Salter-Harris Classification (Epiphyseal Separations)
Type 1 (S) - Straight across; slipped physis
Type 2 (A) - Above; metaphysis only
Type 3 (L) - Lower; epiphysis only
Type 4 (T) - Through; metaphysics + epiphysis
Type 5 (E) - Erasure of growth plate (physis)
Type 6 (R) - Reaction, periosteal (pull away)
Epiphysis
Round, expanded end of the long bone where joint articulation occures
Physis
Growth plate
Metaphysis
Located between epiphysis and diaphysis. Contains the physis
Diaphysis
bone shaft
What is the difference between the periosteum of infant bone compared to mature bone?
In infants, periosteum is loosely attached to the cortex, whereas in adults is firmly anchored
Cortical bone
Dense, compact bone composed of three types of Lamellae (mineralized bone)
Infants and childn mostly have circumfrential lamellae
Composed of structural units of Haversian systems/Osteons, which contain a central blood vessel surrounded by lamella and lacunae containing bone cells
Trabecular bone
Spongy or Calcelloys bone
Interconnecting plates of trabeculea that create a large surface area for cell activity. Bone trabeculae are deposited according to mechanical stress; most abundant on epiphysis and metaphysis of long bone
Serves as calcium reservoir
Timing of radiographic phases of healing (peak)
SPNBF: 10-14 days
Loss of fracture line: 14-21 days
Soft callus: 15-21 days
Hard callus: 21-42 days
Bony findings of congenital syphilis
Lesions most often in tibia, femur and humerous
Spirochetes produce destructive changes to metaphysis and diaphysis. Can cause pathologic fractures
Metaphyseal abnormalities seen in 90% of infants with symptomatic syphilis and 20% or asymptomatic infants with positvie serologies
Wimberger sign
Seen in congeital syphilis
Bilateral metaphyseal dystruction of medial proximal tibias
Scurvy
Insufficient Vit C suppresses normal cellular activity
Changes to metaphysis and epihpyseal area
Fractures uncommon
Thin cortices, osteopenia
Dense Zone of Provisional Calcification
Painful swelling
Bleeding gums, frequent infections, easy bruising, poor wound healing
Vit A intoxication
Vit A (retinoic acid) causes increased bone resorption and SPNBF
Hard, tender swellings over extremities
Xrays show SPNBF
Increase ICP and widening of sutures
Copper deficiency (Menkes)
Can occure in very preterm infants or those with short gut syndrome
Hypotonia, hypopigmentation, anemia, neutropenia, osteoporosis, cupping of metaphysis and SPNBF
Plasma copper <40 and plasma ceruloplasma <13
*Menkes is X-linked, can also have wormian bones, seizures, FTT, “kinky hair”
Caffey Disease
Painful SPNBF and cortical thickening found on multiple bone
Due to mutation in COL1A1
Mandible involved in 75% of case, clavical and ulna also common
NO Metaphyseal irregularity
In what conditions can you see metaphyseal abnormalities?
OI (+/-)
Scurvy
Osteomylitis
Congenital Syphilis
Menkes
Copper deficiency
Methotrexate (impaction fractures)
Rickets
Congenital syphilis
Congential Rickets
Rare, MOC have sever Ca deficiency
Fetal hypocalemia and hyperparathyroidism
Swollen wrists and ankles, frontal bossing, wide anterior fontanelle
Nutritional Rickets
Low Vt D, elevated alk phos, elevated PTH, low phos, low or normal Ca
Stage 1: decreased 25D leads to decreased 1,25D2 and hypocalcemia -> elevated PTH whcih mobilizes Ca from bone. Radiographically normal
Stage 2: Secondary Hyperparathyroidism and hypophosatemia. Changes on xray
Stage 3: Rachitic changes. Xrays with: Widening of physis, metaphyseal fraying, flaring of CCJ (rachitic rosary). Fractures are RARE
What does PTH do?
Increased reabsorption of Ca from renal tubules
Decreased reabsorption of Phos from renal tubules (excrete phos in urine)
Converts 25 OH-D to the active form of 1,25OH-D
Mobilizes Ca from bone to maintain appropriate serum levels
Ca goes up
Phos goes down
Physiology behind OI
Can’t make triple helix
(Fibroblasts make collagen and collagen is a triple helix)
Most common types of OI
Type 1 and Type IV
OI Type 1
Milder, normal facies
Hearing loss 50%
Fx in preschool
Wormian bones, demineralization
1A: Blue sclera bue normal teeth
1B: Dentiongenesis imperfecta
Family History, Autosomal dominant
OI Type II
Letal in perinatal period
OI Type III
Severe deforming
Short stature, bowed legs, Dentinogesis imperfecta, wormian bones
Blue sclera common
