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Chapter 3 · Endocrinology andMetabolism
Vacuum phenomenon , also known as “intervertebral cle
sign,” is a term used to describe a condition characterized by
accumulation of gas, mostly nitrogen (95 %), within the vertebral bodies, intervertebral disks, and synovial joints. e
gas is produced from the surrounding so tissues, and its
3
accumulation mechanism is poorly understood. e main
hypothesis of vacuum phenomenon suggests ischemic origin. Osteonecrosis of the vertebral end plates with negative
pressure between the bone fragments is mandatory to release
gas from the surrounding tissue, a situation that can be classically seen in osteoporotic vertebral fractures and collapse.
Vacuum phenomenon is also seen in osteonecrosis due to
long-term corticosteroid therapy, diabetes mellitus, arteriosclerosis, multiple myeloma, and alcoholism.
e main di erential diagnosis of the intravertebral vacuum phenomenon is gas produced by osteomyelitis and
malignancies. In infectious gaseous production, the gas has
high pressure and tends to accumulate in small collections,
plus extends into the adjacent so tissues, which is not seen
in vacuum phenomenon where gas is limited to the bony or
intradiskal areas.
Kümmel’s disease is a term used to describe vacuum phe-
nomenon within a vertebra that arises from vertebral end
plates osteonecrosis and vertebral collapse. Kümmel’s disease
represents healing failure of an osteoporotic vertebral fracture with the formation of pseudoarthrosis (false joint).
. Fig. 3.4.1 A plain radiograph of the knee shows diminished
bone mineral density (BMD) with thinning of the cortex
( arrowheads )
Signs on Plain Radiograph and CT
5 Thinning of the cortex (compact bone) is the main
radiographic feature of osteoporosis (. Fig. 3.4.1 ).
It is best seen in the second metacarpal bone
diaphysis. Normally, the cortex in the mid-shaft of
the second metacarpal should be almost one third
the thickness of the metacarpal width. This sign is
seen in up to 50 % of cases.
5 Dowager’s hump is an osteoporotic multiple
thoracic vertebrae causing wedge deformities
(. Fig. 3.4.2 ).
5 Pathologic fractures mostly occur at the neck of the
femur, distal radius, and humeral neck.
5 Intracortical tunneling is a sign of rapid bone loss. It
is typically seen as long lucent lines parallel to the
long axis of the bone (. Fig. 3.4.3 ). When the
tunneling is severe, a double cortical line is seen.
5 Diffuse bone resorption occurs in 50 % of cases and
is characterized by loss of the trabecular bone.
5 Linear translucent bands of 4–8mm thickness are
seen within the bone in radiograph. They are
commonly seen with disuse osteoporosis and
leukemic patients.
5 Patchy bone resorption : seen as multiple lucent
patches usually in the carpal or tarsal bones. It can
be mistaken with lytic lesions of Ewing’s sarcoma
and multiple myeloma (. Fig. 3.4.4 ).
. Fig. 3.4.2 A lateral thoracic vertebrae radiograph shows
kyphosis of the thoracic vertebrae due to osteoporosis
(dowager’s hump)
3.4 · Osteoporosis
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3
. Fig. 3.4.4 Anteroposterior plain wrist radiograph in a
patient with osteoporosis shows patchy areas of radiolucent
opacities representing patchy osteoporosis ( arrowheads )
. Fig. 3.4.3 A plain radiograph of osteoporosis of the femoral
shaft demonstrates clearly the intracortical tunneling sign
( arrowheads )
5 Vacuum phenomenon is seen as a gas collection in
a collapsed vertebra or in intervertebral disk space
(. Fig. 3.4.5 ).
5 Singh index is a simple method to estimate the
level bone mineral density (BMD) on radiograph by
analyzing the changes in the trabecular pattern of
the proximal femur. A scale of six grades is
classically described, with the first grade showing
only basic trabecular structures (low BMD, severe
osteoporosis), and the sixth grade showing
trabecular structures in all areas of the proximal
femur (high BMD, normal bone).
. Fig. 3.4.5 Sagittal lumbar CT image in a patient with
osteoporosis shows severe osteopenia, collapse of L4 vertebra
(vertebra plana), and vertebroplasty of L3, with gas formation
located in the intervertebral disk space between L4 and L5
( arrowheads )
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Chapter 3 · Endocrinology andMetabolism
Regional Migratory Osteoporosis oftheHip
Signs on MRI
5 The area of vacuum phenomenon may appear as
an area of fluid signal intensity on T2W images.
This finding is explained by the fact that fluid
3
replacement tends to fill the area of vacuum gas
on long supine position. This T2 flow signal
depends on the time of scanning. In the first
10min of the scan, the vacuum area is seen as a
hypointense area on T2W images. The signal turns
into T2 hyperintense signal between 20 and
40min after positioning.
5 I n Kümmel’s disease , the vertebral end plates are
seen compressing over the fractured area in
flexion. In extension, the gap between the
fractured end plates open. Intervertebral air can
be seen on CT and MRI, with no signs of
inflammation on T2W images.
Dual Energy X-Ray Absorptiometry (DEXA) Scan
5 DEXA scan is a quantitative method for measuring
bone mass by using low-energy X-ray beam. The
bone mass is measured in units of gram per cubic
centimeter of bone. The World Health
Organization (WHO) defines the T -scores as
follows: between +1 and −1 indicates normal
bone; between −1 and −2.5 indicates osteopenia;
and osteoporosis is diagnosed when the T -score is
less than −2.5.
Pitfall : sclerosis and osteophytes in the vertebral column
can increase the values of the DEXA scan giving a false
impression of a good bone density. For this reason, DEXA
report should always be written a er comparison of the
results with plain frontal and lateral radiographs of the vertebral column to avoid misinterpretation.
Secondary Osteoporosis
Secondary osteoporosis is seen in association with other clinical conditions such as endocrine diseases (e.g., Cushing’s
syndrome), nutritional diseases (e.g., scurvy), drug induced
(e.g., heparin), neoplasms (e.g., multiple myeloma), metabolic diseases (e.g., diabetes mellitus), and chronic in ammatory conditions (e.g., rheumatoid arthritis). Radiological
manifestations are same as primary osteoporosis.
(Bone Marrow Edema Syndrome)
Regional migratory osteoporosis (RMO) is a rare condition
characterized by migrating arthralgia of weight-bearing
joints in the lower limbs (hips, knees, and ankles).
RMO typically a ects males between 50 and 60 years of
age presenting with pain con ned to a single joint. Patients
experience progressive pain in one joint that can last from
weeks to months. Peak intensity of the pain is experienced
usually in the second and third months a er the initial presentation. ere is no history of trauma or signs suggesting joint
infection (e.g., septic arthritis). e symptoms resolve spontaneously o en between 4 and 11 months a er presentation.
Signs on Radiographs
Typically, there is osteopenia of the a ected joint
compared to the other joint which normally shows no
osteopenia (unless the patient is generally osteoporotic).
Unfortunately, this sign is seen after 3–6 weeks from the
start of symptoms. Remineralization of the a ected area
may take up to 2 years to complete after the symptoms
are resolved.
Signs on MRI (Four Morphological Criteria at T1W
Images Are Needed to Indicate RMO of the Hip)
5 The bone marrow edema must involve the
femoral head and often spares the subchondral bone
resulting in a thin rim of una ected subchondral
marrow. The edema may extend to the femoral neck.
5 The bone marrow lacks the definite margins or
transitional zone between the lesion and the
adjacent marrow.
5 The signal is homogeneous with areas of high- or
low-intensity foci.
5 The signal intensity of the marrow is moderately
reduced. All the above four criteria must be
evaluated on T1W images.
5 Joint effusion is seen in 75 % of patients.
5 RMO of the knee has the same diagnostic criteria as
the RMO of the hip and typically involves the
lateral femoral condyle, although it can affect any
part of the knee (. Fig. 3.4.6 ) .
3.5 · Rickets andOsteomalacia
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a
. Fig. 3.4.6 Anteroposterior plain radiograph of the left knee ( a ), with coronal T1W image ( b ) and coronal PD image ( c ) of a 57-year-old
lady who presented with nonspeci c knee pain for 3 weeks’ duration. The plain radiograph shows no signs of obvious pathology or
diminished bone density. On the MR images, the lateral femoral condyle showed bone marrow edema signal with no sign of a fracture of
cortical destruction. The knee showed no signs of abnormalities that explain the knee pain. The diagnosis was regional migratory
osteoporosis (RMO) of the knee and the patient was advised a 3-month MRI follow-up examination
b
c
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3
RMO Di erential Diagnoses
5 Avascular necrosis : usually with history of trauma,
steroid use, chemotherapy, or renal disease. No such
history is associated with RMO.Risk factors for RMO
include low dietary calcium and tobacco smoking.
5 Reflex sympathetic dystrophy : there are atrophic
skin changes and history of neurological disease,
which are not seen in RMO.
5 Chronic recurrent multifocal osteomyelitis : has the
same picture as RMO on MRI, but plain radiographs
show both lytic and sclerotic lesions, which is not
characteristic of RMO.
Further Reading
Akpinar E etal. e intravertebral vacuum phenomenon. Eur
J Radiol Extra. 2008;66:e55–7.
Aloia JF etal. Risk for osteoporosis in black women. Calcif
Tissue Int. 1996;59:415–23.
Cahir JG etal. Regional migratory osteoporosis. Eur J Radiol.
2008;67:2–10.
Freedman BA etal. Kummel disease: a not-so-rare complica-
tion of osteoporotic vertebral compression fracture. J Am
Board Fam Med. 2009;22:75–8.
Goldring SR etal. Metabolic bone disease: osteoporosis and
osteomalacia. Dis Mon. 1981;27:1–103.
Hauschild O etal. Evaluation of Singh index for assessment
of osteoporosis using digital radiography. Eur J Radiol.
2009;71:152–8.
Karantanas AH.Acute bone marrow edema of the hip: role of
MR imaging. Eur Radiol. 2007;17:2225–36.
Kumpan W etal. e intravertebral vacuum phenomenon.
Skeletal Radiol. 1986;15:444–7.
Libicher M etal. e intravertebral vacuum phenomenon as
a speci c sign of osteonecrosis in vertebral compression
fractures: results from a radiological and histological
study. Eur Radiol. 2007;17:2248–52.
Lorenc RS.Idiopathic juvenile osteoporosis. Calcif Tissue Int.
2002;70:395–7.
Lutwak L etal. Osteoporosis. Dis Mon. 1963;9:1–39.
Sarli M etal. e vacuum cle sign: an uncommon radio-
logical sign. Osteoporos Int. 2005;16:1210–4.
Vande Berg BC et al. Bone marrow edema of the femoral
head and transient osteoporosis of the hip. Eur J Radiol.
2008;67:68–77.
Williamson MR etal. Osteoporosis: diagnosis by plain chest
lm versus dual photon bone densitometry. Skeletal
Radiol. 1990;19:27–30.
3.5 Rickets andOsteomalacia
Rickets is a group of conditions characterized by accumulation of nonmineralized bony matrix (osteoid) within the
skeleton in children, while osteomalacia is an accumulation
of nonmineralized bony matrix in the mature skeleton of
adults (the bone quantity is normal, but the bone quality is
abnormal).
Understanding bone physiology and metabolism is
crucial for understanding the pathology of rickets and
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Chapter 3 · Endocrinology andMetabolism
osteomalacia. Bones are made up of bony cells surrounded
by extracellular matrix. e extracellular matrix has
organic and inorganic components. e organic compo-
nent, also called “osteoid,” is made of type I collagen bers
embedded in a ground substance composed of proteogly-
3
cans and other components. e osteoid is secreted by the
osteoblasts, and it accounts for 35 % of the bone mass. In
5 Congenital rickets due hypophosphatemia (low
phosphates). It can be X-linked, autosomal dominant, or
autosomal recessive.
5 Acquired rickets due to hypocalcemia.
5 Acquired rickets due to renal failure. Reasons for
developing rickets or osteomalacia are loss of the
hydroxylation step of vitamin D and raised PTH levels.
contrast, the inorganic component is composed of osteoid
plus calcium and pyrophosphate (mineral salts). e inorganic materials are what give bone its density and account
for 65 % of the bone mass. Rickets and osteomalacia are
diseases of matrix mineralization, while osteoporosis is a
Patients with rickets o en present with bowing of the
legs, swollen joints, bone pain, and muscle weakness. Patients
with rickets due to vitamin D resistance may present with
alopecia.
disease of bony matrix.
A er osteoid mineralization, the mineralized collagens
are arranged in either woven or lamellar pattern. Woven bone
D i erential Diagnoses andRelated Diseases
is immature bone with its bers not arranged in any direction. Normally it presents in life as a transitional stage and
then is replaced by lamellar bone. Woven bone is not found in
mature skeleton normally; however, it is produced during
healing of fractures or remodeling (callus formation). Its
presence indicates abnormality when found in mature skeleton. Lamellar bone , on the other hand, is mature bone with its
bers arranged in a certain pattern to withstand mechanical
pressure. e mature skeleton is made only of lamellar bone,
and the bers are arranged in vertical form in the cortical
Dent’s disease is a rare disease characterized by X-linked
recessive hypophosphatemic rickets, idiopathic low molecular weight proteinuria, and X-linked recessive nephrolithiasis. Patients with this disorder commonly present with
hypercalciuria, nephrocalcinosis, and renal failure at
advanced stage of the disease. Radiological investigations in
these patients include plain radiographs of the bone to show
signs of rickets and renal ultrasound to detect urinary stones
and medullary calcinosis.
bone and arranged in transverse form in the trabecular bone.
Some sheets of lamellar bone are circumferentially arranged
around a bundle of blood vessels and lymphatics, forming
what are known as “Haversian canals or osteons.” ese
Haversian canals are found in the cortical bone and arranged
along the long axis of the bone, and they communicate with
each other through channels of interstitial lamellae.
e physis is the cartilaginous growth plate in immature
skeleton which is responsible for adding length to bone. e
growth plate functions as a one-way barrier to blood vessels,
allowing the blood from epiphyseal capillaries to supply the
metaphysis but not vice versa.
Hormones that a ect bone metabolism and hemostasis
include the parathyroid hormone (PTH) and the active form
of vitamin D, 1,25-dihydroxyvitamin D (1,25(HO)
D). PTH
2
is secreted in response to low plasma calcium concentration.
PTH promotes bone formation on the physiological level, but
it causes bone resorption at high concentrations. Vitamin D
undergoes two hydroxylation steps in the liver and the kidney before it becomes metabolically active, promoting calcium absorption from the intestines. Calcitonin is a hormone
that opposes the action of both PTH and vitamin D.
From the latter explanation of the bone metabolism, any
condition that can result in hormonal imbalance or matrix
mineralization defects can result in the development of rickets or osteomalacia. Causes of rickets include:
5 Acquired rickets due to vitamin D de ciency (most
common form).
5 Congenital rickets due to vitamin D enzyme
hydroxylation de ciency.
5 Congenital rickets due to vitamin D resistance and
Signs of Rickets on Plain Radiograph
5 Flaring of the epiphysis.
5 Bending of the diaphysis of long bones, commonly
the tibia (. Fig. 3.5.1 ).
5 Cupping deformity of the metaphysis due to
herniation of the hypertrophied physis into the
metaphysis (. Fig. 3.5.2 ). The metaphyses may
also show fine bony speculation (. Fig. 3.5.3 ).
5 Looser’s zone fracture ( pseudofractures ) is a very
distinctive feature of osteomalacia, which is
characterized by a fracture through a large osteoid
area within the bone. This type of fracture is rare
and tends to occur in the scapula or the pelvis.
5 Rachitic rosary is swelling of the costochondral
junction of the middle ribs.
5 Osteomalacia presents with signs of osteopenia on
radiographs. It cannot be differentiated from
osteoporosis with radiographs alone. History of
chronic renal failure is a helpful clue.
5 Rickets due to hypophosphatemia are usually
associated with craniosynostosis (e.g., scaphocephaly).
5 Skull radiographs in patients with rickets show soft
skull bones (craniotabes), flattening of the skull,
hot-cross-bun skull (caput quadratum), and
delayed closure of the fontanels.
5 Hypocalcemic rickets characteristically show
hypoplasia of the dental enamel, whereas
abscesses of the teeth occur more often in rickets
due to hypophosphatemia.
receptors mutation.
3.5 · Rickets andOsteomalacia
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3
. Fig. 3.5.1 Anteroposterior plain radiograph of the right
knee in a child with rickets shows mild bowing of the proximal
tibial metaphysis ( arrowheads )
. Fig. 3.5.2 Anteroposterior plain radiograph of the left knee
in a child with rickets shows focal cupping of the distal femoral
metaphysis ( arrowhead )
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Chapter 3 · Endocrinology andMetabolism
DeJong AR etal. Pseudotumor cerebri and nutritional rick-
ets. Eur J Pediatr. 1985;143:219–20.
Mays S etal. Skeletal manifestations of rickets in infants and
young children in a historic population from England. Am
J Phys Anthropol. 2006;129:362–74.
3
McBride A et al. Vitamin D-resistance rickets (X-linked
hypophosphatemic rickets). Curr Orthop. 2007;21:
369–99.
Ramavat LG.Vitamin D, de ciency rickets at birth in Kuwait.
Indian J Pediatr. 1999;66:37–43.
Tosetto E etal. Dent’s disease and prevalence of renal stones
in dialysis patients in Northeastern Italy. J Hum Genet.
2006;51:25–30.
3.6 S c u r v y
Scurvy is disease that arises due to vitamin C de ciency. Most
cases of scurvy arise due to severe malnutrition, alcoholism,
and drug abuse.
Vitamin C (ascorbic acid) functions as a cofactor, enzyme
complement, co-substrate, or a strong antioxidant in a variety
of metabolic activities. It provides electrons needed to reduce
molecular oxygen. It also works as a cofactor for collagen
synthesis and norepinephrine synthesis. Vitamin C is present
. Fig. 3.5.3 A plain wrist radiograph of a patient with rickets
shows metaphyseal bony speculations ( arrowhead )
in marine sh, vegetables, and citrus fruits (in high concentrations).
Vitamin C absorption occurs in the small intestine and is
excreted by the kidneys. e maximum concentration of
vitamin C is found in the pituitary gland, leukocytes, the
Further Reading
Brickley M et al. Evaluation and rickets interpretation of
residual rickets deformities in adults. Int J Osteoarchiol.
2008. doi:10.1002/oa.1007.
Cheong HI etal. Phenotype and genotype of Dent’s disease in
three Korean boys. Pediatr Nephrol. 2005;20:455–9.
Currarino G.Sagittal synostosis in X-linked hypophospha-
temic rickets and related diseases. Pediatr Radiol.
2007;37:805–12.
brain, adrenals, and the eye.
Patients with scurvy usually present with irritability, limb
pain, and tenderness with pseudoparalysis. Unusual manifestations of scurvy include subdural and subarachnoid hemorrhage, hematuria, melena, pleural hemorrhage, and
retro-orbital hemorrhage causing proptosis. Patients improve
within 2 days to 1 week from starting vitamin C therapy.
Scurvy is o en found in children, and radiographic abnormalities are rare before 6 months of age.
3.6 · Scurvy
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Signs on Plain Radiograph
5 Subperiosteal hemorrhage is seen as elevated
periosteum from the bone (. Fig. 3.6.1 ).
5 Wimberger’s sign : sclerotic rim surrounding the
epiphysis in children.
5 White line of Frankel : dense sclerotic metaphyseal
line over the metaphysis (. Fig. 3.6.2 ).
5 Pelkin’s fracture : metaphyseal avulsion fracture.
5 Scurvy is a frequent cause of osteoporosis in
children (. Fig. 3.6.2 ), and it can predispose to
slipped distal femoral epiphysis due to
epiphysiolysis.
. Fig. 3.6.1 Anteroposterior left femoral radiograph shows
periosteal hemorrhage in a baby with scurvy seen as
radiolucent shadow that surrounds the distal femur shaft
( arrowheads )
. Fig. 3.6.2 Anteroposterior plain knee radiograph in
another child with scurvy shows dense sclerotic metaphyseal
line ( white line of Frankel ). Notice the di use osteoporosis
a ecting the entire knee joint
Further Reading
Akikusa JD etal. Scurvy: forgotten but not gone. J Paediatr
Child Health. 2003;39:75–7.
Brickley M etal. Skeletal manifestations of infantile scurvy.
Am J Phys Anthropol. 2006;129:163–72.
Firth N etal. Oral lesions in scurvy. Aust Dent J. 2001;46:
298–300.
Ratageri VH et al. Scurvy in infantile tremor syndrome.
Indian J Pediatr. 2005;72:883–4.
Suvarna J et al. Hemorrhagic pleural e usion: can it be
scurvy? Indian J Pediatr. 2007;74:1050–1.
Verma S etal. Unilateral proptosis and extradural hematoma
in a child with scurvy. Pediatr Radiol. 2007;37:937–9.
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Chapter 3 · Endocrinology andMetabolism
3.7 Fluorosis
Fluorosis is a clinical condition characterized by excessive
ingestion of uoride, which causes toxicity and systemic
manifestations that can be disabling.
3
Fluoride is an element that is found in water, soil, and air.
It results from the combination of the “ uorine” gas with different natural elements. Fluoride can be found in food, seawater, and tea. Each cup of tea may supply 0.3–0.5mg of
uoride. e safe daily intake of uoride for an adult is
<4mg/day. Skeletal uorosis results from ingesting uoride
>10mg/day for at least 10 years.
Fluorosis classically results from ingestion of water or
food with high uoride content in endemic areas. Fluorosis
toxicity may also develop from chronic intake of sodium
uoride as a long-standing therapy for osteoporosis, using
Te on-coated pots, chewing tobacco, and the overuse of
ni umic acid (nonsteroidal anti-in ammatory drug).
. Fig. 3.7.1 An illustration demonstrates the clinical appearance of
dental uorosis
Fluoride absorption in the body can be reduced by taking
calcium or magnesium salts. In contrast, phosphate, sulfates,
and molybdenum increase gastrointestinal absorption of
uoride and lead to uoride toxicity.
Up to 99 % of the absorbed uoride combines with the
mineralized bones, mostly in the teeth, pelvis, and vertebrae.
Dental uorosis deposits mainly in the enamels and causes
brown or black dental pigmentation (. Fig. 3.7.1 ). Pitting,
chipping, and mottling of the teeth may also occur.
Patients with uorosis o en complain from pain in the
joints and back, which is o en mistaken with rheumatic disorders like rheumatoid arthritis and ankylosing spondylitis.
Back sti ness, limb paresthesia, and restricted spine movement are early signs of uorosis. In severe form of back uorosis, the vertebral column becomes one continuous column
of bones due to calci cation of the paravertebral ligaments, a
condition known as poker back ( . Figs. 3.7.2 and 3.7.5 ).
Development of genu varum, genu valgum, and kyphosis
may occur. Involvement of the ribs by uorosis results in a
barrel- shaped chest with restricted respiratory breathing.
Abdominal breathing becomes the main breathing mechanism in severe cases.
Neurological manifestations of uorosis usually are
related to the spinal cord compression due to vertebral canal
stenosis. Patients experience radiculopathy and di culty in
walking due to muscle weakness. Cranial nerve compression
may occur when uorosis a ects the skull base foramina.
Some patients develop hyperparathyroidism for unknown
reasons. It is thought that the resistance of the osteoclastic
activity by the sclerotic bones causes parathyroid hormone
overactivity.
Diagnosis is con rmed by detecting high level of uoride
in the urine (main path of uoride excretion), serum, and
bone. A 24 h sampling of urine is the most reliable method
for con rming uorosis. e serum alkaline phosphatase
level is usually high.
. Fig. 3.7.2 An illustration demonstrates a patient with poker back
due to uorosis
3.7 · Fluorosis
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3
Signs on Radiographs
5 The axial skeleton is mainly affected in the form of
sclerosis of the trabecular bone and thinning of
the cortical bone, mostly affecting the vertebrae
and the iliac wings (. Fig. 3.7.3 ). Although the
pelvis shows sclerosis, the long bones may show
osteopenia. A theory to explain this finding states
that bones which accumulate fluoride are resistant
to the osteoclastic activity of bone remodeling.
The hyperparathyroidism resulting from fluorosis
causes high resorption of the long bones which do
not contain fluorosis, but not of the sclerotic axial
bones. This may explain the mixed sclerotic–
osteoporotic radiological picture seen in fluorosis.
5 Subperiosteal new bone formation causes the long
bones to become uneven (. Fig. 3.7.4 ).
5 Ligament calcification is a very characteristic sign
of fluorosis, affecting commonly the sacrotuberous
and the petroclinoid ligaments. Paravertebral
ligament calcification causes vertebral column
restriction (. Fig. 3.7.5 ).
5 Prominence of the occipital protuberance with
formation of exostosis occasionally is another
minor manifestation.
. Fig. 3.7.4 Lateral knee radiograph of the same patient
shows di use sclerosis with sclerosis and osteophytes
formation of the quadriceps and patellar tendons insertion at
the superior and the inferior poles of the patella ( arrowheads ).
Sclerosis of the popliteal vessels can be observed too ( arrows )
. Fig. 3.7.3 Anteroposterior pelvis radiograph shows severe
systemic uorosis with di use skeletal sclerosis. Calci cation
can be seen a ecting even the femoral vessels ( arrowheads )
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