2. Learning Objectives
• To identify the different kinds of metabolic
bone diseases and their features.
• To know the pathophysiology behind the
metabolic bone diseases.
3. What is Bone Metabolism?
• Is the complex sequence of bone turnover
(osteoclastogenesis) and bone formation
(osteoblastogenesis)
– bone has structural and metabolic functions
– metabolic functions of bone largely involve the
homeostasis of calcium and phosphate
– release of calcium, or absorption of calcium, by
bone is largely regulated by hormones and, less so,
by steroids
4. Hormones and steroid that affect Bone
metabolism
• Hormones
– PTH
– Calcitonin
– Sex Hormones (eg. estrogen, androgens)
– Growth Hormone
– Thyroid Hormones
• Steroids
– Vitamin D
– Glucocorticosteroids
11. What is Metabolic Bone Diseases?
• Any of several diseases that cause various
abnormalities or deformities of bone.
• are disorders of bone strength usually caused
by abnormalities of minerals (such as calcium
or phosphorus), vitamin D, bone mass or bone
structure, with osteoporosis being the most
common.
13. Hyperparathyroidism
• Epidemiology
– incidence
• occurs in 0.1% of the population
• 90% result form a single adenoma
• remaining 10% from parathyroid hyperplasia
– demographics
• more common in women
• hyperparathyroidism and maligncacy make up the
majority of patients with hypercalcemia
14. Hyperparathyroidism
• PTH indirectly stimulates osteoclasts by
binding to its receptor on osteoblasts, inducing
RANK-L and M-CSF synthesis
• Excessive PTH leads to over-stimulation of
bone resorption
– cortical bone affected more than cancellous
16. Hyperparathyroidism
• Primary
– typically the result of hypersecretion of PTH by a
parathyroid adenoma/hyperplasia
– may result in osteitis fibrosa cystica
• breakdown of bone, predominantly subperiosteal bone
• commonly involves the jaw
17. Hyperparathyroidism
• Secondary
– secondary parathyroid hyperplasia as compensation from
hypocalcemia or hyperphosphatemia
• ↓ gut Ca2+ absorption
• ↑ phosphorous
– associated conditions
• chronic renal disease
– renal disease causes hypovitaminosis D
» leads to ↓ Ca2+ absorption
• renal osteodystrophy
– bone leisons due to secondary hyperparathyroidism
22. Hyperparathyroidism
• Urinalysis
– primary
• hypercalciuria (renal stones)
• ↑ cAMP
• Radiograph
– cystic bone spaces ("salt and pepper")
• often in the skull
– loss of phalange bone mass
• ↑ concavity
https://www.google.com/search?q=cystic+bone+spaces+(%22salt+and+pepper%22)&sxsrf=ALeKk00lKlck61_ozaOS1RrfXcLgvuqKEQ:15884678
00030&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjjxtTXv5bpAhX-
xosBHc68DkcQ_AUoAXoECAwQAw&biw=1366&bih=657#imgrc=lUrK6JK4g1FPSM
23. Hyperparathyroidism
• Treatment
– Acute hypercalcemia
• IV fluids
• Loop diuretics
– Symptomatic hypercalcemia is treated surgically
• treat with parathyroidectoy
• complications include post-op hypocalcemia
• manifests as numbness, tingling, and muscle cramps
• should be treated with IV calcium gluconate
24. Hyperparathyroidism
• Complications
– Peptic ulcer disease
• ↑ gastrin production stimulated by ↑ Ca2+
– Acute pancreatitis
• ↑ lipase activity stimulated by ↑ Ca2+
– CNS dysfunction
• anxiety, confusion, coma
• result of metastatic calcification of the brain
– Osteoporsis
• Bone loss occurs as result of bone resorption due to excess PTH
• Orthopedic surgeons should recognize lab abnormalities as patients
may present with fragility fractures
25. Hypoparathyroidism
• Decreased production of parathyroid hormone
(PTH) by chief cells of the parathyroid gland
resulting in
– decreased plasma calcium levels
– increased plasma phosphate levels
– decreased 1,25(OH)2 Vitamin D levels
• Iatrogenic (usually due to thyroidectomy)
26. Hypoparathyroidism
• Prognosis
– No current hormone replacement therapy
available
– Treatment is aimed at supplementing vitamin D
and calcium levels
27. Hypoparathyroidism
• Symptoms
– hypocalcemia
• more common in hypoparathyroidism
– neuromuscular irritability
» Chvostek's sign
» seizures
» tetany
– cataracts
– fungal infections of the nail
– hair loss
– skin changes
» vitiligo
» blotchiness of skin
https://www.google.com/search?q=chvostek%27s+sign&sxsrf=ALeKk017bG_LL-
jnuP5d_xbZWzSTK-
4keA:1588397262869&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiL9fX0uJTpAhWFEqYKHc
1mDhYQ_AUoAnoECA8QBA&biw=1366&bih=657#imgrc=yEtp6Yvmx-PspM
29. Hypoparathyroidism
• Labs
– decreased
• PTH
• calcium
• 1,25-Vit D
• urinary calcium
– increased
• serum phosphate
– normal
• alkaline phosphatase
• pH
– alkalosis increases albumin binding to ionized calcium
• leads to hypocalcemia
30. Hypoparathyroidism
• Treatment
– Nonoperative
– calcium and vitamin D supplementation
• indications
– decreased serum calcium level
– decreased levels of vitamin D
• outcomes
– must monitor labs on a regular basis
31. Renal Osteodystrophy
• a spectrum of disease seen in patients with
chronic renal disease.
• characterized by bone mineralization
deficiency due
to electrolyte and endocrine abnormalities
• common cause of hypocalcemia
32. Renal Osteodystophy
• Hypocalcemia
– due to the inability of the damaged kidney to convert
vitamin D3 to calcitriol (the active form)
– because of phosphate retention (hyperphosphatemia)
• Hyperparathyroidism and secondary
hyperphosphatemia
– caused by hypocalcemia and lack of phosphate
excretion by damaged kidney
33. Renal Osteodystrophy
• Associated conditions
– orthopaedic manifestations
• osteomalacia (adults) and growth retardation (children)
• AVN
• tendinitis and tendon rupture
• carpal tunnel syndrome
– deposition of amyloid (β2 microglobulin)
• pathologic fracture
– from brown tumors (hyperparathyroidism) or amyloid deposits
• osteomyelitis and septic arthritis
34. Renal Osteodystrophy
• High-turnover renal bone disease (high PTH
disease)chronically elevated phosphate leads to
secondary hyperparathyroidism
– hyperphosphatemia lowers serum Ca, stimulating PTH
– phosphorus impairs renal 1α-hydroxylase, reducing 1,25(OH)2
vitamin D3 production
– phosphorus retention directly stimultes PTH production
– hyperplasia of chief cells of parathyroid gland
• associated lab values
– decreased calcium, increased serum phosphate, increased
alkaline phosphate, increased parathyroid hormone
35. Renal Osteodystrophy
• Low turnover renal bone disease (normal PTH
disease)characterized by lack of secondary
hyperparathyroidism
• normal levels of PTH with characteristic bone
lesions marked by low levels of bone formation
• excess deposition of aluminium into bone affects
bone mineralization
– impairs differentiation of precursors into osteoblasts, and
osteoblast proliferation
– impairs PTH release from parathyroid gland
– disrupts mineralization
38. Renal Osteodystrophy
• Physical exam
– provocative tests for tetany
• Trousseau's Sign
– carpalpedal spasm after blood pressure readings
• Chvostek's Sign
– facial muscle contractions after tapping on the facial nerve
39. Renal Osteodystrophy
• Radiographic fingings
• Looser's zones
• brown tumor
• osteosclerosis
– from mineralization of osteomalacic bone
– rugger jersey spine
• widened growth plate and zone of
provisional calcification (children)
• varus deformity of the femurs (children)
• fracture
• soft-tissue calcification
• osteopenia
43. Rickets
• is a defect in mineralization of osteoid matrix
caused by inadequate calcium and phosphate
that occurs prior to closure of the physes
– known as osteomalacia if it occurs after physeal
closure
– can be congenital or acquired
– treatment is usually non-operative with
supplementation
44. Rickets
• Vitamin D and PTH play an important role in
calcium homeostasis
• poor calcification of cartilage matrix of growing
long bones occurs at zone of provisional
calcification
• Leads to increased physeal width and
cortical/bowing
45. Rickets
• Orthopedic manifestations
– brittle bones with physeal cupping/widening
– bowing of long bones
– Ligamentous laxity
– flattening of skull
– enlargement of costal cartilage (rachitic rosary)
– kyphosis (cat back)
48. Classification of Rickets
• Vitamin D-resistant (familial
hypophophatemic)
• Vitamin D-deficient (nutritional)
• Vitamin D-dependent (type I and II)
49. Vitamin D-resistant (familial hypophophatemic)
• Most common form of heritable rickets
• Presents at 1-2 years of age
• Caused by inability of renal tubules to absorb
phosphate
– GFR is normal
– vitamin D3 response is impaired
50. Vitamin D-resistant (familial hypophophatemic)
• Genetics
– X-linked dominant
• most common form
• results from mutation in PHEX gene
• leads to increased levels of FGF23, which decreases
renal phosphate absorption and suppresses renal 25-
(OH)-1α-hydroxylase activity
51. Vitamin D-resistant (familial hypophophatemic)
• Genetics
– Autosomal dominant results from mutation
in FGF23
• leads to decreased FGF23 degradation
– Autosomal recessive
• Results from mutation in dentin matrix protein 1 (DMP1
gene)
• Leads to impaired osteocyte maturation and bone
mineralization, and increased levels of FG23
52. Vitamin D-deficient (nutritional)
• Results from decreased dietary intake of Vitamin D
– rare now that Vitamin D is added to milk
• Presents at 6 months - 3 years of age
• Risk factors
– premature infants
– black children > 6 months who are still breastfed
– patients with malabsorption syndromes (celiac sprue) or chronic
parenteral nutrition
– Asian immigrants
– patients with unusual dietary choices (vegetarian diet)
53. Vitamin D-deficient (nutritional)
• Pathophysiology
– low Vitamin D levels lead to decreased intestinal
absorption of calcium
– low calcium levels leads to a compensatory
increase in PTH and bone resorption
– bone resorption leads to increased alkaline
phosphatase levels
54. Vitamin D-dependent (type I and II)
• Rare disorder
• Leads to clinical features similar to Vitamin D-
deficient rickets but more severe
• Clinical characteristics
– type I
• hypotonia, muscle weakness, growth failure, hypocalcemic
seizures, joint pain/deformity, fractures in early infancy
– type II
• hypotonia, muscle weakness, growth failure, hypocalcemic
seizures, growth retardation, bone pain, severe dental caries
or dental hypoplasia
55. Vitamin D-dependent (type I and II)
• Pathophysiology
– type I
• results from autosomal recessive mutation in renal 25-
(OH)-1α-hydroxylase
• prevents conversion of inactive form of vitamin D to
active form
• responsible gene 12q14
– type II
• results from autosomal recessive mutation
in intracellular receptor for 1,25-(OH)2-vitamin D
58. Rickets
• Physical exam
– tibial bowing
• due to widened proximal tibial physes
– rachitic rosary
• enlargement of costochondral junction
– bowing of knees
– retarded bone growth
– muscle hypotonia
– waddling gait
– dental abnormalities
• delayed dental eruption
• defective enamel
– pathologic fractures
59. Rickets
• Radiographic finidings
– physeal widening
– metaphyseal cupping
– decreased bone density
– Looser's zones
• pseudofracture on the
compression side of bone
– Rachitic rosary
• prominence of rib heads at the
osteochondral junction
– Lower extremity bowing
• often genu varum
– Codfish vertebrae
– Cat back
• dorsal kyphosis
60. Rickets
• Calcitriol
• 20-30 mg/kg/day split into 2-3 doses in children
• 0.5-0.75 μg/day split into 2 doses in adults
• Phosphate replacement
• 20-40 mg/kg/day split into 3-5 doses in children
• 750-1000 mg/day split into 3-4 doses in adults
61. Rickets
• Vitamin D
• 5000 IU/day for 6-10 weeks
• Corrective surgery (multilevel osteotomy)
• variety of fixation devices including K-wires, plates,
intramedullary nails, and/or external fixation
63. Rickets
• Treatment
– Nonoperative
• calcitriol
– indications
» Vitamin D-resistant (familial hypophosphatemic) rickets
» type I Vitamin D-dependent rickets
• phosphate replacement
– indications
» Vitamin D-resistant (familial hypophosphatemic) rickets
• Vitamin D
– indications
» Vitamin D-deficient (nutritional) rickets
» type II Vitamin D-dependent rickets
– Operative
• corrective surgery (multilevel osteotomy)
– indications
» severe tibial bowing
64. Hypophosphatasia
• Metabolic bone disease characterized by a
generalized impairment of bone
mineralization
• Incidence
– estimated to be 1 in 100,000
65. Hypophosphatasia
• Pathophysiology
– low levels of alkaline phosphate result in
decreased synthesis of inorganic phosphate
necessary for bone matrix formation
– osteoid that forms in the hypertrophic zone of the
growth plate fails to mineralize
– the zone of provisional calcification never forms
and growth is inhibited
67. Hypophosphatasia
• Associated conditions
– Orthopaedic manifestations
• similar to rickets
• bow legs
• short stature
– Non-orthopaedic manifestations
• abnormal tooth formation
• loss of teeth
74. Scurvy
• Pathophysiology
– humans are unable to synthesize L-ascorbic acid because the
enzyme L-gluconolactone oxidase is nonfunctional
– Vitamin C deficiency leads to decrease in chondroitin sulfate and
collagen synthesis and repair
– impaired intracellular hydroxylation of collagen peptides
– net effect is altered bone formatin with the greatest effect
occuring in the metaphysis
– defect in spongiosa of the metaphysis at the growth plate
– because the demand for type I collagen is greatest during new
bone formation
75. Scurvy
• History
– infant diet consisting of evaporated or condensed milk
– "tea and toast" diet in elderly
• Symptoms
– malaise and fatigue
– pain
• bone pain
• myalgia, because of reduced carnitine production
– bleeding
• gum bleeding and loosening of teeth
• hematuria
• hematemesis
• hemorrhage
• iron deficiency
76. Scurvy
• Physical exam
– petechiae and ecchymosis
– joint effusion
– swelling over long bones because of subperiosteal
hemorrhage
– scorbutic rosary (costochondral separation)
• angular step-off deformity in children
• differentiated from rachitic rosary, which is rounded and
nodular
78. Scurvy
• Findings
• the white line of Frankel
– widened zone of provisional calcification
– between epiphysis and metaphysis
• Trummerfeld zone
– transvese radiolucent band in
the metaphysis adjacent to the Frankel line
– also known as the scurvy line
• Wimberger ring
– ring of increased density surrounding epiphysis
• Pelkin spur and fracture
– metaphyseal spurs and fractures
79. Scurvy
• Findings
• corner sign of Park
– metaphyseal clefts
• thin cortices ("pencil-point" cortex)
• decreased trabeculae with ground-
glass osteopenia
• subperiosteal elevation
• epiphyseal separation
• fractures and dislocations
80. Scurvy
• The diagnosis is usually made based on history, clinical
and radiological picture, and resolution of symptoms
following vitamin C administration. Lab tests are usually
not helpful.
• Labs
– fasting serum ascorbic acid level is low
• Histology
– replacement of primary trabeculae with granulation tissue
– areas of hemorhage
– widening zone of provisional calcification of the physis
81. Scurvy
• Treatment
– Nonoperative
• vitamin C replacement
• indications
– signs and symptoms of scurvy
– chronic malnutrition
• techniques
– oral vitamin C at 250mg qid x 1 week in adults
82. Paget’s
• A condition of abnormal bone remodeling
– original osseous tissue is reconstructed through
active interplay between excessive bone resorption
and abnormal new bone formation
83. Paget’s
• Pathophysiology
– increased osteoclastic bone resorption is the
primary cellular abnormality
– cause is thought to be a slow virus infection (intra-
nuclear nucleocapsid-like structure)
• paramyxovirus
• respiratory syncytial virus
84. Paget’s
• Epidemiology
– peak incidence in the 5th decade of life
– common in Caucasians (northern European /
Anglo-Saxon descent)
– males = females
– location
• may be monostotic or polyostotic
• common sites include femur > pelvis > tibia > skull >
spine
85. Paget’s
• Genetics
– Inheritance
• most cases are spontaneous
• hereditary
– familial clusters have been described with ~40% autosomal dominant
transmission
– Genetics
• most important is 5q35 QTER (ubiquitine binding protein
sequestosome 1) SQSTM1 (p62/Sequestosome)
– tend to have severe Paget disease
• also insertion mutation in TNFRSF11A for gene
encoding RANK
86. Paget’s
• Orthopaedic manifestations
– bone pain
– long bone bowing
– fractures, due to brittle bone and tend to be
transverse
– large joint osteoarthritis
• excessive bleeding during THA
• malalignment during TKA
– secondary sarcoma
87. Paget’s
• Prognosis & malignancy
– Paget's sarcoma
• less than 1% will develop malignant Paget's
sarcoma (secondary sarcoma)
• osteosarcoma > fibrosarcoma and chondrosarcoma
• most common in pelvis, femur, and humerus
• poor prognosis
– 5-year survival for metastatic Paget's sarcoma < 10%
– treatment includes chemotherapy and wide surgical resection
88. Paget’s
• Classification
Phases
–lytic phase
• intense osteoclastic resorption
–mixed phase
• resorption and compensatory bone
formation
–Sclerotic phase
• osteoblastic bone formation
predominates
–all three phases may co-exist in the
same bone
https://www.google.com/search?q=pagets+phase&sxsrf=ALeKk01kjuSX_fw52_u5rRiWWFhNENpmp
A:1588469592704&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiY1byuxpbpAhXfwosBHa4JAqoQ_A
UoAXoECA4QAw&biw=1366&bih=608#imgrc=k1bP4wYA1zWMgM
89. Paget’s
Symptoms
• asymptomatic
– frequently asymptomatic and found incidentally
• pain
– pain may be the presenting symptom due to
• stress fractures
• increased vascularity and warmth
– new intense pain and swelling
• suspicious for Paget's sarcoma in a patient with history of Paget's + new intense
pain and swelling
• cardiac symptoms
– can present with high-output cardiac failure particularly if
large/multiple lesions & pre-existing diminished cardiac function
90. Paget’s
• Radiographs
– coarsened trabeculae which give the bone a blastic
appearance
• both increased and decreased density may exist depending
on phase of disease
– lytic phase
» lucent areas with expansion and thinned, intact cortices
» 'blade of grass' or 'flame-shaped' lucent advancing edge
– mixed phase
» combination of lysis + sclerosis with coarsened trabeculae
– sclerotic phase
» bone enlargement with cortical thickening, sclerotic and lucent
areas
91. Paget’s
– remodeled cortices
• loss of distinction between cortices and medullary cavity
– long bone bowing
• bowing of femur or tibia
– fractures
– hip and knee osteoarthritis
– osteitis circumscripta
• (cotton wool exudates) in skull
– Paget's secondary sarcoma
• shows cortical bone destruction
• soft tissue mass
92. Paget’s
• MRI
– may show lumbar spinal stenosis
• Bone scan
– accurately marks site of disease
– intensely hot in lytic and mixed phase
– less hot in sclerotic phase
• CT scan
– cortical thickening and coarsened trabeculae
94. Paget’s
• Characteristic histology
– woven bone and irregular broad
trabeculae with disorganized cement lines in a mosaic
pattern
– profound bone resorption - numerous large osteoclasts
with multiple nuclei per cell
• virus-like inclusion bodies in osteoclasts
• Paget's osteoclasts larger, more nuclei than typical
osteoclasts
– fibrous vascular tissue interspersed between trabeculae
95. Paget’s
• Treatment
– observation and supportive therapy treatment
for asymptomatic Paget's disease
• physiotherapy, NSAIDS, oral analgesics
96. Paget’s
– medical therapy aimed at osteoclast
inhibition bisphosphonates are 1st line treatment for
symptomatic Pagets
• oral
– alendronate and risedronate
– etidronate disodium (Didronel)
» older generation medication
» inhibits osteoclasts and osteoblasts
» cannot be used for more than 6 months at a time
• intravenous
– pamidronate, zoledronic acid (Zometa)
» newer generation medications that only inhibit osteoclasts
» disadvantageous in that they only come in IV form
97. Paget’s
– calcitonin are 2nd line (after bisphosphonates)
• causes osteoclasts to shrink in size and decreases their
bone resorptive activity within minutes
• administered subcutaneously or intramuscularly
– teriparatide is contraindicated in Paget's disease
due to risk of secondary osteosarcoma
98. Paget’s
• Operative
– THA / TKA
• indications
– affected patients with degenerative joint disease
– technique
• treat Paget's with pharmacologic agents prior to arthroplasty
to reduce bleeding
– outcomes
• greater incidence of suboptimal alignment secondary to
pagetoid bone
• the most common complications include
– malalignment with knee arthroplasty
– bleeding with hip arthroplasty
99. Paget’s
• metaphyseal osteotomy and plate
fixation indications
– fractures through pathologic bowing of long bones
– impending pathologic fracture of long bone with
bowing
100. Osteopetrosis
• Marble bone disease
• term for a group of bone disorders
characterized by increased sclerosis and
obliteration of the medullary canal.
• Result of decreased osteoclast (and
chondroclast) function: failure of bone
resorption
102. Osteopetrosis
• Pathophysiology
– osteoclast dysfunction leads to dense bone and
obliterated medullary canals
• caused by osteoclast inability to acidify Howship's
lacuna
– leads to predisposition to fracture
• lower extremity > upper extremity > axial skeleton
• lifelong prevalence of fracture ~ 40-50%
103. Osteopetrosis
• Associated conditions
– head
• cranial nerve palsies
– from overgrowth of skull foramina
– optic n. > auditory n. > trigeminal n. > facial n.
• osteomyelitis
– due to lack of marrow vascularity and impaired WBC function
– spine
• lower lumbar pain
– increased prevalence of spondylolysis
104. Osteopetrosis
• Associated conditions
– pelvis
• coxa vara
– commonly due to femoral neck fracture nonunion or repeated stress
fractures
– increased risk of degenerative joint arthritis
– extremities
• increased tendency for long bone fractures
– often low energy
– transverse
– increased risk of delayed union and malunion
• Carpal tunnel syndrome
106. Osteopetrosis
• Autosomal recessive forms
– frequent fractures
– progressive deafness and blindness
– severe anemia (caused by encroachment of bone on marrow)
beginning in early infancy or in utero
• bleeding risk
• frequent infections
• physical exam
– macrocephaly
– hepatosplenomegaly (caused by compensatory
extramedullary hematopoiesis)
– dental abscesses and osteomyelitis of the mandible
107. Osteopetrosis
• Autosomal dominant form
– usually asymptomatic
– fractures
• first learn of disease after fracture
• usually a low energy pathologic fracture to lower extremity
– anemia (fatigue)
– joint pain
• lower back pain common
• early hip osteoarthritis
• physical exam
– general
• normal height and appearance
• generalized osteosclerosis
– range of motion
• usually normal unless underlying osteoarthritis
– head and neck
• high risk of cranial nerve palsy
108. Osteopetrosis
• Radiographsrecommended views
– AP and lateral of bone of interest
• general findings
– increased cortical thickening
– increased overall bone density
– loss of medullary canal diameter
• bone-in-bone appearance
• additional findings
– "erlenmeyer flask" proximal humerus and distal
femur
– "rugger jersey spine" with very dense bone
– block femoral metaphysis
– coxa vara
https://www.google.com/search?q=erlenmeyer+flask+deformity&sxsrf=ALeKk02aY
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mgrc=ZViT2xDf_pwZwM
109. Osteopetrosis
• Histology
– histology shows defective osteoclasts
• lack ruffled border and clear zone
• islands of calcified cartilage within mature trabeculae
– empty lacunae and plugging of the haversian canals also
seen
• Laboratory studies
– autosomal recessive
• increases acid phosphatase
• may have increased PTH +/- calcium
– autosomal dominant
• usually normal
110. Osteopetrosis
• Medical management
– bone marrow transplant
• indications
– autosomal recessive (infantile-malignant) form
– high dose calcitriol (1,25 dihydroxy vitamin D), bone
marrow transplant
• indications
– autosomal recessive (infantile-malignant) form
– interferon gamma-1beta
• indications
– autosomal dominant form
111. Osteopetrosis
• Cranial nerve impingment
– Neurosurgical decompression
• Fracture management
– nonoperative
• indications
– diaphyseal long bone fractures
– upper extremity fractures
• techniques
– prolonged casting and non-weight bearing
– acceptable bone alignment, rotation and length
• outcomes
– healing may be delayed
– fracture remodeling limited
» increased risk of malunion and refracture
112. Osteopetrosis
• Operative
– indications
• proximal femur fractures
– techniques
• plate and screws
– avoid intramedullary devices
– slow steady drilling
– constant cooling and change of drill bit
– outcomes
• increased risk of hardware failure
• higher union rates and lower malunion rates compared to
non-operative management
– decreased risk of coxa vara
113. Osteopetrosis
• Degenerative joint disease
– total hip arthroplasty
• indication
– end stage osteoarthritis
• techniques
– femur
» cannulated reamers under fluoroscopy
» short stemmed implants
» usually uncemented components are used
– acetabulum
» small, sharp reamers
» irrigation
» multiple screws
114. Osteopetrosis
– total knee arthroplasty
• indications
– end stage osteoarthritis
• technique
– consider navigation
115. Osteopetrosis
• Complications
– Refracture
• caused by
– hard brittle bones
– hardware failure
– Infection
• increased risk due to reduced tissue vascularity
– Malunion
– Non-union
scorbutic rosary is distinguished from rickety rosary (which is knobby and nodular) by being more angular and having a step-off at the costochondral junction
Spondylosis is a type of arthritis spurred by wear and tear to the spine. It happens when discs and joints degenerate, when bone spurs grow on the vertebrae, or both.
