Young MSK

Question 1

What is the early embryonic membrane formed of?

Answer 1

Early embryonic membrane entirely made up of fibrous membrane and hyaline cartilage.

Question 2

By which 2 routes does ossification of the bones occur?

Answer 2

-> Intramembranous ossification where osteoid is laid down by osteoblasts within mesenchymal connective tissue

-> Endochondral ossification where ostroid is deposited on cartilage scaffolds.

Question 3

When does intramembranous ossification occur?

Answer 3

-During foetal development
-fracture healing
-subperiosteal bone growth. - – - Forms flat bones.

Begins in-utero, hence at birth, the skull and clavicles are not completely ossified and the cranial sutures (junctions between the skull bones) are not closed, allowing deformation during passage through the birth canal.

Question 4

What is the process of intramembranous ossification?

Answer 4

1. Mesenchymal stem cells proliferate in fibrous tissue.
2. Mesenchymal stem cells differentiate into blood vessels, osteoblasts and osteogenic cells.
3. Osteoblasts form ossification core and secrete non-mineralised matrix (osteoid)
4. Mineralisation of matrix (osteoid) and osteoblasts embedded in the matrix become osteocytes.
5. Trabecular matrix forms around blood vessels. 6. Periosteum arises from mesenchyme and surface osteoblasts.
6. Cortical bone forms below periosteum; blood vessels condense into red marrow.

Question 5

When does endochondral ossification occur?

Answer 5

How most of the skeleton develops e.g. at physis for longitudinal growth and non-rigid fracture healing.

Question 6

What is the process of endochondral ossification at the primary ossification centre?

Answer 6

Replaces diaphyseal cartilage with bone.

Formation of the periosteum and collar:

1. In early foetal development mesenchymal cells differentiate into chondrocytes and form the cartilaginous skeleton precursor.
2. Perichondrium that forms on the surface of foetal bone transitions to become periosteum and produces a thin layer of bone on the surface called periosteal collar.

Calcification of the matrix:

3. As more cartilage matrix is produced chondrocytes at the centre of scaffold enlarge and begin to calcify their surrounding matrix, calcification blocks nutrients from chondrocytes.
4. Without nutrients chondrocytes die, and the cartilage surrounding them disintegrates allow blood vessels to invade the space they left carrying osteogenic cells with them.

Question 7

What is the secondary ossification centre?

Answer 7

A secondary ossification center appears in each end (epiphysis) of long bones.

Periosteal buds carry mesenchyme and blood vessels in and the ossification is similar to that occurring in a primary ossification center.

Question 8

What is the epiphyseal plate.

Answer 8

The cartilage between the primary and secondary ossification centers is called the epiphyseal plate, and it continues to form new cartilage, which is replaced by bone, a process that results in an increase in length of the bone.

Question 9

Endochondral ossification:

Answer 9

Formation of periosteum:

The perichondrium becomes the periosteum. The periosteum contains a layer of undifferentiated cells (osteoprogenitor cells) which later become osteoblasts.

Formation of bone collar

The osteoblasts secrete osteoid against the shaft of the cartilage model (Appositional Growth). This serves as support for the new bone.

Calcification of matrix

• Chondrocytes in the primary center of ossification begin to grow (hypertrophy).
• They stop secreting collagen and other proteoglycans and begin secreting alkaline phosphatase, an enzyme essential for mineral deposition.
• Then calcification of the matrix occurs and osteoprogenitor cells that entered the cavity via the periosteal bud, use the calcified matrix as a scaffold and begin to secrete osteoid, which forms the bone trabecula.
• Osteoclasts, formed from macrophages, break down spongy bone to form the medullary (bone marrow) cavity.

Question 10

What is the function of the secondary ossification centre?

Answer 10

Secondary centre replaces epiphysis with bone.

They begin to form at or after birth in a predictable way.

Question 11

Where do longitudinal and circumferential bone growth occur?

Answer 11

Longitudinal bone growth occurs at the physis

Circumferential bone growth continues to occur at the periosteum.

Question 12

When does bone growth stop?

Answer 12

Bone growth stops when the epiphyseal plates (aka the physis) close - 14 in females and 16 in males.

Question 13

What are is the physis/ epiphyseal plate?

Answer 13

Physis is the hyaline cartilage plates at the ends on long bones separating the epiphysis from the metaphysis and is responsible for longitudinal growth of long bones

Question 14

What at the 3 main routes for blood supply to the bone?

Answer 14

Epiphyseal, perichondrial and metaphyseal arteries.

Question 15

What is the perichondrial ring and what is its function?

Answer 15

perichondrial ring is continuous with the metaphyseal periosteum and increases strength of attachment between the physis and the rest of the bone.

Question 16

Describe the resting zone of microscopic bone?

Answer 16

Sparsely packed chondrocytes that don’t change in size or produce matrix. Has stores of lipids, glycogen and protoglycans. Blood supplied by epiphyseal arteries.

Question 17

Describe the proliferative zone of microscopic bone.

Answer 17

Cells begin to stack in column and multiply at increasing rate.

Begin to produce cartilaginous ECM.

Question 18

Describe the hypertrophic zone of microscopic bone.

Answer 18

Is a relatively weak point in the physis where SUFE and SH fractures occur.

Cells increase in size and begin to collect and store calcium to release upon their death.

Has 3 subzones:
- Zone of maturation (x2)
- Zone of degradation (x5)
- Provisional calcification (apoptosis) where cells die and release Ca2+ calcifying the surrounding matrix.

Question 19

What are primary and secondary spongiosa?

Answer 19

Primary spongiosa has haematogenous infiltration, and is where immature woven bone is formed

Secondary spongiosa is where woven bone is remodelled to laminar bone.

Question 20

What is achondroplasia? What is it caused by?

Answer 20

The most common skeletal dysplasia, caused by a gene defect that increases inhibition of chondrocyte proliferation in the proliferate zone.

Also known as disproportionate dwarfism. Can be inherited as dominant gene and 80% of cases new mutations.

Question 21

What is Gigantis?

Answer 21

A condition where there is excess growth hormone caused by pituitary adenoma. Causes increased proliferation of chondrocytes in the proliferate zone.

Question 22

What is acromegaly?

Answer 22

Where pituitary adenoma causes production of too much growth hormone after physeal closure (in adults).

Question 23

What age do children have a matured gait?

Answer 23

7 years old `

Question 24

What age ranges link to different limping child symptoms?

Answer 24

• DDH 0-2 (hopefully diagnosed before 6 weeks)
• Transient Synovitis (2-5 yrs)

Question 25

What is DDH? What are the causes/risk factors and presentation?

Answer 25

Developmental dysplasia of the hip = abnormalities of either the femoral head or the acetabulum, or both resulting in infantile hip instability, shallowness of the hip socket or hip dislocation.

Causes/risk factors: hereditary influence, breech after 32 weeks, cesarean, 1st borns, 5:1 females.

Presentation: skin crease asymmetry, barlows (brittle), Ortolani (out) tests, Leg length discrepancy, Reduced abduction.

Question 26

What is transient synovitis?

Answer 26

Transient synovitis of the hip is a self-limiting inflammatory disorder of the hip that commonly affects young children between 2 and 12 years of age

Question 27

What are the key diagnostic factors and risk factors for transient synovitis?

Answer 27

Key diagnostic factors:
limited movement, pain, limp, abducted and externally rotated hip, fever.

Risk factors:
- 2 to 12 years of age
- male sex
- history of recent viral illness

Question 28

What is perthes disease?

Answer 28

idiopathic osteonecrosis of the femoral epiphysis seen in children majority 4-8 years

More common in boys 4:1

Generally occurs secondary to the abnormal or damaged blood supply to the femoral epiphysis, leading to fragmentation, bone loss, and eventual structural collapse of the femoral head.

Question 29

How do you treat perthes disease of the hip?

Answer 29

Containment, prevention of stiffness and keeping epiphysis in acetabulum. Physiotherapy and rest.

Question 30

What is SUFE, what are teh risk factors and symptoms and how do you treat it?

Answer 30

Slipper upper femoral epiphysis

more common in males 3:1 age 13-16 years, often obses or slender.

Caused by rapid growth although genetic component

Leg will look externally rotated as metaphysis twists of epiphysis.

Presents with pain in the groin, knee, thigh, limp and antalgic gait.

Treatment is pin placed in surgery across epiphysis in both sides to avoid leg length discrepancy.

Question 31

What could these limping child red flags be a sign of:

• Neonate with painful/paralysed arm/leg
• Asymmetry of spine or limbs
• school age child with limp
• knee pain in adolescence
• back pain

Answer 31

• Neonate with painful/paralysed arm/leg = SEPTIC ARTHRITIS OR INFECTION
• Asymmetry of spine or limbs = SCOLIOSIS OR DDH
• school age child with limp = PERTHES DISEASE
• knee pain in adolescence = SUFE OR TUMOUR
• back pain = DISCITIS

Question 32

What possible infections could result in a limping child?

Answer 32

Cellulitis, osteomyelitis, septic arthritis.

Question 33

What is Discitis?

Answer 33

An infection of the intervertebral disc space.

Presentation is subtle hence MRI usually required to decide inflammation vs. infection.

Question 34

What is an epidural abscess?

Answer 34

Spinal epidural abscess represents infection of the epidural space, located between the spinal dura mater and the vertebral periosteum.

It can present with rapidly deteriorating neurological function due to compression.

Imaging is best performed with MRI and emergency surgery is often required.

Question 35

What can atraumatic painful swelling be a sign of in children?

Answer 35

Tumours

Question 36

What are some examples of incomplete fractures?

Answer 36

greenstick fractures and Buckle/Torus fractures.

Question 37

What are greenstick fractures?

Answer 37

A bone cracks on one side only, not all the way through the bone. It is called a “greenstick” fracture because it can look like a branch that has broken and splintered on one side

more commonly less than 10 years of age.

Is more unstable and requires hard cast

Question 38

What are buckle/torus fractures?

Answer 38

Buckle fractures are common injuries sustained by children >2 years old, typically following a fall on the outstretched hand.

As the developing bone is relatively soft, the trabeculae is compressed, resulting in the appearance of a bulge.

This is most frequently seen on the dorsal aspect of the distal radius but can appear on distal ulna or both distal ulna and radius. The bulge may be seen at both the ulnar and radial aspects of the bone.

This doesn’t require hard cast as heals well on its own.

Question 39

What is special about periosteum in children?

Answer 39

Periosteum is much thicker in children, and a clinical benefit is that it is easier to reduce fractures in children, the bones don’t tend to displace as much.

Question 40

When is there greatest potential for remodelling of a fracture?

Answer 40

Greatest potential for remodelling is at a young age, with deformity is near to the joint. There is no potential for remodelling with rotational deformities.

Question 41

What is wolff’s law

Answer 41

Bone is formed depending on mechanical stress.

Bone is Deposited on the compression side and absorbed on the tension side.

Question 42

Explain the 5 different types of salter harris fractures:

Answer 42

S - straight. Fracture goes straight across the physis. Difficult to diagnosed, least likely to have growth deformity.

A - above. Fracture line exits above the physis with metaphyseal wedge attached to epiphysis. Most common.

L - lower. Fracture line exits below physis with epiphyseal fragment. Intra-articular and chance of growth deformity due to fusion of physis.

T - through. Fracture directly through physis forming both metaphyseal and epiphyseal fragments. intra-articular, chance of growth deformity due to fusion of physis.

R - ruined. Crush injury to the physis with worst prognosis and causes growth arrest.

Question 43

What are the positive and negatives of paediatric fractures?

Answer 43

Positive: heal rapidly, non union is rare and there is less morbidity with bed rest.

Negative: difficult to diagnose and physeal plate injuries may halt growth.

Question 44

What are some child and some parent risk factors for Non Accidental Injury (NIA)

Answer 44

Child: First born, unplanned, premature, disabilities, step-children.

Parent: single parents, unemployed, substance abuse, personal history of abuse, low SE background.

Question 45

How can you distinguish between accidental and Non accidental soft tissue injury?

Answer 45

Head/face injuries rare in patients <18 months old.

Lumbar injures unusual in patients < y/o

Accidental bruising of hands, feet and lower legs most common.

Nonaccidental have bite marks, burns, grip mark bruising, paticial bruising, torn frenulum and retinal hemorrhage.

Question 46

What fractures are common in NIA?

Answer 46

metaphyseal corner fractures in children ,2 y/o, small enough to be shaken but cannot protect with muscles.

Rib fractures especially on posterior ribs diagnosed on skeletal survey.

Question 47

What can make children more susceptible to fractures? (3)

Answer 47

BBD, prematurity and copper deficiency

Question 48

What is genu valgum?

Answer 48

aka knock knees.
condition that is common in toddlers but usually resolves spontaneously around 18 months.

If it persists or is more severe then suspect rickets or blount disease.

Question 49

What is genu varum?

Answer 49

less common angular variant in children. Even if severe usually resolves spontaneously around 9 years. Necessary to exclude skeletal dysplasia and hypophosphatasia.

Question 50

Rickets

Answer 50

Rickets = deficient mineralisation at the growth plate of long bones in growing children. If not treated, bone deformity occurs, typically causing bowed legs and thickening of the ends of long bones.

primarily as a nutritional deficiency of vitamin D.

Can also be caused by deficiencies of calcium or phosphorus.

Osteomalacia is impaired mineralisation of the bone matrix and can occur after growth plates have fused.

Question 51

What is blount disease?

Answer 51

• Is a developmental growth disorder of the tibia that causes the lower leg to angle outwards, causing bowing of the leg.
• It is characterised by progressive multiplanar deformities of the leg caused by disordered endochondral ossification of the proximal medial tibial physis.

Question 52

What is skeletal dysplasia?

Answer 52

a category of rare genetic disorders that cause abnormal development of a baby’s bones, joints, and cartilage. affects different parts of the body in different children.

Question 53

How can you check for apparent bowing?

Answer 53

Bowing seeing when stood as hips and knees are flexed, but when child lies down and extents hip and knees, lower limb is straight.

Question 54

When can genu varus and valgus bee pathological?

Answer 54

When asymmetrical
resistant,
shorter stature
varus greater than 11 degrees
if there is traumatic or systemic causes.

Question 55

How are genu varus and valgus treated in children?

Answer 55

Observation -> growth -> osteotomy.
Eight plates are used to guide growth by inserting into one side of growth plate.

Question 56

How do rotational growth deformities present?

Answer 56

clumsiness, tripping and limping, looking ‘deformed’

Question 57

What can cause rotational growth deformities.

Answer 57

femur, tibia, foot.

• Femoral anteversion
• external/internal tibial torsion

Question 58

What is miserable malalignment?

Answer 58

Consists of proximal femoral anteversion, leading to internal rotation of the thigh, inward squinting of the patella, and significant external tibial torsion.

Question 59

What are some causes of out-toeing?

Answer 59

Femoral retroversion
Metatarsus adductus
Clubfoot (CTEV)
Planovalgus (flat footedness)

Treatment only given when symptomatic, can have subtalar implant.

Question 60

Common forearm fracture pattern:

Answer 60

breaking bone in both radius and ulnar, disrupting the circle.

Question 61

how are femoral fractures treated in children?

Answer 61

bed traction and flexible intramedullary nails.