Osteochondrosis Flashcards
General features of osteochondrosis
common during middle years of growth, boys>females, lower limbs more frequently involved, about 15% are bilateral
Early phase of necrosis (phase of avascularity)
osteocytes and bone marrow cells die, ossific nucleus of epiphysis ceases to grow, articular cartilage remains alive and grows, disuse atrophy (osteoporosis), asx
Phases of osteochondrosis
early phase of necrosis (phase of avascularity), phase of revascularization with bone deposition and resorption, phase of bone healing, phase of residual deformity
Phase of revascularization with bone deposition and resorption
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
What is the most vulnerable stage of osteochondrosis?
phase of revascularization with bone deposition and resportion
Phase of bone healing
bone resorption ceases, but bone deposition continues, newly formed bone still exhibits biological plasticity
Phase of residual deformity
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
Legg-Calve-Perthes Disease general facts and etiology
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
Signs and sx of Legg-C-P disease
pain in hip (synovial effusion), antalgic gait, limited ROM (abduction and internal rotation), disuse atrophy
Four stages of LCPD
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
First and second stages of development of LCPD
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
Third and fourth stages of development of LCPD
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
Classification for LCPD
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
Tx of LCPD
aimed at preventing deformity of femoral head and degenerative changes to hip, abduction cast or some time of abduction brace is most common treatment
Osgood’s Schlatter’s disease general
osteochondrosis of tibial tuberosity, males 10-15, radiographs little use because tibial tuberosity commonly looks abnormal
Sx and dx of Osgood’s Schlatter’s disease
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
Differential dx of Osgood’s Schlatter’s
tendonitis, osteogenic sarcoma, infecetion, tibial tubercle fx
Radiographic findings of Osgood’s Schlatters acute and chronic phase
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
Tx of Osgood’s Schlatter’s disease
withdrawal from sports that cause pain, Ice, NSAIDS, pad to protect tuberosity, infrapatellar strap, no steroid injections, cast immobilization for 6wks if sx severe
Complications of Osgood’s Schlatter’s disease
proximal segment fails to unite remainder of tubercle (remains as a local source of pain)
Kohler’s disease general
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
Etiology of Kohler’s disease
mechanical-longitudinal strain during locomotion
compressive forces during locomotion-compromise vascular source
Weissman: talus projects further distal than nl
Sx of Kohler’s disease
antalgic gait (weight bearing on lateral side), local pain and tenderness over navicular, posterior tibial tendon inflamed at its insertion site
Radiographic findings of Kohler’s disease
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
Tx of Kohler’s disease
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
Freiberg’s Infarction general
avascular necrosis of met head, between 13-18 (females), unilateral generally, structurally weak feet, 2nd met 68%, 3rd met 27%
Differentials of Freiberg’s infarction
fx/stress fx, synovitis/capsulitis, extensor/flexor tendonitis, metatarsalgia, Morton’s neuroma, JRA
Etiology of Freiberg’s infarction
Simillie: occurs 2ndary to a traumatic process (stress)
Braddock: Secondary to fx modified by its proximity to epiphyseal plate
Presentation of Freiberg’s infarction
local pain, tenderness, swelling, limitation of MPJ motion
Classification of Freiberg’s infarction
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
Radiograph findings of Freiberg’s infarction
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
Tx of Freiberg’s infarction
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
Sever’s disease general
Osteochondrosis of calcaneus, nl ossification appearance varies b/w 8-13 yo, x-rays not helpful, apophysis usally has greater density than the calcaneus
contributing factors to Sever’s disease
gastroc-soleus equinus and activity level most common, any foot deformity resulting in excessive pronation and decreased shock absorption, cavus foot, obesity, inflammatory conditions
Differentials of Sever’s disease
fx/stress fx, lytic lesion, infeciton, tendonitis
Radiographic findings of sever’s disease
dx cannot be made, need contralateral films, will see multiple centers of ossification, apophyseal sclerosis
Presentation of sever’s disease
pain, tnd to palp, antalgic gait, exacerbated by activity, little pain in morning or after rest, may be associated with trauma
Tx of sever’s disease
decreased activity, short leg cast 2-4 weeks, NSAIDs, control pronatory force, treat gastroc-soleus equinus
Thiemann’s general
osteochondrosis of phalanges (proximal epiphyses), may be associated with activities (repeat trauma)
Islen’s disease general and etiology
osteochondrosis of styloid process, traction apophysitis from peroneus brevis, metatarsus adductus
Buschke’s disease
osteochon of cuneiform bones, x-rays show irregularity of contour and framentation-similar to Kohler’s
Diaz disease
osteochon of talus
Treve disease
osteocon of sesamoids
Osteochondritis Dessicans general
juvenile and adult type, basic disturbance d/t eiphyseal development, trauma, knee most commonly affected, areas affected: medial femoral condyle, femoral head, talus
Etiology of osteochondritis dessicans
unknown, may be familial, assoc with other osteochondrosis, assoc with abnl of epiphysis, local trauma may be aggravating factor to initiate lesion
Sx, x-ray findings and tx of osteochondritis dessicans
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
