Hip dysplesia radiology

1. Dysplastic Hip - Radiology
Dr. Bhanupriya Singh
JR-1.

11. X-Ray views:-
AP radiograph of the pelvis or hip is taken with the patient supine, and both feet in
approximately 15° of internal rotation.
This reduces the normal 25 to 30° femoral anteversion, allowing better visualization of the
femoral neck

12. X-Ray views:-
Judet views (anterior and posterior oblique view of pelvis) are performed with the
patient in a 45° oblique position. When the affected hip is in a posterior oblique position, the
posterior column and anterior acetabular rim are well seen. Conversely, with the affected hip
in the anterior oblique position, the anterior column and posterior acetabular rim are well
seen.
Forty-five-
degree posterior
oblique view of
the left
acetabulum
reveals a non-
displaced
fracture through
the posterior
column.

13. X-Ray views:-
The frogleg lateral view is performed with the patient supine, feet together, and thighs
maximally abducted and externally rotated.The radiographic tube is angled 10 to 15° cephalad,
directed just above the pubic symphysis. The anterior and posterior aspects of the femoral
neck, as well as the lateral aspect of the femoral head, are seen with this projection.

14. X-Ray views:-
Pelvic outlet (Ferguson) view, is performed in the same position as the AP view,
with the radiographic tube angled 30 to 35° cephalad, and the central beam
directed at the center of the pelvis. This projection allows excellent visualization of
the sacroiliac joints, the pubic rami, and the posterior acetabular rim

15. X-Ray views:-
Pelvic inlet view is performed in the same position as the AP view, with 30 to 35° of caudal
angulation of the radiographic tube. This view allows visualization of the sacral promontory,
the iliopectineal line (anterior column), the ischial spine, and the pubic symphysis

16. X-Ray views:-
Groin-lateral view of the hip is performed with the patient supine, the nonaffected leg
elevated and abducted, and the affected leg extended. The radiographic tube is directed
horizontally toward the medial aspect of the affected hip, with 20° of cephalad angulation
Long-leg lateral view of the
left hip shows prominent
femoral
head–neck junction,
narrowing of the
anterosuperior joint
space, and sclerosis of the
anterosuperior acetabulum.
Heterotopic
bone formation is seen from
previous hip arthroscopy for
anterior
labral debridement in a
patient with
femoroacetabular
impingement.

44. Ligaments ( increase stability)
The only intracapsular ligament is the ligament of head of femur. It is a
relatively small ligament that runs from the acetabular fossa to the fovea of the
femur. It encloses a branch of the oburator artery, which comprises a small
proportion of the hip joint blood.
Extracapsular There are three extracapsular ligaments. They are continuous
with the outer surface of the hip joint capsule.
Iliofemoral: Located anteriorly. It originates from the ilium, immediately
inferior to the anterior inferior iliac spine. attaches to the intertrochanteric line
in two places, giving the ligament a Y shaped appearance. It prevents
hyperextension of the hip joint.
Pubofemoral: Located anteriorly and inferiorly. It attaches at the pelvis to the
iliopubic eminance and obturator membrane, and then blends with the
articular capsule. It prevents excessive abduction and extension.
Ischiofemoral: Located posteriorly. It originates from the ischium of the pelvis
and attaches to the greater trochanter of the femur. It prevents excessive
extension of the femur at the hip joint.

52. Neurovascular Structures
Vascular supply to the hip joint is achieved via the medial and
lateral circumflex femoral arteries, and the artery to head of
femur.
The circumflex arteries are branches of the profunda femoris
artery.
They anastamose at the base of the femoral neck to form a ring,
from which smaller arteries arise to the supply the joint itself.
The medial circumflex femoral artery is responsible for the
majority of the arterial supply (the lateral circumflex femoral artery
has to penetrate through the thick iliofemoral ligament to reach
the hip joint).
Damage to the medial circumflex femoral artery can result in
avascular necrosis of the femoral head.
The hip joint is innervated by the femoral nerve, obturator nerve,
superior gluteal nerve, and nerve to quadratus femoris.

53. Hip Dysplasia
• Is a condition where Femoral Head(ball) and Acetabulum(socket) are
misaligned.
The condition is common in children, but is also found in adolescents and adults
with no history.
• It becomes difficult for femoral head to remain properly positioned within
the acetabulum if hip is poorly angled or rotated femoral head/neck or
shallow acetabulum.
• A severe or prolonged misalignment of Hip’s ball and socket results in
increased friction which causes joint’s cartilage to wear out quickly- leading
to cartilage(labral) tears and eventually Osteoarthritis.
• A dysplastic hip socket usually causes discomfort and pain beginning in
adolescence and gradually becomes worse with time.
A shallow acetabulum may develop during infancy but may not be evident until
after puberty- and may not cause pain until teen years or later.
SYMPTOMS:-May range from mild-severe, uni/bi lateral. Discomfort or stiffness
in hip may occur when attempts are made to move the leg away from
body(abduction) or form a bend 90 degree to a straight extended position.

54. Later Pt may develop limp. Leg lengths may appear unqual with difficulty in
rotation of thigh.
X RAYS:- Assess alignment of Femoral Head and Acetabulum.
MRI:- Assess Hip’s soft tissue and labrum(cartilage).

55. Dysplasias and Congenital Anomalies
Sclerosing Bone Dysplasias
• The various types of sclerosing bone dysplasias occur either from excess bone
production due to abnormal osteoblastic activity or from failure of bone
resorption and remodeling due to defective osteoclastic activity.
• The excess bone accumulation affects endochondral bone formation in
osteopetrosis,pyknodysostosis, or osteopathia striata. Intramembranous
bone formation is primarily affected in progressive diaphyseal dysplasia and a few
rare endosteal hyperostosis.
• Both endochondral and intramembranous bone formation are affected in
melorheostosis and metaphyseal dysplasia.
• There are three types of osteopetrosis,
• infantile-malignant type, which is autosomal recessive, and the most severe
form
• intermediate type, also autosomal recessive presenting typically in the first
decade of life,
• an autosomal dominant- type with full life-expectancy.

56. Osteopetrosis
• Albers-Schonberg disease
• Presentation in the majority of cases is with fracture because
of the weakened bones. They are often transverse fractures
with multiple areas of callus formation and normal healing.
• there is crowding of the marrow, so bone marrow function is
affected resulting in myelophthisic anaemia
and extramedullary haematopoiesis with splenomegaly. This
may terminate in acute leukaemia.
• defective osteoclasts and overgrowth of bone.
• bones become thick and sclerotic, but their increased size
does not improve their strength.

57. • In the infantile type, pancytopenia, cranial nerve dysfunction, and mental
retardation occur. Radiographs of the hip may demonstrate curvilinear bands of
sclerosis in the ilium, with a “bone-inbone” appearance. The vertebrae may show
similar bands of sclerosis along the vertebral endplates, with a “sandwich
vertebrae” appearance. In the long bones, undertubulation, broadened
metaphyses, and pathologic fractures are seen
All visualized bones are sclerotic.
Previous fractures of the
right femoral shaft and left
femoral neck with residual
deformity.
Osteopetrosis.

58. Pyknodysostosis
• osteopetrosis acro-osteolytica or Toulouse-
Lautrec syndrome
• rare autosomal recessive - osteosclerosis and
short stature.
• Delayed closure of fontanelles, short stature,
undertubulation of long bones, and diffuse
sclerosis are seen.
• Bones are brittle and prone to fracture.
• Genetic research has demonstrated a mutation
causing inactivation
of the gene encoding cathepsin K, which is
involved in osteoclastic function.
• Patients present in early childhood with:
-short stature, particularly limbs
-delayed closure of cranial sutures
-frontal and occipital bossing
-short broad hands and hypoplasia of nails
-multiple long bone fractures following minimal
trauma
named after the famous French artist
who was thought to be afflicted with it

59. Pyknodysostosis is with radiographic characteristics of both osteopetrosis and cleidocranial
dysplasia. The diffusely sclerotic bones, undertubulation,and fractures resemble
osteopetrosis. Pyknodysostosis.
Hands: short, stubby fingers
partial agenesis/aplasia of terminal
phalanges, simulating acro-osteolysis
delayed bone age
Cranial and maxillofacial
marked delay in sutural closure
frontoparietal bossing
calvarial thickening
Wormian bones (lambdoidal region)
relative proptosis
nasal beaking
obtuse mandibular gonial angle often
with relative prognathism
persistence of primary teeth
Others:sclerosis of vertebral bodies
increased lumbar lordosis
vertebral segmentation
anomalies particularly upper cervical
and lower lumbar, hypoplastic
clavicles, erosion of distal clavicles

60. Melorheostosis
• In Melorheostosis (also known as Leri disease)both
endochondral and intramembranous bone formation
are abnormal. It is characterized by hyperostosis,
typically of one side of the cortex, with a lobulated,
wavy appearance resembling dripping candle wax
• Although changes occur in early childhood age at
presentation is often later, and the condition often
remains occult until late adolescence or early
adulthood. In only approximately half of cases is the
diagnosis made before the age of 20
• Whenit does manifest clinically, the most common
presentation is of joint contracture or pain. This is
more common in adults
• can be either monostotic or polyostotic and tends to
be monomelic
• predilection for long bones of the limbs, although it
can be seen almost anywhere
• Five patterns have been described :- classic
-osteoma - like
-myositis ossificans - like
-osteopathia striata - like
-mixed

61. Osteopoikilosis
• sclerosing bony dysplasia with multiple enostoses. Autosomal Dominant.
• bone islands of osteopoikilosis develop during childhood and do not regress and
therefore are seen in all age groups. There is no gender predilection
• asymptomatic and does not degenerate into malignancy. Bone strength is normal.
• often found concurrently with osteopathia striata, andmelorheostosis, and it is
thought by some that they represent a spectrum of the same condition. Indeed
recent genetic evidence suggests that these conditions are related by a loss of
function mutation of the LEMD3 gene
Plain film and CT
The bone islands of osteopoikilosis are typically clustered around joints and align
themselves parallel to surrounding trabeculae (thus predominantly longitudinally in the
metaphyses) . Most lesions are found in the appendicular skeleton and pelvis. The axial
skeleton is largely spared. It is rare for the skull vault to be involved .
The lesions vary in size, usually a 5-10 mm, but ranging from only 1-2 mm up to 1-2
cm.
MRI
Appearances on MRI are the same as individual bone islands. Each lesion is small and
dark on both T1 and T2 weighted images, as it is composed of mature dense bone

62. Ossifications and fibrosis in periarticular soft tissues are also common. The abnormalities
may follow a dermatomal distribution. Treatment includes soft-tissue releases
and excisions, and if necessary, osteotomies. It commonly recurs. In osteopoikilosis and
osteopathia striata, there are localized foci of cortical bone in which resorption and
remodeling fail,while in the remainder of bone, the process of endochondral ossification
proceeds normally. The result is numerous foci of sclerotic bone (enostoses or “bone-
islands”) throughout the skeleton in osteopoikilosis ,or linear striations of sclerotic bone in
osteopathia striata. Differentiation from sclerotic metastases may at times be difficult by
plain radiographs. Although radionuclide bone scan has been thought to be critical to
differentiate osteopoikilosis from osteoblastic metastases, there are reports of increased
radiopharmaceutical uptake in osteopoikilosis, particularly in young patients.
Punctate sclerotic lesions (bone
islands) scattered diffusely
bilaterally.
Osteopoikilosis.

63. “Osteopoikilosis, osteopathia striata, and/or melorheostosis can coexist in the same
patient and probably represent a range of manifestations of the same disease process”
(A) Dense sclerotic, wavy cortical thickening in the femoral shaft and superolateral
acetabulum are noted.
(B) Wavy cortical thickening in the distal femoral shaft is seen indicative of
melorheostosis. Linear striations in the medullary bone are areas of osteopathia striata.

64. Osteogenesis Imperfecta
Osteogenesis imperfecta (OI) is a hereditary disorder characterized by abnormal type I
collagen, resulting in weakened, fragile bones, ligament laxity, abnormal dentition,
blue sclerae, and hearing impairment. Most subtypes of OI are inherited as autosomal-
dominant mutations in the COL1A1 and COL1A2 genes that encode for the pro alpha 1
and pro alpha 2 chains in type I collagen. Types I-IV, described
by Sillence and coworkers, are as follows:
type I,autosomal-dominant and relatively mild, with relatively normal stature, blue
sclerae, and hearing impairment;
type II, with subtypes described as autosomal-dominant or autosomal-recessive, the
most severe form, lethal in the fetal or newborn period, with severe deformity and
intrauterine growth retardation;
type III, also with both autosomal-dominant and autosomal-recessive cases described,
severe and progressive but with longer survival than type II;
type IV, rare, autosomal dominant and mild with normal sclera and normal hearing.
More recently, additional types V-VII have been described, which are not associated
with defects in the genes encoding type I collagen.
Treatment with biphosphonates improves bone mass in all types, but long-term
outcomes from biphosphonate therapy are not known.

65. Severe deformity and osteopenia, with multiple fractures in different stages of healing.
The pelvis is deformed and narrow.
Osteogenesis imperfecta.

66. Developmental Dysplasia of the Hip
The etiology of (DDH)involves both genetic and
environmental factors.
Risk factors include oligohydramnios, breech
delivery, positive family history,. Diagnosis can
be made at birth in the vast majority of cases.
If diagnosed at birth, the likelihood of
successful nonoperative treatment such as a
Pavlik harness, and the overall prognosis, is
much better than with delayed diagnosis.
Ultrasound is more sensitive than radiography
for diagnosis. Radiographically, dislocation or
subluxation of the hip can be demonstrated by
discontinuity of the Shenton arc, a curvilinear
line connecting the medial femoral neck
with the undersurface of the superior pubic.
With hip dislocation, the femoral head moves
into the upper outer quadrant. If the
dislocated hip is in contact with the ilium, a
pseudoacetabulum will form. Essentially all
patients with hip subluxation or dislocation will
develop osteoarthritis, usually in the 3rd or 4th
decade of life.
Superior dislocation of the left hip, with
pseudoacetabulum
formation. Mild subluxation also of the
right hip.

67. Radiographic features
Once there is significant ossification then x-ray examination is required.
For some reason the left hip is said to be more frequently affected . One third of cases are
affected bilaterally .
Ultrasound
Ultrasound is the test of choice in the infant (<6 months) as the proximal femoral
epiphysis has not yet significantly ossified. Additionally it has the advantage of being a
real time dynamic examination allowing the stability of the hip to be assessed with stress
views.
A number of values are used to 'objectively' assess morphology.
Alpha angle (Depth of bony acetabular roof)
Angle formed by the acetabular roof to the vertical cortex of the ilium. This is a similar
measurement as that of the acetabular angle.The normal value is greater than or equal to
60 degrees.
Beta angle (Cartilagenous Coverage)
Angle formed between the vertical cortex of the ilium and the triangular labral
fibrocartilage (echogenic triangle). The normal value is less than 77 degrees, but is only
useful in assessing immature hips when combined with the alpha angle

69. Bony coverage
The percentage of the femoral epiphysis covered by the acetabular roof. A value of greater
than 58% is considered normal.
Plain film
The key to plain film assessment is looking for symmetry and defining the relationship of the
proximal femur to the developing pelvis. The ossification of the superior femoral epiphyses
should be symmetric. Delay of ossification is a sign of DDH.
Hilgenreiner line is drawn horizontally through the superior aspect of both triradiate
cartilages. It should be horizontal, but is mainly used as a reference for Perkin line and
measurement of the acetabular angle.
Perkin line is drawn perpendicular to Hilgenreiner line, intersecting the lateral most aspect of
the acetabular roof. The upper femoral epiphysis should be seen in the inferomedial quadrant
(i.e below Hilgenreiner line, and medial to Perkin line)
The acetabular angle is formed by the intersection between a line drawn tangential to the
acetabular roof and Hilgenreiner line, forming an acute angle. It should be approximately 30
degrees at birth and progressively reduce with maturation of the joint.
Shenton line is drawn along the inferior border of the superior pubic ramus and should
continue laterally along the inferomedial aspect of the proximal femur as a smooth line. If
there is superolateral migration of the proximal femur due to DDH then this line will be
discontinuous.

73. Acetabular Dysplasia in Adults
Dysplasia of the acetabulum may occur without hip dislocation, and mild dysplasia may
go undiagnosed until adulthood. Acetabular dysplasia occurs in females more often than
males and has been demonstrated to lead to development of hip joint osteoarthritis.
Evaluation for acetabular dysplasia can be performed using the center-edge angle of
Wiberg, performed by measuring the angle between a line drawn vertically from the
center of the femoral head and a line from the center of the femoral head through the
edge of the acetabulum.Angle measures less than 20° are dysplastic; 20 to 25° are
classified as borderline dysplasia, and greater than 25° are normal.
Bilateral acetabuli are dysplastic, with
only partial covering
of the femoral head. On the left, early
osteoarthritis has begun to
develop.

74. Bilateral acetabuli are dysplastic, with only partial covering
of the femoral head. On the left, early osteoarthritis has begun to
develop.

75. Femoroacetabular Impingement
The theory behind femoro acetabular impingement is that certain anatomic variations
lead to impingement between the proximal femur and acetabular rim with flexion and
internal rotation. This leads to shearing and impaction of the anterior articular cartilage
of the femoral head, as well as anterior labral tears. There are two types of
femoroacetabular impingement.
• The first is the “cam” type, femoral waist defeciency; thought to be caused by an
enlarged femoral head or an abnormal contour of the femoral head/neck junction,
which causes impingement anteriorly against a normal acetabulum.
• The second, or “pincer” type, is thought to be due to “over-coverage” of the femoral
head anteriorly from either coxa profunda or a retroverted acetabulum. Radiographs
may demonstrate reduced offset of the femoral head–neck junction, acetabular
abnormalities such as retroversion, coxa valga, coxa profunda, or protrusio acetabuli,
and the eventual development of osteoarthritis. MR imaging is more sensitive to the
early findings of labral tear and cartilage injury.

76. Long-leg lateral view of the left hip shows prominent femoral head–neck junction,
narrowing of the anterosuperior joint space, and sclerosis of the anterosuperior
acetabulum. Heterotopic bone formation is seen from previous hip arthroscopy for
anterior labral debridement in a patient with femoroacetabular impingement.

77. Cam Impingement: Pistol Grip
Deformity
Mechanism: Femoral cause
• Jamming of an abnormal femoral
head into the acetabulum
during forceful motion, especially
flexion and internal rotation
„Classic“ Imaging finding
• abnormal femoral head with a
laterally increasing radius
• femoral waist deficiency
„Classic“ Patient
• young and athletic male

81. Cartilage Lesions: Localization
Acetabulum >> Femur
• Antero - superior
• Labral tears often
associated
• Junction of labrum and
cartilage

83. Pincer Impingement:deep acetabulum
Mechanism: Acetabular cause
• Contact between acetabular rim and femoral head-neck junction
„Classic“ Imaging finding
• General ‘overcoverage’ (coxa profunda / protrusio)
• Local anterior ‘overvoverage’ (acetabular retroversion)
„Classic“ Patient
• Middle-aged women

87. Achondroplasia
congenital disorder of endochondral bone
formation affecting fetuses in utero,
transmitted as an autosomal-dominant
trait.The genetic defect involves an allele
encoding fibroblast growth factor receptor
3, on chromosome 4p, which is the same
allele implicated in both hypochondroplasia
and thanatophoric dwarfism.
Patients have short stature, with limb
shortening affecting more severely the
proximal extremities. Short pedicles can
predispose to spinal stenosis. Narrowing of
the interpedicular width in the lower
lumbar spine is seen, along with
horizontally oriented acetabular roofs,
small sciatic notches, and rounded, “ping-
pong-paddle”-shaped iliac bones;short
femur with widened femoral metaphysis.
Cervicomedullary compression has been
shown to be associated with sudden death
in infants with achondroplasia.

88. • horizontal acetabular roof
(decreased acetabular angle)
• small squared (tombstone) iliac wings
• small trident pelvis
• champagne glass type pelvic inlet
• short sacroiliac notches
• metaphyseal flaring : can give a trumpet
bone type appearance
• femora and humeri are particularly
shortened (rhizomelic shortening)
• long fibula
• they may also appear thickened but in
fact normal in absolute terms compared
to the normal adult diameter (thickening
is perceived due to reduced length)
• V shaped growth plates
• trident hand

89. Multiple Epiphyseal Dysplasia
dysplasia epiphysealis multiplex the abnormal growth of the femoral head epiphysis
typically leads to a varus alignment of the femoral neck. This occurs due to overgrowth of
the trochanteric ossification center and infundibulum, a cartilaginous connection between
the femoral head and trochanteric ossification centers in the infant. Secondary
osteoarthritis eventually develops. non-rhizomelic dwarfism characterized by flattening and
fragmentation of epiphyses. inherited as autosomal dominant.
Broad, dysplastic femoral
heads, with varus angulation
of the femoral necks
bilaterally. Multiple
epiphyseal dysplasia.

90. Proximal Focal Femoral Deficiency
• Proximal focal femoral deficiency (PFFD) represents a congenital disorder characterized by
varying severity of shortening and dysplasia of the proximal femur and acetabulum, and
varus angulation of the proximal femur- with shortening of the entire lower limb.
• A common classification system divides the disorder into types, A-D, in increasing order
of severity.
In type A, the femur is shortened compared with the normal size, but the femoral head is
present and located within the acetabulum.
In type B, the femur is short with a varus angulation, and there is a gap between the femoral
head, which is located within the acetabulum,and the femoral neck.
In type C, the femoral head is rudimentary or absent. The femur is markedly short, and
theacetabulum is dysplastic.
In type D, the entire femur is rudimentary,with absent femoral head and acetabulum.
• Various treatments have been used for patients with this disorder. In one recent report,
patients reported similar mobility and improved satisfaction with nonoperative treatment
using extension prosthesis, compared with surgical ankle disarticulation with fitting of an
above-knee prosthesis.

92. Proximal Focal Femoral Deficiency
MRI
The role of MR imaging in patients with this condition is to help define the cartilaginous
proximal femur and the presence or absence of a cartilaginous connection to the femoral
head. Therapeutic decisions are based on the detection of a femoral head and the
presence of a connection. Also, the severity of coxa vara, if present, will influence
treatment selection. The ability of imaging to clearly depict cartilage is of particular value
in this setting. Routine coronal and axial MR images may be adequate, however, oblique
images may be useful in some patients.
T 1 T 2

93. Mucopolysaccharidoses
This represents a heterogeneous group of disorders characterized by accumulation of
various mucopolysaccharides as a result of congenital lack of certain enzymes. Many if not
all of these exhibit similar radiographic findings in the pelvis, including flared and
dysplastic femoral heads, narrowed and distorted pelves, and flared iliac wings
The iliac wings are broad,
the pelvis narrow, and the
femoral heads dysplastic
in this patient with
Hurler’s syndrome.

94. Fibrodysplasia Ossificans Progressiva
(FOP) represents a rare congenital
disorder characterized by progressive
heterotopic
ossification of tendons, ligaments,
muscles, and other soft tissues with
deformity of the great toe. No known
treatment or preventive measure
exists. The typical course of the
disease is progressive restriction of
movement, frequent
falls, and eventual respiratory
difficulty from involvement of the
chest wall. Most patients die of
pulmonary complications in their 40s
or 50s. Recent advances include
mapping of the gene for FOP to
chromosome 4q, and identification
of a key protein found in lesion cells
and lymphocytes.These findings may
prove beneficial in treating this
condition in the future. Marked heterotopic ossification bridging the hip joint
medially and laterally

95. Characteristic features include:
hallux valgus
monophalangic first toe
shortened metacarpals
pseudoexostoses (ossification of ligamentous insertions)
microdactyly of the first metacarpal / metatarsal
neck muscles oedema