This document discusses metabolic and endocrine skeletal diseases. It covers the composition of bone tissue, production of bone, and evaluation of metabolic and endocrine disorders through radiography. Specific diseases covered include osteoporosis, rickets, scurvy, and their radiographic manifestations such as bone density changes, growth plate abnormalities, and fractures. Osteoporosis can be generalized or regionalized. Common sites of involvement are the spine, pelvis and femur.
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.
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
4. EVALUATION OF METABOLIC
AND ENDOCRINE DISORDERS
• Most metabolic and endocrine disorders are
characterized radiographically by
abnormalities in bone density
increased bone
production
increased
bone
resorption
inadequate
bone
mineraliz
ation
5. Radiologic modalities most often used to evaluate
metabolic and endocrine bone disorders are:
simplest and most widely used
• Conventional radiography method of evaluating bone
density
• Computed tomography (CT)
• Radionuclide imaging (Scintigraphy , Bone scan)
• Magnetic resonance imaging (MRI)
• Ultrasound (US).
8. OSTEOPOROSIS
• Osteoporosis is a reduction in bone quantity
, with the actual quality of the bone remaining
normal.
• Most commonly encountered metabolic
disease of bone
• Generalized metabolic bone disease
10. Basic distinction in osteoporosis is
between two types
Generalized or diffuse – bone
density is decreased in the
majority of the skeleton,
especially the axial components of
the spine, pelvis, and proximal
long bones
Regional - Loss of bone density
confined to a region or segment
of the body
Localised - Focal losses of bone
density affecting a relatively small
area of bone
11. GENERALISED OSTEOPOROSIS
• Bone density is decreased in the majority of
the skeleton, especially the axial components
of the spine, pelvis, and proximal long bones.
• MCC - Postmenopausal status and aging.
14. SENILE OSTEOPOROSIS
• Osteoporosis associated with advancing age in
male and female individuals is termed senile
osteoporosis, senescent osteoporosis, or old-
age osteoporosis.
• In the female an additional designation used is
postmenopausal osteoporosis.
15. CLINICAL FEATURES
Gradual reduction in skeletal mass
• Pain
• Spinal compression fractures and other
fractures of bone— especially the proximal
femur, ribs, humerus, and radius
16. RADIOGRAPHIC FEATURES
• Increased radiolucency
• Cortical thinning
• Altered trabecular patterns
• Fracture deformity
decreased bone mass
30–50% loss of bone
tissue must occur
before an observable
radiographic change
becomes evident.
Generalized thinning
of cortex
increase in the
marrow cavity size
As trabeculae are resorbed, those
that remain appear accentuated,
along the regions of greatest stress.
In severe disease , the internal
trabecular architecture may be
completely lost, giving the bone a
washed-out appearance
17. Target sites
Spine
Pelvis and femur
Sacrum
Pubis
Other sites – Sternum , Acetabulam , Neck of
femur , Tibia , Fibula ,
18. SPINE
Curve changes - Increased thoracic kyphosis
risk for compression fractures
• Decreased bone density – density of the
vertebral body, diminishes in parallel with loss
of bone mass
19. • Trabecular changes - preferential resorption of
the horizontal trabeculae, allowing easier
delineation of vertical trabeculae- pseudo-
hemangiomatous appearance of osteoporosis
remaining
20. • Cortical Thinning - Cortical outlines of the
vertebral body and neural arch are thinned. This
is best depicted at the vertebral body endplates,
which are normally relatively thick.
• Changes in Shape - rare in the cervical spine, less
common in the upper thoracic spine, and most
common in the midthoracic and thoracolumbar
regions.
21. 1. Wedged Vertebra. Compression deformities causing
loss of the anterior vertebral body height with
preservation of the posterior height are termed
wedged vertebrae
2. Vertebra plana / Pancake vertebra - compression
deformity of the vertebral body characterized by a loss
in both the anterior and posterior vertical heights
3. Fish vertebra - Central depression of the vertebral
body endplates causes exagerrated concavity .
22.
23. 4. Isolated endplate deformity - Central endplate
fractures are most frequent at L1 and L4.
24.
25. Schmorl’s Nodes
• intravertebral disc herniations - protrusions
of the cartilage of the intervertebral
disc through the vertebral body endplate and
into the adjacent vertebra.
• Localized intrabody discal herniations are
frequently superimposed on the osteoporotic
spinal column.
• Most commonly occur in the thoracic and
upper lumbar spines
26. OSTEOPOROSIS: SEVERE SENILE KYPHOSIS.
Lateral Thoracic Spine. Note the severe
postural alteration, which is a complication
owing to loss of disc height and anterior
wedging of the vertebral bodies. This underlies
the physical appearance of the buffalo or
dowager’s hump deformity.
27. PELVIS AND FEMUR
• Manifestations
are identical to
most other sites
with decreased
bone density,
trabecular
changes, cortical
thinning, and
fracture-related
deformities.
30. SACRUM
• MCC of fracture of the sacrum is senile and
postmenopausal osteoporosis with a history
of a recent fall onto the buttocks.
• Second most common occurrence is fracture
secondary to radiotherapy of the pelvis.
• Corticosteroid therapy (rheumatoid arthritis,
chronic airways disease), alcohol abuse,
multiple myeloma, osteomalacia, osteogenesis
imperfecta, and recent hip replacement
31. • Most sensitive method of detection is isotopic
bone scan.
• Three patterns of sacral insufficiency fractures
occur based on bone scan appearance.
• H pattern (butterfly or “Honda” sign).
• I pattern
• Arc pattern.
32. • H pattern (butterfly or “Honda” sign).
Bilateral vertical fractures through the sacral
ala are connected by a transverse fracture
through the S2, S3, or S4 bodies
33.
34. I pattern
• A single vertical fracture passes through the sacral ala.
• most common form of sacral insufficiency fracture
• Bone scan - focal linear increased tracer uptake
• Misdiagnosed as Sacroiliitis owing to the proximity of the
fracture to the adjacent sacroiliac joint
Arc pattern
A linear or curvilinear transverse fracture passes horizontally
across the sacrum
35. MRI
T1-weighted images - decreased signal
intensity
T2-weighted images - increased signal
intensity .
This is especially helpful when the fracture
line cannot be seen through the sacral ala and
is, therefore, readily overlooked.
38. REGIONALISED OSTEOPOROSIS
• Reflex Sympathetic Dystrophy Syndrome
• Disuse and Immobilization Osteoporosis
• Transient Regionalized Osteoporosis
1. Transient Osteoporosis of the Hip
2. Regional Migratory Osteoporosis
39. REFLEX SYMPATHETIC DYSTROPHY SYNDROME
• Post-traumatic osteoporosis / Sudeck’s
atrophy / Acute bone atrophy / causalgia /
complex regional pain syndrome.
• Acute onset of a painful regional osteoporosis,
usually following trivial antecedent trauma
40. Joint spaces and margins are
normal, assisting in differentiating
from infection or rheumatoid
arthritis.
RADIOGRAPHIC FEATURES
• Most characteristic radiographic change - rapidity of the
appearance and progression of the osteoporosis
INITIAL FEATURES
• Mottled appearance – Rapid resorption
• Metaphyseal osteoporosis
• Tunneled cortices
• Endosteal resorption
LATE CHANGES - entire bone density is diminished, appearing no
different from other types of osteoporosis
41.
42. DISUSE AND IMMOBILIZATION
OSTEOPOROSIS
Traumatic injuries that
are immobilised
Motor paralysis Inflammatory lesions of
the bones and joints.
• Inhibits osteoblastic activity
• Accelerates osteoclastic mediated resorption
43. • Acetabulum - the superior cortex appears as a
double cortical line (double cortical line sign).
• Changes in the spine and pelvis are less
apparent than in the appendicular skeleton
44. Radiologic features after acute immobilization
can be recognized by four patterns of
osteoporosis
• Uniform. All bones involved exhibit a similar
degree of bone loss. most common form.
• Spotty. Localized circular lucencies predominate,
especially within the epiphyseal portions of the
bones.
• Bands. Linear transverse subchondral or
metaphyseal lucent zones.
•Cortical - Lamination or scalloping loss of
definition in the outer and inner cortical margins.
45.
46.
47.
48. TRANSIENT REGIONALIZED
OSTEOPOROSIS
• Transient regionalized osteoporosis is
described as osteoporosis ocurring suddenly
which is reversible with predilection for
periarticular bone and has no associated
causal factor.
• With the advent of MRI, the disorder has also
been termed transient bone marrow edema
syndrome.
49. Transient Osteoporosis of the Hip
• Reversible stage of avascular necrosis
• Slightly more frequent in males
• Onset - sudden, with pain, antalgia, and limp
• Radiologic features
–Marked osteoporosis of the femoral head
–Less severe osteoporosis of the femoral
neck and acetabulum.
–Joint space is normal
50. MRI
MRI demonstrates bone marrow oedema
pattern involving the femoral head, neck, and
even intertrochanteric region
T1: decreased signal with loss of normal fatty
marrow signal
T2: high signal / heterogeneous signal intensity
51. Regional Migratory Osteoporosis
• Middle-aged males are most commonly
affected.
• Most frequent joints – lower extremity - knee,
ankle, foot, and hip .
• Radiologic features - localized osteoporosis of
the intraarticular components , which
subsequently regresses over 9-month period
to reappear in another joint .
52. LOCALISED OSTEOPOROSIS
• Rapidly developing osteoporosis that usually affects
the periarticular regions and has no definite etiology
like trauma or immobilization.
• It is a self-limiting and reversible disorder, of which
three subtypes have been described.
53.
54. Periarticular osteoporosis. Anteroposterior (A) and lateral (B) radiographs of an ankle
reveal sparse trabecular pattern and increase radiolucency in the subchondral areas.
55.
56. • Involutional
osteoporosis. Lateral
radiograph of the lumbar
spine of an 89-year-old
woman demonstrates a
relative increase in the
density of the vertebral
end plates and
resorption of the
trabeculae of spongy
bone, creating an empty
box appearance
57. RICKETS
• Rickets is a systemic disease of the infant and
young child.
• Faulty mineralization of bone matrix.
58. ETIOLOGY
Inadequate intestinal absorption
Vitamin D metabolism defects
Renal tubular disorders
Renal osteodystrophy secondary to renal
failure
Inadequate exposure to ultraviolet radiation,
intestinal malabsorption
Aluminum intoxication, and chronic
administration of anticonvulsants
59. CLINICAL FEATURES
• Muscle tetany
• Pain
• Irritability
• Weakness
• Delayed development
• Small stature
• Bone deformities
60. RACHITITIC
ROSARY
• Soft tissue swellings
occurring around the
growth plates owing
to hypertrophied
cartilage.
• At the anterior rib
cage, these are seen
as multiple
costochondral bumps
(rachitic rosary)
61. PATHOLOGICAL vs RADIOLOGICAL
• Decrease in the quantity of
calcified osteoid and an
increase in uncalcified
osteoid.
• Cartilage cells at the physis
grow normally but fail to
calcify and degenerate.
• Lack of osteoid mineralization
generalized
radiolucency
widening
the region
metaphyseal
zone of prov
calcification
be absent
62. RADIOGRAPHIC FEATURES
• Abnormalities will be found at the growth
plate regions of long bones.
– Generalized osteopenia
– Coarse trabecular changes
– Widened growth plates
– Frayed and cupped paintbrush metaphyses
63. RADIOGRAPHIC FEATURES
– Absent zone of provisional calcification
– Bowing deformities
– Fractures, decreased bony length, scoliosis,
and pseudofractures.
64.
65. HEALING RICKETS
• No distinct white line of the zone of
provisional calcification is visible.
• Reappearence of this line is a useful indicator
of a good therapeutic response.
• Epiphyses also appear frayed at the borders.
66.
67. Classic Vitamin D-Resistant rickets
• Hypophosphatemic rickets / familial vitamin D-
resistant rickets
• Mutation of PHEX gene found on the X
chromosome
• Short, stocky, and bowlegged
• Ectopic calcifications and ossifications in the axial
and the appendicular skeleton
68.
69. SCURVY
A/K/A barlow’s disease / hypovitaminosis C
Long-term deficiency of vitamin C
Infants between the ages of 4 and 18 months
are primarily affected.
70. CLINICAL FEATURES
• Clinical hallmark - Tendency toward spontaneous
hemorrhage owing to capillary fragility.
• Cutaneous petechiae, bleeding gums, melena,
and hematuria
• Joint swelling, irritability, pain, and a tendency to
lie supine and motionless with the thighs
abducted (frog-leg position)
71. PATHOLOGIC FEATURES
Vitamin C
osteoid endothelial linings
formation of intercellular substances
generalized
osteopenia
collagen
Bleeding
manifestations
72. RADIOGRAPHIC FEATURES
• Osteopenia - generalized decrease in bone
density with thinning of the cortex and loss of
trabecular definition
• White line of frankel - Dense zone of provisional
calcification. Enhancement of the dense
metaphyseal zone of calcified cartilage occurs
owing to delayed conversion into bone
73. • Wimberger’s sign - Ring epiphysis. The
peripheral margin of the epiphysis appears
dense, whereas the central portion is more
radiolucent.
• Corner (angle) sign. Irregularity of the
metaphyseal margins frequently occurs
secondary to infractions of the epiphyseal–
metaphyseal junction.
74. • Pelken’s spurs. These bony protuberances
occur at the metaphyseal margins and extend
at right angles away from the shaft axis.
• Scorbutic zone (Trümmerfeld’s zone). Directly
beneath thezone of provisional calcification a
radiolucent band may be visible, representing
disordered osteoid formation.
75. • Subperiosteal hemorrhage. Extensions of
extravasated blood frequently lift the
periosteum away from the bone and will later
calcify, especially during healing
76.
77.
78. OSTEOMALACIA
• Osteomalacia is a metabolic disorder that
alters the quality of bone
• Occurs only after bone growth has ceased
• MC clinical presentation - bone pain and
muscle weakness
79. CAUSES OF OSTEOMAACIA
Cause
– faulty absorption of fat-
soluble vitamin D from
the gastrointestinal
tract secondary to
malabsorption
syndrome.
– dysfunction of the
proximal renal tubules -
Renal osteomalacia
80. RADIOGRAPHIC FEATURES
No definitive radiologic diagnosis can be made
without the appropriate clinical and
laboratory support, owing to the non-specific
nature of the skeletal changes
81. • Decreased Bone Density
•
Bones will appear more radiolucent
due to diminished bone mineral
content
• Coarsened Trabecular Pattern
Decrease in the overall number of bony trabeculae within
all bones enhances the contrast of those remaining
Texture of the spongiosa may appear coarse and mottled.
Loss of Cortical Definition Cortex reveals it to be thinner and
altered in structure
82. Pseudo-Fractures
• Pseudo-fractures are linear radiolucencies that
usually occur bilaterally and symmetrically in
predictable locations.
• MC sites - femoral necks, pubic and ischial
rami, ribs, and axillary margins of the
scapulae.
83. Deformities
• Majority of the deformities occur in the weight-bearing
bones.
• In the pelvis, inferior displacement of the sacrum produces a
triradiate shape to the pelvic canal. Medial acetabular
migration forms a protrusio acetabuli deformity.
• Bowing of the femur and tibia also are seen.
• In the spine, kyphoscoliosis and increased endplate concavity
predominate. Bellshaped thoracic cage has also been
described.
88. HYPERPARATHYROIDISM
• A/K/A generalized osteitis fibrosa cystica or
Recklinghausen disease of bone
• Hyperparathyroidism is the general term applied to
overactivity of the parathyroid gland.
THREE BASIC FORMS OF HYPERPARATHYROIDISM
Primary hyperparathyroidism-
Most common cause of hypercalcemia
Due to a parathyroid adenoma , carcinoma,
hyperplasia, or ectopic tumors, producing a
parathormone type of substance.
89. elevated levels of parathormone, hypercalcemia, and
hypophosphatemia.
Secondary hyperparathyroidism
Most common complications of chronic renal
disease, allowing for persistent loss of calcium and
phosphorous and thus stimulating parathormone
release.
Tertiary hyperparathyroidism
In dialysis patients, the parathyroid gland may act
independently of serum calcium levels.
91. CLINICAL PROFILE
30 to 50 years old female
Weakness, lethargy, polydipsia, and polyuria
Hypercalcemia - muscles will be hypotonic and
formation of renal calculi
Elevated Parathormone concentration
92. RADIOGRAPHIC FEATURES
• Radiologic differentiation between primary and
secondary hyperparathyroidism is usually not
possible
Bones
•Subperiosteal
resorption
•Decreased bone
density
•Accentuated
trabecular pattern
•Loss of cortical
definition
•Subligamnetous bone
resorption
•Brown tumors
Soft tissues
Joints
Dialysis-related
arthropathy (DRA)
Dialysis-related
spondyloarthropathy
(DRSA)
Urinary Tract
Articulations
Miscellaneous Tissues
- Periarticular
structures, such as
blood vessels,
ligaments, tendons,
muscle, and
subcutaneous tissues
93. TARGET SITES
Hands
• Demonstration of subperiosteal resorption is the
hallmark of hyperparathyroidism.
• MC Location - proximal and middle phalanges of
second and third digits along radial margins
• outer cortex will appear frayed and irregular
94.
95. Skull
• Diffuse granular deossification produces a mottled
appearance to the calvaria (salt and pepper or
pepper pot skull
96. Spine and Pelvis
• All vertebral segments show generalized
deossification and trabecular accentuation.
• Endplate concavities due to bone softening
• Uniform condensation in the sub-endplate zones of
the bodies (rugger-jersey spine).
97.
98.
99. • Subchondral resorption at the sacroiliac and pubic
articulations produces marked apparent widening of
these joints and can be readily confused with erosive
spondyloarthropathies, such as ankylosing spondylitis.
• Discovertebral destructive lesions (e.g., DRSA) are most
common in the cervical spine and appear identical to
infection
100. Shoulder
Resorption of the distal clavicle subchondral bone
bilaterally is an early and reliable indicator of
hyperparathyroidism.
Articular surface is indistinct and frayed.
Infection and post-traumatic osteolysis
101.
102. ACROMEGALY
• In adulthood, excessive growth hormone secretion
from a pituitary eosinophilic adenoma produces
growth of intramembranous bone tissue and
subcutaneous hypertrophy
• Prominent in the hands and feet
103. CLINICAL FEATURES
• Physical features - malocclusion, prominent
forehead; thickened tongue; and broad, large hands.
• Bitemporal hemianopia, headache, and carpal tunnel
syndrome are common.
• Acromegalic patients are predisposed to
degenerative arthritis, especially of the spine and
weight-bearing joints.
104. RADIOGRAPHIC FEATURES
Skin changes
• usual site for skin changes actually measured
is the heel pad thickness.
• heel pad thickness > 20 mm is suggestive of
acromegaly
107. Hand
• Widened shafts of the phalanges and metacarpals
• Bony protuberances
• Prominent ungual tufts - spade-like appearance
• A reliable indicator - generalized increase in joint
space width owing to cartilage overgrowth.
108. Figure 14-39 ACROMEGALY. A. PA Hand. Note
the characteristic features of widened joint
spaces and periosteal neW bone formation. B.
Close-Up, Distal Tufts. Note that the distal
tufts are classically enlarged, showing the
spade-like deformity (arrows).
109. ACROMEGALY. AP Hip. Note the
widened axial joint cavity, reflecting
the overgrowth of intra-articular
cartilage (arrowheads). Despite this
joint widening weight-bearing
superior compartment is narrowed,
with evidence of a degenerative
lateral acetabular osteophyte
(arrow). A subchondral cyst can be
seen in the femoral head.
COMMENT: The appearance of
degenerative joint changes is
common in acromegaly
110. SPINE
• Vertebral dimensions increase in both sagittal
and transverse planes, especially in the
lumbar spine.
– vertical height – unchanged vertebral
bodies appearing flattened and increased in
their sagittal dimensions platyspondyly.
• Premature degeneration with exuberant
osteophytes and widened disc heights
complete the most typically observed
changes.
• posterior body scalloping may be observed
from dural ectasia.
111. • The atlantodental interspace may be increased up to
6 mm owing to cartilage overgrowth, not transverse
ligament instability.
• Widening of the facet joints
• Hyperostosis of the tips of the spinous processes
• Spinal stenosis - thickened laminae and articular
process with the spinal ligaments thickened and
calcified.
112. HYPERVITAMINOSIS A
• Hypervitaminosis A can occur both in adults and in
children.
• C/F - Dermatitis, Pruritus, Alopecia, and Yellowing of
the skin. Hepatosplenomegaly can be present.
113. RADIOLOGICAL FEATURE
• Solid, periosteal new bone along the shafts of
the long bones - femurs, tibia, fibula,
metatarsals, humerus, ulna, radius, and
metacarpals.
• Diastasis of the cranial sutures, most marked
at bregma, is also common.
• Increased radioisotope uptake on bone scan
• Diffuse osteopenia
114. HYPERVITAMINOSIS D
• C/F - nausea, anorexia, polyuria, and
polydipsia.
• Hypercalcemia
• The most characteristic radiologic feature is
the extensive calcification in blood vessel
walls, kidneys, and periarticular tissues
115. LANGERHANS CELL
HISTIOCYTOSIS
• Histiocytosis X is a disease of unknown origin that
encompasses a wide spectrum of clinical, pathologic, and
radiologic features
• Hallmark - abnormal proliferation of reticuloendothelial cells
• Three entities are encompassed under this term:
• Letterer-siwe disease
• Hand-schüller-christian disease
• Eosinophilic granuloma
116. LETTERER SIWE DISEASE
• Acute, fulminating, fatal disease affecting children <
3 years of age.
• C/F – Critically ill with a high fever, skin rash, bleeding
gums, malaise, lymphadenopathy,
hepatosplenomegaly, and respiratory symptoms.
117. • Skeletal lesions are infrequent owing to the
rapidity of its progression.
• MC bone change - lytic lesionsin the calvaria.
• Long bone lesions - aggressive, with irregular
rarefaction of the diaphysis and surrounding
laminated periosteal response closely
simulating Ewing’s sarcoma.
119. RADIOLOGICAL FEATURES
• radiologic hallmark - polyostotic destructive
foci in an immature skeleton particularly in
the skull, pelvis, and long bones
• Long bones- multiple lytic defects affecting
the entire bone from the diaphysis to the
metaphysis coalesing to create larger defects
marked by endosteal scalloping and beveling
of the cortex - hole-within-hole appearance
120. • In the skull, confluence of these individual
lesions generates large map-like regions of
radiolucency (geographic skull ) with a
peripheral beveled edge and a hole-within-
hole appearance
121. EOSINOPHILIC GRANULOMA
• Least severe but most common of all histiocytoses.
• Typically lacks the systemic features of hand-schüller-
christian or letterer-siwe disease
• Vertebral involvement – pain
• Temporal bone involvement – om like symptoms
122. • Monostotic presentations are three times
more common than polyostotic presentations
• Pain may be the primary symptom (6), and the
diagnosis often requires histopathologic
analysis of the lesions
123. RADIOGRAPHIC FEATURES
• Most lesions are visible on plain films.
• CT and MRI are useful in defining a soft tissue mass,
periosteal response, and characteristics of the lesion.
• Once a lesion is isolated, a bone scan may well
identify additional lesions.
Solitary and geographic
Round to oval in shape
Sharply demarcated borders
Prominent endosteal scallopingwith solid or
laminated periosteal response
124. SKULL
• Sharply demarcated round to oval osteolytic lesion of
1–4 cm is characteristic
• Beveled edge sign / Hole within hole - Involve one
table greater than the other to produce a double
contour
• Button sequestrum - within the lesion a central focus
of bone may remain isolated, identified on CT
examination.
• The lesion does not respect suture lines and readily
infiltrates into adjacent parts of the calvaria.
125. MANDIBLE
• Pain is the primary symptom
• Radiographically, the lesion is osteolytic,
expansile, and does not involve the teeth
except to leave them displaced and isolated
floating teeth sign.
• Early lesions typically begin near last molar
and enlarge predominantly forward without
destroying the lower mandibular border.
126. Spine
• Involve the thoracic spine , lumbar spine; and < 15%,
the cervical spine.
• Vertebral body is usually involved with relative
sparing of the neural arch structures.
• Ghostly appearance – When Neural arch is involved
destruction of internal matrix with preserved the
cortical outline is noted.
127. • Vertebra plana, Silver dollar vertebra, Coin-on-edge
vertebra - most prominent feature in the lumbar and
thoracic spine is pathologic fracture, with dramatic
loss of vertebral height involving both the anterior
and posterior vertebral body surfaces.
132. CRETINISM
• Congenital hypothyroidism
• Exerts considerable growth and developmental-inhibiting
factor to the skeleton.
• Cretinoid epiphyses delayed closure and fragmented
epiphyses
• Occasional wormian bones
• Wedged thoracolumbar sail vertebra.
• Bilateral slipped capital femoral epiphysis (rare)
133. Juvenile hypothyroidism. (A) Dorsovolar radiograph of the right hand of a 13-year-
old boy demonstrates skeletal immaturity; the bone age is approximately 8 years.
Note the “fragmented” secondary ossification centers of the distal ulna and distal
phalanges. In fact, they represent separated foci of ossification.
(B) The hand of a healthy boy of the same age is shown for comparison
134. Congenital hypothyroidism (cretinism). Anteroposterior radiograph of the pelvis of a 5-year-old
boy shows pseudofragmentation of both capital femoral epiphyses. This process may be
mistaken for Legg- Calvé-Perthes disease
135. THYROID ACROPACHY
• Thyroid acropachy is an unusual complication to a
treated hyperthyroid patient who is now maintaining
normal thyroid activity.
• C/F - digital swelling that is painless and progressive.
• Radiological feature - thick and dense periostitis
arising from the radial aspect of the small hand
bones. Similar changes exhibited on the tibial aspects
of the foot bones
136. Figure 14-41 THYROID ACROPACHY. A. PA Hands. Observe the thick, dense periosteal new bone a
the metacarpals and phalanges (arrows). B. PA Feet. Note that similar changes are
seen on the medial surface of the first metatarsal (arrows), a distinctively characteristic site for
thyroid acropachy of the foot
137. PAGETS DISEASE
• Chronic, progressive disturbance in bone metabolism
that primarily affects older persons.
• More common in men than in women
• Skeletal abnormalities seen in paget disease are
frequently asymptomatic.
• Frequency of bone involvement - pelvis, femur, skull,
tibia, vertebrae, clavicle, humerus, and ribs
138. HALLMARK
Disordered and extremely active bone
remodeling, secondary to both osteoclastic
bone resorption and osteoblastic bone
formation in a characteristic mosaic pattern.
139. • increase in osteoblastic activity - elevated
levels of serum alkaline phosphatase
• the increase in osteoclastic bone resorption -
high urinary levels of hydroxyproline,
140. IMAGING EVALUATION
EARLY PHASE- THE OSTEOLYTIC OR HOT PHASE
Active bone resorption is evident as a
radiolucent wedge or an elongated area with
sharp borders that destroys both the cortex and
cancellous bone as it advances along the shaft.
This phenomenon are advancing wedge, candle
flame, and blade of grass.
141. Osteolytic phase of Paget disease. (A)
Anteroposterior radiograph of the
lower leg of a 68-year-old
woman shows an advancing wedge of
osteolytic destruction in the midportion
of the tibia (arrow). (B) Magnification
study of the midfemur in another
patient shows the purely osteolytic
phase of Paget disease. In
both examples, the lesion resembles a
blade of grass or a candle flame
142. (A) Lateral radiograph of the skull shows an osteolytic lesion in the parietooccipital area. This
sharply demarcated defect, known as osteoporosis circumscripta, represents a hot
phase of the disease. (B) Radionuclide bone scan shows a characteristic localized increased
uptake of the radiopharmaceutical tracer resulting in the appearance of a “yarmulke” sign. (C)
Lateral radiograph of the skull reveals osteoporosis circumscripta in the frontoparietal area.
143. INTERMEDIATE OR MIXED PHASE
• Bone destruction is accompanied by new bone
formation, with the latter process tending to
predominate.
• Bone remodeling appears radiographically as
thickening of the cortex and coarse
trabeculation of cancellous bone
144. • Intermediate phase of
Paget disease. (A) In the
intermediate phase
thickening of the cortex
and a coarse trabecular
pattern in the medullary
portion of the bone are
characteristic features.
Note the anterior
bowing. (B) intermediate
phase is seen in the
pubic and ischial bones.
(C) Mixed phase
affecting the proximal
phalanx of the middle
finger with monostotic
form of the disease
145. • Spine - the thin cortex of the vertebral body,
which disappears in the hot phase, is later
replaced by broad, coarsely trabeculated
bone, forming what appears to be a “picture
frame” around the body .
• Skull - focal patchy densities with a “cotton
ball” appearance are characteristic
146. Intermediate phase of Paget disease.
(A) Involvement of the lumbar spine in
the mixed phase can be recognized by
the “picture frame” appearance of the
vertebral bodies (arrows) created by
dense sclerotic bone on the periphery
and greater radiolucency in the center.
Note the partial replacement of
vertebral end plates by coarsely
trabeculated bone. (B) In another
patient, the picture frame appearance
of the vertebral body of L2 marks the
intermediate phase of Paget disease.
(C) Sagittal STIR MRI of the lumbar
spine in another patient with Paget
disease affecting the L5 vertebral body
shows the MRI-equivalent of picture
frame.
147. Intermediate phase of Paget
disease. Focal patchy densities
in the skull, having a “cotton
ball” appearance, are typical
of the intermediate phase of
Paget disease
148. COOL OR SCLEROTIC PHASE
• a diffuse increase of bone density occurs
together with enlargement and widening of
the bone and marked cortical thickening, with
blurring of the demarcation between cortex
and spongiosa.
• Bowing of long bones may become a striking
feature
• Similar changes are observed in the skull,
where obliteration of the diploic space is also
a typical feature
149. Cool phase of Paget disease. In the cool phase, there is thickening of the cortex and bone
deformity. (A) The pelvic cavity assume a triangular appearance. (B) Involvement of a long bone,
in this case the distal humerus of a 60-year-old woman, exhibits marked cortical thickening,
narrowing of the medullary cavity, and a coarse trabecular pattern.
150. (C) Similar changes are present in the (D)
Anteroposterior radiograph of the skull of an
reveals typical changes of the cool phase of
Paget disease.
151. Cool phase of Paget disease. Anteroposterior
radiograph of the forearm with
polyostotic Paget disease shows enlargement
of the left radius with a marked bowing
deformity. the cool phase of the disease are
seen in the diffuse sclerotic changes and the
indistinct demarcation between
the cortex and the spongiosa
152. Anteroposterior and lateral radiographs of the right leg show thickening of the
cortex and a coarse trabeculation of the proximal tibia. (B) Sagittal and coronal
reformatted CT images demonstrate these abnormalities to the better advantage
lack of distinction between the cortex and the spongiosa (arrows). (C) 3D CT
reconstructed image shows deformity of the tibia
and anterior bowing
153. Magnetic resonance imaging (MRI)
• demonstrate cortical and intramedullary
involvement better
• exclude (or confirm) extension of the process into
the soft tissues.
In general, the pagetic bone exhibits heterogeneous
signal intensity.
• T1-weighted sequences - intermediate-to low SI
• T2 weighting - high, intermediate, or low SI
depending on the stage of the disease and degree
of fibrosis and sclerosis
154. MRI of Paget disease. (A) Anteroposterior radiograph of the left distal femur shows
typical appearance of Paget disease: enlargement of the bone, cortical thickening,
and sclerosis and coarse trabecular pattern of cancellous bone. (B,C) Two coronal T1-
weighted MR images demonstrate cortical thickening (arrow) and low-signal coarse
cancellous trabeculae
155. (D) Coronal T2-weighted MRI
shows heterogeneous signal
in the femoral condyles. (E,F)
Sagittal T1-weighted and
axial T2-weighted MRI of the
knee in another patient
demonstrate the
characteristic coarse
trabecular pattern and
cortical thickening of the
distal femur. Note the
prominent areas of fatty
marrow between the
thickened trabeculae
156. Scintigraphy
• increased uptake of bone-
seeking radiotracer in all
three phases of the
disease, but particularly
in the hot and
intermediate, due to
increased vascularity and
osteoblastic activity in
abnormal bone.
157. DIFFERENTIAL DIAGNOSIS
• familial
idiopathic
hyperphosphat
asia, also called
juvenile Paget
disease -
articular ends
of the bone
may not be
affected.
(A) AP radiograph of the shoulder and arm reveals marked thickening of the cortex of the
humerus and coarsening of the bony trabeculae, resembling pagetic bone. (B) Radiograph of
the hands shows sclerotic changes in the bones and a marked narrowing of the medullary
cavity of the metacarpals and phalanges
158. • Van buchem disease (hyperostosis corticalis
generalisata)
• Vertebral hemangioma
• Rugger-jersey spine seen in secondary
hyperparathyroidism
• Lymphoma
• Extensive osteoblastic metastases
160. Pagets sarcoma
The most serious complication of Paget disease
is sarcomatous degeneration.
Radiographically, it can be recognized by:
• osteolytic bone destruction at the site of the
pagetic lesion
• cortical breakthrough
• soft-tissue mass
161. (A) Radiograph of the pelvis shows extensive involvement of the left ilium, pubis, and ischium by
Paget disease. There is also destruction of the cortex and a large soft-tissue mass accompanied
by bone formation (arrow), typical findings for osteosarcoma. (B) CT scan demonstrates the
softtissue mass more clearly (open arrows).
162. (A) Coronal T1-weighted image
shows Paget disease affecting
the distal femur. Destruction of
the cortex and soft-tissue mass
are well demonstrated.
(B) Coronal STIR and (C) axial T2-
weighted sequences confirm
the presence of a soft-tissue
mass (arrows), thus
corroborating the diagnosis of
malignant transformation
163. Metastasis in Pagets disease
Anteroposterior radiograph of the pelvis shows extensive osteolytic destruction of
the right ilium, ischium, and pubis secondary to metastatic renal cell carcinoma
(hypernephroma). Note the typical involvement of the pelvis by Paget disease. This
metastatic lesion should not be mistaken for Paget sarcoma