UniMelb+DPT+Common+Musc+Conditions+in+Paeds

The secondary barriers to reduction that develop due to chronic dislocation in DDH include:

1. Pulvinar thickening
2. Thickening and elongation of the ligamentum teres
3. Thickening of the transverse acetabular ligament

The anatomical changes associated with chronic dislocation in DDH include:

1. Increased femoral neck anteversion
2. Flattening of the femoral head
3. Increased acetabular anteversion
4. Increased obliquity and decreased concavity of the acetabular roof
5. Thickening of the medial acetabular wall

• Dysplasia: 7:1000
• Dislocation: 1:1000

The incidence of DDH is 6:1 Female to Male, indicating a stronger effect of oestrogen in females.

Risk factors include:

1. Breech position
2. Oligohydramnios (reduced intrauterine fluid)
3. First pregnancy
4. Multiples (twins or more)
5. Ethnic carrying/swaddling practices

Swaddling techniques can lead to hip dysplasia in the following ways:

• Correct Swaddling: Legs should be loosely swaddled to allow movement, keeping hips relaxed and spread out.
• Incorrect Swaddling: Tightly swaddled hips can lead to hip dysplasia and dislocation, as they restrict natural movement.

Ligamentous laxity from oestrogen and relaxin can remain in infants up to 14 days after birth, increasing the risk of DDH.

A positive family history is found in 12-33% of cases of DDH, indicating a genetic predisposition to the condition.

Conditions associated with DDH include plagiocephaly, torticollis, knee hyperextension, and foot deformities. All these conditions should be screened for DDH.

Screening for DDH should be conducted until the age of 3 years.

• Female
• First born
• Family history of hip dysplasia (in first degree relative)
• Breech lie
• Neuromuscular or connective tissue disorder associated with DDH
• Inappropriate swaddling

• 'Clunk' or 'Click' when moving hip
• Uneven thigh creases
• Crooked buttock creases
• Leg(s) difficult to spread apart
• Weight off to one side when sitting
• Different leg lengths
• Avoiding weight bearing
• Walking on tippy toes on one side
• Limping when walking
• Torticollis, Plagiocephaly and Metatarsus adductus

• At birth
• At 1-4 weeks
• At 6-8 weeks
• At 6-9 months
• At 12 months
• Then at normal health reviews until 3.5 years

Early detection is vital to improve outcomes for children with hip dysplasia.

• Positive Barlow sign: Indicates the hip can be dislocated with adduction.
• Positive Ortolani sign: Indicates the hip can be reduced back into the socket with abduction.

Developmental dysplasia of the hip (DDH) is a disorder characterized by abnormal growth and development of the acetabulum and the femur. It results in the femoral head having an abnormal relationship to the acetabulum, making it easy to displace.

Dysplasia leads to subluxation and gradual dislocation of the femoral head, which can be felt to glide in and out of the acetabulum.

The Barlow test is used to dislocate an unstable hip by adduction of 10-20° and depression of the flexed femur. It helps in assessing hip stability in infants.

A positive result in the Barlow test is indicated if the hip can be popped out of the socket, often accompanied by a clunk or click on exit.

During the Barlow test, the examiner's fingers should lie over the greater trochanter, and the thumb should be placed on the inner thigh of the infant.

The Ortolani test is used to reduce a dislocated hip by elevating and abducting the flexed femur. It helps in identifying hip dislocation in infants.

1. Position the infant on their back.

2. Flex the infant's knees and hold the legs.

3. Abduct the legs while applying an upwards force over the greater trochanter.

4. Listen for a clunk or click indicating the hip is relocating.

A positive Ortolani test result is indicated by a clunk or click sound when the hip is relocated during the test, suggesting a previously dislocated hip is being reduced.

The Galeazzi sign is observed when an infant's hips are flexed to 90°. In the case of a unilateral dislocated hip, the thigh on the affected side will appear shorter than the other thigh, indicating a potential hip dislocation.

Reduction of hip abduction can be assessed by observing the range of motion in an infant's hips. Limited ability to move the legs away from the midline may indicate hip dysplasia.

Abnormal skin creases can be a sign of developmental dysplasia of the hip (DDH). These may appear uneven or asymmetrical when comparing the thighs of the infant.

The most sensitive test is a limitation in hip abduction.

Leg length discrepancy may be observed in children with DDH.

Barlow and Ortolani tests are unlikely to be positive as soft tissue contractures have developed around the hip.

The soft tissue around the hip becomes tighter as the child ages from 3 months to 1 year.

• Pelvic obliquity
• Apparent leg length discrepancy
• Toe walking (to compensate for short leg)

• Lumbar lordosis

• Trendelenburg gait

• Subluxable: Barlow test suggestive of subluxation.
• Dislocatable: Barlow test positive indicates dislocatability.
• Dislocated: Ortolani test positive when detected early and reducible; Ortolani test negative when late and irreducible.

An ultrasound evaluates for acetabular dysplasia and/or hip dislocation. It is most effective before 6 months of age when the hip joint is primarily cartilaginous.

The normal values are:

• Alpha angle: > 60° (created by lines along the bony acetabulum and the ilium)
• Beta angle: < 55° (created by lines of the labrum and the ilium)

The femoral head is normally bisected by a line drawn down from the ilium during the ultrasound evaluation.

The ultrasound image displays several anatomical features including:

• Iliac bone
• Tendon of the rectus femoris
• Cartilage of the acetabulum
• Triradiate cartilage
• Labrum (between the acetabulum and femoral head)
• Gluteus minimus
• Gluteus medius
• Capsule
• Femoral head
• Great trochanter

The hip angle is measured using the following components:

• Ilium
• Labrum
• Cartilaginous acetabular roof
• Femoral head
• Bony roof

The angles measured are:

• Alpha angle: 64 degrees
• Beta angle: 44 degrees

The angles measured in an ultrasound for DDH are alpha (α) and beta (β). The alpha angle is 64 degrees, representing the coverage of the femoral head by the acetabular roof, while the beta angle is 44 degrees, indicating the slope of the acetabular roof.

Key indicators include:

• Increased acetabular index
• Disruption of Shenton's line
• Widened teardrop
• Ossific nucleus should be in the lower quadrant where Perkins and Hilgenreiner lines cross

Note: X-rays are not useful in children less than 6 months of age.

Position the baby with their hips bent and knees apart in a frog-like position.

Avoid swaddling the legs tightly or straight down, and do not use sleep sacks that are snug around the thigh.

Following SIDS guidelines is important to ensure the baby's safety during sleep and to prevent risks associated with swaddling.

Swaddling should be stopped once the baby is rolling from back to tummy and onto back again, typically around 4-6 months of age.

Inappropriate swaddling can increase the risk for developmental dysplasia of the hip (DDH).

The primary aim of treatment for DDH is to maintain the reduction of the femoral head in the acetabulum, providing an optimal environment for the development of both the femoral head and the acetabulum.

Early treatment for DDH is considered optimal because it should occur before 6 weeks of age, utilizing observation or bracing to promote abduction of the hip joint.

The two main treatment devices for DDH are the Pavlik Harness and the Denis Browne bar. The Pavlik Harness holds the baby's legs in a frog-like position, while the Denis Browne bar keeps the legs in a wide, frog-like position.

The recommended duration for treatment options in DDH is 3-6 months.

If the hip can be reduced during DDH treatment, a hip spica cast is applied.

If the hip cannot be reduced, an open reduction is performed, followed by the release of tight structures and then a hip spica cast is applied.

Bracing alone may be insufficient for DDH treatment due to too much soft tissue changes that require more intervention.

An arthrogram and examination under anaesthetic are performed to assess and potentially reduce the hip in DDH treatment.

Delayed diagnosis may lead to bony changes in the hip joint, resulting in hip pain and potentially necessitating early knee replacement.

Surgical options include femoral osteotomies and acetabular osteotomies, which aim to enhance the congruency of the hip joint.

The majority will stabilize as the postnatal elasticity resolves, provided they rest in a stable position.

The greater the delay in diagnosis, the poorer the outcome.

If osteotomies are required, the hips will never be normal and may result in osteoarthritis as a young adult, potentially requiring total hip replacement (THR).

Hip dysplasia is the most common cause of hip arthritis before the age of 50.

The assessment of Barlow and Ortolani maneuvers should only be performed by an experienced and trained paediatric physiotherapist.

If DDH is a possibility, a graduate physiotherapist should seek training or refer infants to a paediatrician or MCHCN.

Developmental Dysplasia of the Hip (DDH) is a condition where the ball of the femur is partially or fully dislocated from the socket of the pelvis, unlike a normal hip joint where the ball fits perfectly into the socket. This can lead to hip instability and potential long-term complications if not treated.

Perthes Disease is characterized by an irregular shape of the ball of the femur due to disrupted blood supply. This condition can lead to pain and limited mobility in the affected hip joint, and it typically affects children between the ages of 4 and 8.

Slipped Capital Femoral Epiphysis (SCFE) occurs when the ball of the femur slips off the neck of the femur. This condition can result in hip pain, limited range of motion, and can lead to complications such as avascular necrosis if not addressed promptly.

The exact aetiology remains unknown, but it is characterized by aseptic osteonecrosis of the femoral head in children.

Perthes disease typically presents in children aged 4-10 years.

Approximately 80% of Perthes disease cases are unilateral.

The changes to the femoral head in Perthes disease occur in three stages, which can take 18 months to 2 years to complete.

The incidence of Perthes disease is 10.8 cases per 100,000 in Caucasian children, 0.5 cases per 100,000 in African children, and 1.7 cases per 100,000 in mixed race children.

Boys are 4 times more likely to be affected by Perthes disease than girls.

Perthes disease is associated with:

• ADHD
• High levels of physical activity
• Low birth weight
• Decreased skeletal maturation at the time of diagnosis

• Intermittent limping and pain in the groin, thigh, or knee.
• Difficulty jumping on the affected leg.
• Reduced range of motion in abduction and internal rotation.
• In advanced stages, the presence of Trendelenburg sign.

Ultrasound can detect joint effusion in the early stages of Perthes disease.

The recommended radiographic views for diagnosing Perthes disease are AP pelvis and frog lateral views.

Radiology is often normal in the early stages of Perthes disease because changes may not appear for 2-3 months after the onset of symptoms, so imaging should be repeated if symptoms persist.

The initial stage of Perthes disease is characterized by disrupted blood supply leading to avascular necrosis. This stage can last around 1 year and may show early flattening of the top of the femoral head or a fracture line.

In Stage 1 of Perthes disease, potential radiographic findings include:

• Early flattening of the top of the femoral head
• Possible fracture line

These changes indicate a loss of normal shape of the femoral head, which may be seen on X-ray.

During the fragmentation/resorptive stage, the femoral head appears broken up and flatter due to the resorption of dead bone, which creates spaces where there is no bone. This stage can take approximately 1.5 years to progress.

During the reossification stage, new bone forms where dead bone has been removed. This process starts from the outside and works its way inward, typically taking 2-3 years to complete.

In healed stage 4 Perthes disease, the femoral head may appear similar to the normal side but can also be:

• Enlarged (coxa magna)
• Flattened (coxa plana)
• Have a short broad neck (coxa breva)

The Lateral Pillar Classification includes four groups based on the height of the lateral pillar observed in hip radiographs during the fragmentation stage:

The aims of treatment for Perthes disease are to:

1. Protect the shape of the femoral head by containing it in the acetabulum.
2. Restore normal range of movement.
3. Provide pain relief.

The treatment options for stages 1 and 2 of Perthes disease include:

1. Maintain hip abduction
2. Range of Motion (ROM) exercises to promote femoral and acetabular congruency
3. Use of slings and springs
4. Abduction bracing
5. Casting
6. Restrict activity:
   • Protected or non-weight bearing
7. If an adductor contracture occurs, surgical release may be required followed by broomstick plasters.

Slings and springs are used to improve mobility in children with Perthes Disease, particularly to maintain the ability to move the legs wide apart and prevent stiffness of the hip joint.

The upper slings should be positioned just above the knees, and the lower slings at the ankles. The correct length of the springs is important, allowing the legs to skim the bed with knees straight, promoting free movement of the hips.

In a hospital setting, slings and springs should be used for most of the day and overnight. For home use, they are generally required only overnight.

Children should be encouraged to exercise in the slings and springs for at least five to ten minutes every hour, gently swinging their legs wide apart and then together to increase mobility as comfortable.

One hour of tummy lying daily, out of slings and springs, is recommended to promote further mobility and comfort.

Full weight bearing can be resumed and bracing discontinued if full abduction range of motion (ROM) has been preserved.

If conservative management fails, an osteotomy may be required to contain the head in the acetabulum.

The aim is to return to sport in 5 years.

Younger diagnosis is associated with a more favorable outcome.

Children with bilateral disease have a worse prognosis compared to those with unilateral disease.

Although Perthes disease is more common in males, females who are affected tend to have a worse outcome.

The final shape of the femur will determine the long-term effects, with more deformation leading to a higher likelihood of arthritis and the need for total hip replacement (THR).

The aetiology of DDH includes factors such as:

1. Genetic predisposition: Family history of hip dysplasia.
2. Mechanical factors: Breech presentation during delivery, oligohydramnios, and tight swaddling.
3. Hormonal influences: Relaxin hormone affecting joint laxity during pregnancy.

Common signs and symptoms of Perthes Disease include:

• Hip pain: Often referred to the knee.
• Limping: Due to pain or stiffness.
• Limited range of motion: Especially in internal rotation and abduction.
• Muscle atrophy: Around the hip due to disuse.

Treatment options for SUFE include:

1. Observation: For stable cases with minimal displacement.
2. Surgical intervention:
   • In situ fixation: Using screws to stabilize the femoral head.
   • Osteotomy: In severe cases to realign the femur.
3. Physical therapy: Post-surgery to regain strength and mobility.

The incidence of DDH varies by population but is generally reported as:

• 1-2% in the general population.
• Higher rates in females and those with a family history.
• Increased incidence in breech births, with rates up to 20%.

Diagnostic tests for DDH include:

• Ultrasound: For infants to assess hip joint stability.
• X-rays: For older children to evaluate the acetabulum and femoral head position.
• Physical examination: Including the Barlow and Ortolani tests to check for hip dislocation.

The suspected multifactorial causes of Slipped Upper Femoral Epiphysis (SUFE) include:

1. Obesity
2. Growth spurts
3. Endocrine disorders

These factors contribute to the condition, although the exact aetiology remains unknown.

In cases of Slipped Upper Femoral Epiphysis (SUFE), the femoral neck typically:

• Moves anteriorly
• Rotates externally relative to the femoral head

A metaphor used to describe the condition of Slipped Upper Femoral Epiphysis (SUFE) is: Ice cream falls off the back of the cone. This illustrates the displacement of the femoral head from its normal position.

The primary characteristic of SUFE is the downward slippage of the head of the femur relative to the rest of the femur, which occurs at the growth plate.

The anatomical feature affected in SUFE is the growth plate located at the upper end of the femur, which is where the slippage occurs.

The two classifications of SUFE are Unstable and Stable.

An unstable SUFE patient is characterized by an inability to weight bear.

Acute SUFE is characterized by a sudden onset of symptoms and an inability to weight bear.

Chronic SUFE presents with a gradual onset of symptoms lasting for more than 3 weeks.

Acute on chronic SUFE refers to a sudden exacerbation of symptoms due to an acute displacement of a chronically slipped epiphysis.

A patient with SUFE requires immediate referral to an orthopedic surgeon.

The incidence of SUFE is approximately 10 cases per 100,000 children.

Boys are 60% more likely to be affected by SUFE than girls.

The average age for boys is 12 years and for girls is 11 years.

Approximately 50% of SUFE patients are above the 95th percentile for weight.

SUFE is the most common hip pathology in pre-adolescents and adolescents, and it is also the most common missed or delayed diagnosis in this age group.

• Sudden pain and inability to weight bear

• Most common complaint is knee pain

• May also complain of vague pain in the thigh or groin

• Antalgic gait

• Out toeing gait with femur external rotation

• Loss of internal rotation at the hip

• Increased external rotation

• Possible toe walking on one side due to apparent shortening of the affected limb

• Trendelenburg gait due to hip abductor weakness

The most reliable physical sign of SUFE is that the affected side exhibits obligatory external rotation during hip flexion. As the hip is flexed on the affected side, it will automatically rotate and abduct.

The diagnostic testing for Slipped Upper Femoral Epiphysis (SUFE) includes:

1. AP Pelvis view
2. Frog lateral views of both hips

The Steel sign indicates a specific diagnostic feature in the right femoral head, suggesting the presence of Slipped Upper Femoral Epiphysis (SUFE). It is characterized by a shaded region that highlights the abnormality in the femoral head, which is crucial for diagnosis.

The Widening of physis refers to the increased space around the growth plate observed in bilateral hips, which is a key diagnostic indicator of Slipped Upper Femoral Epiphysis (SUFE). This widening suggests abnormal growth plate behavior, often associated with the condition.

The Relative decreased height of epiphysis indicates a reduction in the height of the femoral epiphysis compared to normal, which is a significant diagnostic sign of Slipped Upper Femoral Epiphysis (SUFE). This finding helps in assessing the severity of the condition.

Klein's line is a diagnostic line drawn along the lateral aspect of the femoral neck. The loss of intersection of the epiphysis by this line indicates a displacement of the femoral head, which is a critical sign of Slipped Upper Femoral Epiphysis (SUFE).

The child should be immediately placed non weight bearing to prevent further injury.

All patients with SUFE will require emergency surgical stabilization to prevent death of the femoral head.

The most commonly performed procedure is in situ fixation with a pin or screw, aimed at preventing further slippage of the femoral head.

Prophylactic pinning of the non-affected side may occur because stabilizing the affected side can sometimes precipitate a slip of the contralateral side.

In severe cases of SUFE, osteotomies may be required to reconstruct the femur, correcting the deformity and optimizing the positioning of the femoral head in the acetabulum.

50% of unstable SUFE cases develop osteonecrosis due to disrupted blood supply post fixation.

Complications post fixation can include:

1. Femoral head osteonecrosis - due to disrupted blood supply.
2. Chondrolysis - resulting in pain and reduced range of motion if the articular surface is penetrated (occurs in 7% of cases).
3. Femoralacetabular impingement - due to failure of femoral remodeling.
4. Slip progression - observed in 2% of cases after fixation.
5. Increased risk of early degenerative joint disease in patients with moderate or severe SUFE.

The aetiology of DDH includes factors such as:

1. Genetic predisposition: Family history of hip dysplasia.
2. Mechanical factors: Breech presentation during pregnancy, oligohydramnios, and tight swaddling.
3. Hormonal influences: Relaxin hormone affecting joint laxity during pregnancy.

Common signs and symptoms of Perthes Disease include:

• Hip pain: Often referred to the knee.
• Limping: Due to pain or stiffness.
• Limited range of motion: Especially in internal rotation and abduction.
• Muscle atrophy: Around the hip due to disuse.

Diagnostic tests for SUFE typically include:

1. X-rays: To visualize the position of the femoral head.
2. MRI: To assess the degree of slippage and any associated changes.
3. Physical examination: Checking for limited range of motion and hip pain.

Treatment options for DDH include:

• Observation: In mild cases, especially in infants.
• Pavlik harness: For infants to maintain hip position.
• Closed reduction: For older infants or those not responding to harness.
• Surgery: In severe cases or when non-surgical methods fail.

The three different anatomic growth regions of a long bone are:

1. Physis - the growth plate, where ligaments are stronger than adjacent bone, making bone injuries more common due to ligament pulling on the bone.
2. Epiphysis - the base of hyaline articular cartilage.
3. Apophysis - the attachment site of major muscle groups to bone, considered a 'weak link'.

Child athletes are still growing, and their bones grow faster than their muscles. This discrepancy can lead to traction at the muscle insertion sites, making them more susceptible to injuries like apophysitis.

Apophysitis is characterized by degeneration of the center of growth or ossification center, leading to chronic inflammation, avulsion of cartilage and bone, tendinous micro-tears, and hemorrhages.

Common sites of apophysitis include:

• Inferior pole of patella (Sinding-Larsen Johansson disease)
• Tibial tubercle (Osgood-Schlatters)
• Calcaneal apophysis at insertion (Severs)
• Plantar fascia
• Medial apophysitis of the humerus

Apophysitis typically occurs in children aged 8-15 years due to rapid bone growth outpacing muscle growth, which results in increased tension on the bones.

Apophysitis is commonly associated with repeated overuse activities such as running, jumping, and throwing.

Irregularities in the growth plate at the tibial tuberosity can indicate Osgood-Schlatter disease, which is characterized by pain and swelling in the knee due to stress on the growth plate from activities such as running and jumping.

A slight irregularity in the calcaneal apophysis can be indicative of Sever's disease (calcaneal apophysitis), which is a common cause of heel pain in growing children, often related to physical activity.

Widening or irregularity at the growth plate around the elbow joint may suggest apophysitis, which can lead to pain and functional limitations in the affected arm, often due to repetitive stress or overuse.

Sinding Larsen Johansson disease is an inflammation of the proximal attachment of the patellar tendon to the inferior pole of the patella. It is caused by the pull of the patellar tendon on the patella, particularly in children engaged in running sports.

The common signs and symptoms include:

• Pain with point tenderness at the inferior pole of the patella
• Pain after or during activity

Diagnostic testing typically involves:

• Ruling out other knee pathologies
• Assessing sports history and tenderness at the inferior pole of the patella
• Knee radiographs may be performed, which can show a spur at the inferior pole of the patella, although they are not always required.

The treatment options include:

1. Activity modification
2. Relative rest
3. Maintenance of quadriceps strength within pain-free limits
4. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
5. Gradual return to sport

The prognosis is generally good:

• Symptoms may linger for months.
• Complete recovery occurs with the closure of the patella growth plate.
• There are no long-term implications associated with the condition.

Osgood-Schlatter disease is a common cause of anterior knee pain characterized by inflammation around the insertion of the patella tendon onto the tibial tuberosity. It often occurs during adolescent growth spurts and is prevalent in jumping sports.

The common signs and symptoms include:

• Pain and tenderness over the tibial tubercle
• Possible swelling in the area
• Pain typically occurs after physical activity
• Possible tightness in the quadriceps
• Possible sub talar pronation, which may be a predisposing factor (e.g., flat feet)

Osgood-Schlatter disease is most commonly seen in adolescents aged 10-15, with a higher incidence in boys than girls, particularly during growth spurts.

Diagnostic testing involves ruling out other knee pathologies through sports history and tenderness at the tibial tuberosity. X-rays are not typically indicated unless there is increased swelling that raises concern for a tumor.

1. Rest and activity modification
2. Ice application post-activity
3. NSAIDs for pain relief
4. Quadriceps and hamstring stretching
5. Patellar tendon strap/taping to offload the tibial tubercles

Symptoms may persist for up to 2 years but will typically resolve at the time of bony fusion of the tibial tubercle. There are no long-term implications associated with the condition.

Calcaneal apophysitis, also known as Sever's disease, is an inflammation of the growth plate in the heel (calcaneus) that commonly occurs during periods of rapid growth, particularly in children aged 10-12 years who participate in running sports or wear very flat shoes.

The signs and symptoms of calcaneal apophysitis include:

• Localised tenderness and swelling at the site of the insertion of the Achilles tendon
• Tight calf muscles

Diagnostic testing for calcaneal apophysitis includes:

• Palpation of the affected area
• Assessment of joint range of motion (ROM)
• A history of symptoms
• X-ray is not indicated unless symptoms persist.

1. Activity modification
2. Calf stretching and strengthening
3. Use of wedges or heel cups gel insoles to prevent stretching to heel in running
4. Supportive shoes
5. Ice post activity

Sever's disease can last up to 2 years and will stop when growth stops. There are no long-term implications associated with the condition.

Children aged 6-15 years are typically affected by medial apophysitis of the humerus.

Common signs and symptoms include:

• Localized tenderness and swelling at the medial epicondyle
• Pain with valgus stress

Diagnostic testing includes:

• Palpation of the joint
• Range of motion (ROM) history
• X-ray is not indicated unless symptoms persist

A common condition associated with medial apophysitis in young athletes is Little League elbow, which occurs in throwing sports.

1. Activity modification: Rest and refrain from overhead activities.
2. Ice post activity: Use NSAIDs for pain relief.
3. Bracing: If severe, to prevent valgus force.
4. Prognosis: 1/3 return to sport; non-union and avulsion fractures may occur if the child continues sport with symptoms; condition resolves with growth plate closure.

Apophysitis is a condition characterized by inflammation of the growth plate (apophysis) where tendons attach to bones. It occurs due to:

• Weakness of bone: The area is more susceptible to injury during growth spurts.
• Tendon pull on bone: Repetitive stress from tendons can lead to inflammation.
• Resolution: The condition typically resolves when the growth plate ossifies, meaning it hardens and matures into bone.

The process of normal bony growth in long bones is called endochondral ossification.

In long bone development:

• Primary Ossification Center: The first area where bone starts to form, typically located in the diaphysis.
• Secondary Ossification Centers: Areas that develop later, usually located in the epiphyses, contributing to the growth of the bone after birth.

The cartilage template serves as a scaffold for bone development, allowing for the gradual replacement of cartilage with bone tissue during the process of endochondral ossification.

Injury to the physis can lead to:

• Increased blood flow
• Increased growth
• Altered growth patterns

Wolff's Law states that "Bones will ultimately achieve the shape and size that best fits their function." This principle highlights how bones adapt to the stresses placed upon them through physical activity and body weight.

Increased pressure stimulates growth at the physis, leading to enhanced bone development and adaptation to loading conditions.

Children's bones adapt to different mechanical stresses due to their growing bodies and changing functional abilities, leading to changes in bone structure and strength.

The healing progression of a bone fracture typically shows significant changes at various time points:

1. Day 1: Initial fracture with hematoma formation.
2. Day 4: Inflammation and early callus formation.
3. Day 7: Continued callus formation and early bone remodeling.
4. 2 Weeks: More organized callus and beginning of ossification.
5. 6 Months: Complete healing with restored bone integrity.

The comparison of bone structure between children and adults highlights several key differences:

The anatomical differences between adult and child bones include:

A greenstick fracture is a type of bone fracture where one side of the bone is broken while the other side remains intact, resembling the way a young tree branch bends and breaks. This differs from complete fractures, where the bone is broken all the way through, and from buckle fractures, which involve compression of the bone without a clear break.

Children's bones are softer and more flexible, leading to unique fracture patterns such as:

1. Greenstick fracture - partial break on one side of the bone.
2. Buckle fracture - compression of the bone causing it to bulge.
3. Plastic deformation - bending of the bone without a clear fracture.

These patterns are less common in adults due to the differences in bone structure and density.

The Salter-Harris classification is used to categorize physeal fractures based on their severity and the involvement of the growth plate in a bone.

The stages of physeal injury in a bone include:

1. Initial fracture
2. Increased blood flow
3. More bone formation in the injury
4. Altered shape of the bone

Monitoring for changes in bone shape is essential during recovery.

The exact aetiology of DDH is unknown, but it can be present at birth or develop over time. It is thought to be influenced by maternal oestrogen and relaxin crossing the placenta, which increases ligamentous laxity.

1. Physis - growth plate; ligaments are stronger than adjacent bone, making bone injuries more common.

2. Epiphysis - base of hyaline articular cartilage.

3. Apophysis - attachment of major muscle group to bone, considered a 'weak link'.