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 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
skeletal disorders of metabolic and endocrine originyashovrattiwari1
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.
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
skeletal disorders of metabolic and endocrine originyashovrattiwari1
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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3. Introduction
• 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.
4. Patho radiological features
Radiological appearances truly portray the histological
changes occurring in the bones.
Disordered proliferation of cartilage cells and defective
mineralization in the zone of provisional calcification.
Decreased quantity of calcified osteoid.
5. Patho radiological features
Owing to the lack of osteoid mineralization the
metaphyseal zone of provisional calcification will also be
absent radiographically.
Bones appear more radiolucent with coarsened trabecular
pattern.
Widened growth plate with irregular, frayed and cupped
metaphyseal margins (paintbrush metaphyses)
6. Apoptosis of hypertrophic
chondrocytes caused by
phosphate ions
Hypophosphatemia
No apoptosis of
hypertrophic
chondrocytes
Normal growth plate Rachitic growth plate
7. Impaired apoptosis of terminally differentiated chondrocytes in the
growth plate are responsible for clinical and radiological signs of rickets
8. RADIOLOGICAL FEATURES
Widening of growth plate:-
Earliest and specific radiological change.
It is due to increase in cartilaginous cell mass.
Metaphyseal fraying:-
Irregular metaphyseal margins occurring due to fraying and
disorganization of spongy bone in the metaphyseal region.
9. RADIOLOGICAL FEATURES
Metaphyseal cupping and widening:-
Protrusion of bulky mass of cartilageneous cells in the zone
of hypertrophy into the poorly mineralized metaphysis.
Normal Rickets
10. RADIOLOGICAL FEATURES
Epiphyseal abnormalities:-
Osteopenia.
Irregular and indistinct borders.
Delayed appearance of ossification centres.
Shaft abnormalities:-
Rarefaction of shaft due to loss of mineral content.
Cortex becomes thin with coarse echotexture.
11. RADIOLOGICAL FEATURES
Growth plate abnormalities:-
Generalised osteopenia.
Coarse trabecular pattern.
Frayed paintbrush metaphyseal margins.
Lack of the zone of provisional calcification.
Widening of the physis.
12. RADIOLOGICAL FEATURES
Wrist:
Widening of growth plates.
Irregular margins of metaphysis with widening and
cupping.
Osteopenia.
Rarefraction in long bones.
13.
14. RADIOLOGICAL FEATURES
Bowing of long bones:
Result of displacement of growth centres owing to
assymetrical musculotendinous pull on the weakened growth
plate.
16. RADIOLOGICAL FEATURES
Craniotabes:
Excessive osteoid deposition in frontal and parietal regions
with posterior flattening of skull due to supine posture of
infant.
Squared configuration of skull.
Demineralisation of skull.
18. RADIOLOGICAL FEATURES OF
HEALING RICKETS
Appearance of line of provisional calcification at the end of
metaphysis.
Metaphysis show cupping and splaying but no fraying.
Periosteum may show double periosteal line due to
subperiosteal deposition of osteoid tissue.
19. RADIOLOGICAL FEATURES OF
HEALED RICKETS
The subperiosteal osteoid tissue is calcified (no double
periosteal line).
Splaying and cupping is corrected.
22. Differential diagnosis
Rickets Scurvy
Epiphyseal centres are invisible or
indistinct
Epiphysis is sharply marginated by
sclerotic rim (Wimberger’s sign)
Loss of zone of provisional calcification
adjacent to metaphysis, thus having a
faint and irregular line (Fraying)
Zone of proviosional calcification at
metaphysis is dense giving a “ White line
of Frenkel’s sign”
Not found Trummerfeld zone and Pelken’s spur
seen
Subperiosteal layer may be found but less
marked effect.
Sub-periosteal hemorrhage due to
capillary fragility giving rise to periosteal;
elevation.
23. Differential diagnosis
RICKETS SCURVY
Epiphyseal centres are
invisible or indistinct
Epiphysis is sharply
marginated by sclerotic
rim (Wimberger’s sign)
Loss of zone of
provisional calcification
zone of provisional
calcification is dense
“White line of Frenkel”
24.
25. Differential diagnosis
Schimid type metaphyseal chondrodysplasia
- Mild type, due to mutation
in type X collagen (COL10A1 gene),
metaphyses are cupped resembling rickets.
26. Differential diagnosis
Blount disease refers to a local disturbance
of growth of the medial aspect of the
proximal tibial metaphysis and/or epiphysis
that results in tibia vara.
Editor's Notes
Low serum phosphate is fundamental to pathogenesis of rickets.
Impaired mineralization of growth plate and osteoid.
Posteroanterior radiograph of both hands shows diffuse osteopenia, age-indeterminate fractures of several metacarpals (solid arrows), and cupped fragmented frayed metaphyses of the distal radii and ulnae (ovals). A peripheral rim of bone along the metaphysis (dashed arrow) occurs by membranous ossification.
Square head appearance – caput quadratum
Beneath the zone of provisional calcification, there is evidence of lucent zone related to lack of mineralized osteoid (Trummerfeld zone).
Lateral projection of white line of frenkel may lead to formation of spur or marginal cleft.