Osteochondrosis

Question 1

General features of osteochondrosis

Answer 1

common during middle years of growth, boys>females, lower limbs more frequently involved, about 15% are bilateral

Question 2

Early phase of necrosis (phase of avascularity)

Answer 2

osteocytes and bone marrow cells die, ossific nucleus of epiphysis ceases to grow, articular cartilage remains alive and grows, disuse atrophy (osteoporosis), asx

Question 3

Phases of osteochondrosis

Answer 3

early phase of necrosis (phase of avascularity), phase of revascularization with bone deposition and resorption, phase of bone healing, phase of residual deformity

Question 4

Phase of revascularization with bone deposition and resorption

Answer 4

stage represents a vascular reaction of the surrounding tissue to dead bone, ossification of the thickened pre-osseous cartilage resumes and new bone is laid down on dead trabeculae, combo of irregular areas of bone deposition and resorption provides radiographic appearance of fragmentation

Question 5

What is the most vulnerable stage of osteochondrosis?

Answer 5

phase of revascularization with bone deposition and resportion

Question 6

Phase of bone healing

Answer 6

bone resorption ceases, but bone deposition continues, newly formed bone still exhibits biological plasticity

Question 7

Phase of residual deformity

Answer 7

once bony healing of the epiphysis is complete, its contour relatively remains unchanged, if any residual deformity is present, it will remain, as well as the associated complications

Question 8

Legg-Calve-Perthes Disease general facts and etiology

Answer 8

ischemic necrosis of femoral capital ossification center, males (4-8), avascularity, self limited disease
etiology: occlusion of blood supply to femoral head-either from excessive fluid pressure of a synovial effusion or inflammatory/traumatic

Question 9

Signs and sx of Legg-C-P disease

Answer 9

pain in hip (synovial effusion), antalgic gait, limited ROM (abduction and internal rotation), disuse atrophy

Question 10

Four stages of LCPD

Answer 10

femoral head becomes more dense with possible fx of supporting bone, fragmentation and reabsorption of bone, reossification when new bone has regrown, healing when new bone reshapes

Question 11

First and second stages of development of LCPD

Answer 11

1: incipient or synovitis phase (soft tissue changes around hip-last 1-3 weeks)
2. Aseptic necrotic/avascular stage: entire head or anterior half of ossific nucleus is dead, lasts months to years, necrotic mass of dead marrow and dead bone in marrow spaces, no evidence of bone regeneration

Question 12

Third and fourth stages of development of LCPD

Answer 12

Regenerative/ fragmentation stage: radiologically the femoral head (compressed and fragmented) secodnary to ingrowing fibrous vascular tissue and immature bone
Residual stage: rarefied area gradually disappear-normal trabecular patterns, residual coxa magna

Question 13

Classification for LCPD

Answer 13

Catterall system
Group 1: anterior epiphysis
2: anterior epiphysis with a clear sequestrum
3: only a small part of epiphysis not involved
4: total head involvement

Question 14

Tx of LCPD

Answer 14

aimed at preventing deformity of femoral head and degenerative changes to hip, abduction cast or some time of abduction brace is most common treatment

Question 15

Osgood’s Schlatter’s disease general

Answer 15

osteochondrosis of tibial tuberosity, males 10-15, radiographs little use because tibial tuberosity commonly looks abnormal

Question 16

Sx and dx of Osgood’s Schlatter’s disease

Answer 16

dx primarily determined by pain and soft tissue edema, enlargement of tibial tuberosity with a max area of tenderness at insertion of patellar tendon, presumed etiology secondary to trauma, pain at the patellar tendon with extension

Question 17

Differential dx of Osgood’s Schlatter’s

Answer 17

tendonitis, osteogenic sarcoma, infecetion, tibial tubercle fx

Question 18

Radiographic findings of Osgood’s Schlatters acute and chronic phase

Answer 18

acute: soft tissue swelling anterior to tibial tuberosity
chronic: Type 1: tibial tuberosity prominent and irregular
Type 2: same as above with small free particle of bone located at anterior tuberosity
Type 3: nl tuberosity with bone particle

Question 19

Tx of Osgood’s Schlatter’s disease

Answer 19

withdrawal from sports that cause pain, Ice, NSAIDS, pad to protect tuberosity, infrapatellar strap, no steroid injections, cast immobilization for 6wks if sx severe

Question 20

Complications of Osgood’s Schlatter’s disease

Answer 20

proximal segment fails to unite remainder of tubercle (remains as a local source of pain)

Question 21

Kohler’s disease general

Answer 21

osteochondrosis of navicular, 4x more frequent in males, 3-7 yo, ossification (18-24 mo for females, 24-30 mo in males), may occur with LCPD

Question 22

Etiology of Kohler’s disease

Answer 22

mechanical-longitudinal strain during locomotion
compressive forces during locomotion-compromise vascular source
Weissman: talus projects further distal than nl

Question 23

Sx of Kohler’s disease

Answer 23

antalgic gait (weight bearing on lateral side), local pain and tenderness over navicular, posterior tibial tendon inflamed at its insertion site

Question 24

Radiographic findings of Kohler’s disease

Answer 24

flattening of navicular, irregular rarefactions and sclerosis, two patterns: 1: flattened navicular with patchy areas of increased bone density and loss of nl trabeculae (discoid navicular), 2: nl shape navicular with increased density
use contralateral x-ray

Question 25

Tx of Kohler’s disease

Answer 25

below knee walking cast (foot in 10-15 degrees varus and 20 degrees equinus) 6-8 wks, first 2 wks non weight bearing, decrease activity, rigid orthoses or thomas heel, follow through with soft longitudinal arch support

Question 26

Freiberg’s Infarction general

Answer 26

avascular necrosis of met head, between 13-18 (females), unilateral generally, structurally weak feet, 2nd met 68%, 3rd met 27%

Question 27

Differentials of Freiberg’s infarction

Answer 27

fx/stress fx, synovitis/capsulitis, extensor/flexor tendonitis, metatarsalgia, Morton’s neuroma, JRA

Question 28

Etiology of Freiberg’s infarction

Answer 28

Simillie: occurs 2ndary to a traumatic process (stress)
Braddock: Secondary to fx modified by its proximity to epiphyseal plate

Question 29

Presentation of Freiberg’s infarction

Answer 29

local pain, tenderness, swelling, limitation of MPJ motion

Question 30

Classification of Freiberg’s infarction

Answer 30

Stage 1: epiphyseal fissure fx

2: central portion of bone resorption and slightly depressed
3: met head begins to flatten
4: articular loose body
5: complete flattening of met

Question 31

Radiograph findings of Freiberg’s infarction

Answer 31

widening of joint space with effusion, initial lesion (subchondral bone fx), central and dorsal head detaches, loose fragment becomes encompassed in a cavity, collapse of lateral margin

Question 32

Tx of Freiberg’s infarction

Answer 32

acute stage: below knee walking cast (3-4wks) or until sx subside, use of met pad after cast removal (proximal to met head), orthoses
adult: surgical-arthroplasty, implant, med head resection

Question 33

Sever’s disease general

Answer 33

Osteochondrosis of calcaneus, nl ossification appearance varies b/w 8-13 yo, x-rays not helpful, apophysis usally has greater density than the calcaneus

Question 34

contributing factors to Sever’s disease

Answer 34

gastroc-soleus equinus and activity level most common, any foot deformity resulting in excessive pronation and decreased shock absorption, cavus foot, obesity, inflammatory conditions

Question 35

Differentials of Sever’s disease

Answer 35

fx/stress fx, lytic lesion, infeciton, tendonitis

Question 36

Radiographic findings of sever’s disease

Answer 36

dx cannot be made, need contralateral films, will see multiple centers of ossification, apophyseal sclerosis

Question 37

Presentation of sever’s disease

Answer 37

pain, tnd to palp, antalgic gait, exacerbated by activity, little pain in morning or after rest, may be associated with trauma

Question 38

Tx of sever’s disease

Answer 38

decreased activity, short leg cast 2-4 weeks, NSAIDs, control pronatory force, treat gastroc-soleus equinus

Question 39

Thiemann’s general

Answer 39

osteochondrosis of phalanges (proximal epiphyses), may be associated with activities (repeat trauma)

Question 40

Islen’s disease general and etiology

Answer 40

osteochondrosis of styloid process, traction apophysitis from peroneus brevis, metatarsus adductus

Question 41

Buschke’s disease

Answer 41

osteochon of cuneiform bones, x-rays show irregularity of contour and framentation-similar to Kohler’s

Question 42

Diaz disease

Answer 42

osteochon of talus

Question 43

Treve disease

Answer 43

osteocon of sesamoids

Question 44

Osteochondritis Dessicans general

Answer 44

juvenile and adult type, basic disturbance d/t eiphyseal development, trauma, knee most commonly affected, areas affected: medial femoral condyle, femoral head, talus

Question 45

Etiology of osteochondritis dessicans

Answer 45

unknown, may be familial, assoc with other osteochondrosis, assoc with abnl of epiphysis, local trauma may be aggravating factor to initiate lesion

Question 46

Sx, x-ray findings and tx of osteochondritis dessicans

Answer 46

intermittent pn in joint, stiff, swelling, clicking and locking, giving away
fragment of subchondral bone
tx: conservative, long leg plaster cast, for a lesion of talus a short leg cast, arthrotomy and insertion of graft