth metacarpals.
  • 75.
    AP radiograph ofthe hand in another child with pseudohypoparathyroidism shows short 3rd , 4th , and 5th metacarpals.
  • 76.
    Pseudopseudohypoparathyroidism • Incomplete geneticmanifestation of PHP. • End-organ resistance to parathyroid hormone. • Share most of their clinical and radiologic features of pseudohypoparathyroidism.
  • 77.
    RENAL OSTEODYSTROPHY • Bone diseasein patients with chronic renal insufficiency. • It combines features of rickets, osteomalacia, secondary hyperparathyroidism, and osteoporosis. • Aluminum toxicity is an additional component that may be seen in patients undergoing dialysis. • In children with chronic renal failure, the findings of rickets dominate, whereas in adults the findings of secondary hyperparathyroidism are more prominent.
  • 78.
    Radiologic findings in RENALOSTEODYSTROPHY • Combination of the findings of rickets, osteomalacia, secondary hyperparathyroidism, and osteoporosis • Periosteal neostosis (lucency between the periosteum and subjacent bone) may be present. • It is usually seen in asymmetric distribution in the metatarsals, femur, and pubic rami.
  • 79.
    The differential diagnosisof RENAL OSTEODYSTROPHY • Periosteal neostosis • – hypertrophic osteoarthropathy, osteomyelitis, or neoplasm. • Soft tissue calcification • – Collagen-vascular diseases, idiopathic tumoral calcinosis, hydroxyapatite crystal deposition disease, and hypervitaminosis D.
  • 80.
    • The mostcommon complications in patients with renal osteodystrophy are insufficiency fractures. • In patients who have had renal transplantation, osteonecrosis, insufficiency fractures, tendinitis, and tendon ruptures are common.
  • 81.
    Frog-lateral radiograph ofthe hip in a patient with osteonecrosis of the femoral head shows a characteristic subchondral lucency ( arrow) and collapse of the femoral head.
  • 82.
    PAGET'S DISEASE • Acommon disorder of unknown aetiology that is characterized by excessive and abnormal remodelling of bone. • Men > women • Age > 40 years. • Polyostotic > monostotic.
  • 83.
    PAGET'S DISEASE • Asymptomatic. •• Bone pain, progressive bony enlargement, bowing of long bones, or fractures at presentation. • • Deafness • – from cranial-nerve compression at the skull base or from middle-ear ossicle involvement. • • The spinal cord compressed • – basilar invagination of the skull or enlargement of • the vertebrae.
  • 84.
    Radiologic findings of PAGET'SDISEASE • Epiphyseal involvement with sharply demarcated lysis that advances down the diaphysis is quite specific. • Three sequential stages may be seen: • 1. Lytic - most common in skull and long bones. • 2. Mixed • 3. Sclerotic - typically involves the axial skeleton. • The hallmarks of advanced Paget's disease are bone enlargement and increased bone sclerosis. • Cortical and trabecular thickening and distortion are also frequently present.
  • 85.
    Radiologic findings of PAGET'SDISEASE • Spine • – M/C in lumbar region: picture-frame vertebra, ivory vertebra, or compression fractures. • • Skull • – Lytic phase, or osteoporosis circumscripta, usually begins in the frontal or occipital bones. • – More advanced disease in the skull manifests a cotton wool appearance of mixed sclerosis and lysis. • • Pelvis • – The earliest finding = thickening of the iliopectineal line. • – Occasionally, patchy areas of lucency and sclerosis. • – Protrusion deformity of the acetabula is a well-recognized complication of advanced disease of the pelvis.
  • 86.
    Radiologic findings of PAGET'SDISEASE • Long bones • – Lysis of subarticular bone is seen initially. • – A wedge of lucency down the diaphysis: flame- shaped or blade-of-grass. • – In the tibia, the lytic phase occasionally begins in the diaphysis. • – Advanced disease of the long bones is characterized by coarsened trabecula , bony sclerosis, bony enlargement, and deformity.
  • 93.
    A, Frontal radiographof the pelvis in a patient with advanced Paget's disease shows bony enlargement, bone sclerosis, and trabecular disorganization involving the right femur, right hemipelvis, and sacrum. B, Frontal radiograph of humerus in another patient with advanced Paget's disease shows bony enlargement, cortical and trabecular thickening, and trabecular disorganization.
  • 94.
    Frontal radiograph ofthe femur in a patient with advanced Paget's disease shows bowing deformity of the femur along with bony enlargement, bone sclerosis, cortical thickening, and trabecular disorganization.
  • 95.
    Complications of PAGET'S DISEASE •Basilar invagination • Spinal stenosis • Premature osteoarthritis • Insufficiency fractures • Osteomyelitis • Neoplasms: osteosarcomas. • Sarcomatous degeneration: common in patients with widespread disease
  • 96.
    Frontal radiograph ofthe pelvis in a patient with widespread Paget's disease shows enlargement and cortical thickening of the pelvis. Additionally, there is an expansile lytic lesion ( arrows) in the ischium, representing malignant degeneration of Paget's disease into fibrosarcoma.