McCance CH 46 - Musculoskeletal Alterations & Bone Formation

• Musculoskeletal alterations in children can be congenital, hereditary, or acquired.
• Some disorders are acute with complete recovery, while others are chronic or terminal.
• Understanding the pathophysiology is crucial for providing optimal care.

Bone Formation

• Begins around the sixth week of gestation, involving delivery of bone cell precursors and their aggregation at ossification centers.
• Some precursors are in fetal connective tissues, others migrate via blood vessels.
• Cellular aggregation and maturation occur in two fetal tissues: mesenchyme and cartilage.

Intramembranous Bone Formation

• The cranium, facial bones, clavicles, and parts of the jawbone develop from mesenchyme, resulting in flatbones.
• Mesenchyme vascularizes, immature bone cells aggregate and mature into osteoblasts, forming ossification centers and osteoid.

Endochondral Bone Formation

• New bone is formed from cartilage.
• Mesenchymal tissue forms a cartilage anlage by 6 weeks' gestation, defining bone shape.
• Blood vessel invasion leads to primary calcification centers by 8 weeks.
• The perichondrium, a dense connective tissue layer, contains cells that develop into osteoblasts, forming a periosteal collar.
• Cartilage degenerates within the collar, capillaries invade, delivering osteoblast and osteoclast precursors.
• Ossification progresses from the primary center towards the ends.
• Secondary ossification centers (epiphyseal centers) develop at the ends.
• Ossification spreads until cartilage is replaced by bone.
• Articular cartilage and the physeal plate remain at the ends of long bones.
• The physeal plate retains the ability to form and calcify new cartilage until skeletal maturity (11-15 years in females, 15-18 in males).

Bone Growth

• Until adulthood, long bone length increases at the physeal plate through endochondral ossification.
• Cartilage cells multiply and enlarge on the epiphyseal side.
• Cartilage cells are destroyed and replaced by bone on the metaphyseal side.
• Compact bone is thicker where stress is maximal, usually in the middle of the shaft.
• The distal physis in areas such as the femur contributes 80% to the overall length, whereas the proximal physis at the hip contributes only 20%.
• Undulating patterns such as that of the distal femur, increase resistance to sheer force, but growth disturbance is highly likely if injured.
• The distal radius, with a flat smooth physis, is more resistant to injury.
• Bone diameter increases by deposition of new bone on the periosteal surface.
• Bone resorption occurs on the endosteal surface.
• Endosteal resorption increases the medullary cavity diameter.
• Factors affecting growth include growth hormone, peptide regulatory factors, cell interactions, extracellular matrix, nutrition, general health, and hormones.
• Skeletal dysplasias, like achondroplasia, occur when these factors are poorly controlled.
• Bone is constantly destroyed and re-formed, rapidly in children and slowly in adults.
• Peak bone mass is achieved in the mid-to-late twenties.
• Intake of calcium, phosphorus, weight-bearing exercises, and minimizing caffeine intake are important to avoid osteoporosis.
• Vitamin D levels are also crucial; insufficiency increases fracture incidence and severity.

Skeletal Development

• The axial skeleton changes shape with growth; the newborn spine is kyphosed.
• The cervical spine becomes lordotic with head control in the first 3 months.
• The lumbar spine develops a lordotic curve with sitting.
• The appendicular skeleton grows faster than the axial skeleton during childhood.
• Spine growth is 50% complete by age 1 and over 70% by age 8.
• Extremities undergo changes in rotation and alignment.
• Proximal femur is rotated forward up to 40 degrees in newborns, and tibia is rotated inward.
• Femur alignment normalizes by age 12.
• Tibial rotation neutralizes at age 8.
• Bowlegs and knock knees are normal at certain stages.
• Newborns have bowlegs due to in utero stresses.
• Genu varum (bowleg) peaks at 30 months.
• Genu valgum (knock knee) maximizes at 5-6 years.
• Persistent genu varum or valgum may indicate Blount disease, rickets, skeletal dysplasias, trauma, or infection.
• Genetic predisposition may also contribute to genu valgum.

Muscle Growth

• Fetal muscle tissue has high water content and intercellular matrix.
• After birth, muscle fibers enlarge by accumulating cytoplasm.
• Muscle nuclei increase 14 times in boys and 10 times in girls between birth and maturity.
• Muscle fibers reach maximal size at approximately 10 years in girls and 14 years in boys.
• Length growth occurs at muscle ends with increased nuclei.
• Fiber diameter increases with more fibrils. Fibrils themselves do not increase in diameter.
• Connective tissue grows at the tendon-muscle junction.
• Muscle growth is stimulated by separation of attachments during skeletal growth.
• Fiber length depends on intended range of movement.
• Tendon formation is stimulated by muscle pull on connective tissue.
• Paralysis of opposing muscles can lead to contracture.
• Muscle growth is a significant factor in adolescent weight gain.

Muscle Growth Pt.2

• Gender differences in muscle size are minor in childhood, but significant with puberty.
• Muscle accounts for 25% of infant body weight vs. 40% in adults.
• Lower limb muscles make up approximately 55% of adult muscle weight, while axial musculature predominates in infants.
• Respiratory and facial muscles are well developed at birth.
• Pelvic muscles develop over several years.
• Exercise increases skeletal muscle weight throughout life.

Syndactyly

• Syndactyly, or webbing of the fingers, is the most common congenital defect of the upper extremity.
• Simple webbing involves soft tissue only and is surgically released at 6 months to 1 year.
• Complex syndactyly involves fusion of bones and nails and may include absence or anomaly of bony or neurovascular units.
• Surgery aims for maximal function and appearance and is ideally performed at 1-2 years, before school.
• Vestigial tabs, such as an extra digit, are best removed in the neonatal period.
• Radial arm anomalies often associate with blood, heart, or kidney abnormalities.
• Ulnar-sided defects are less often associated with systemic anomalies and are extremely rare.

Developmental Dysplasia of the Hip (DDH)

• DDH involves abnormal development of the proximal femur, acetabulum, or both.
• Incidence of true hip dislocation or dislocatable hip is 1 in 1000 live births.
• Some degree of instability occurs in approximately 10 per 1000 live births.
• The left hip is affected in 60% of cases, the right in 20%, and bilateral DDH occurs 20% of the time.
• Risk factors include family history, female gender (6:1), metatarsus adductus (20%), torticollis (10%), oligohydramnios, first pregnancy, and breech presentation.
• Breech presentation accounts for possibly up to 40% of infants with DDH despite only 2% of births having a breech history.
• Maternal hormones increase joint laxity.
• DDH is more common in whites and cultures that swaddle infants with hips extended and adducted.
• It is almost unknown in African cultures where infants are carried with abducted legs.

DDH Pathophysiology

• The hip can be subluxated (partial contact), dislocated (no contact), or display acetabular dysplasia (shallow acetabulum).
• The subluxated hip maintains contact but is not well seated, with a dysplastic acetabulum and normal femur.
• The dislocatable hip is located but easily dislocated.
• The dislocated hip has no contact between the femoral head and acetabulum.
• Acetabular dysplasia is present in almost all cases.
• Hip dysplasia develops within the second and third trimesters, often due to breech positioning.
• There may be a genetic component.
• 2% of DDH cases are teratologic, caused by syndromes like arthrogryposis or spina bifida.

Untreated DDH

• DDH left untreated in children leads to secondary changes.
• Subluxation or dislocation leads to a shallow acetabulum and shortened soft tissues.
• Subluxation leads to early osteoarthritis (OA), accounting for possibly up to 60% of all OA of the hip.
• Dislocation causes the acetabulum to fill with soft tissue, forming a false acetabulum where the femoral head contacts the iliac crest.
• Limb length inequity and hip muscle weakness lead to a waddling gait.
• Back and hip pain develop in adulthood.
• Adult reconstruction is very difficult, even with an artificial hip.

Clinical Manifestations of DDH

• Asymmetry of gluteal or thigh folds
• Limb length discrepancy (Galeazzi sign)
• Limitation of hip abduction
• Positive Barlow maneuver (hip reduced, but dislocatable)
• Positive Ortolani sign (hip dislocated, but reducible)
• Positive Trendelenburg gait (waddling)
• Pain (very late)
• Examine for associated anomalies like torticollis or metatarsus adductus.
• Clinical examination is the most important diagnostic tool in newborns.
• Real-time ultrasound is valuable in newborns.
• Radiographs are used after age 6 months when the ossific nucleus of the femoral head appears.

DDH Evaluation and Treatment

• Treatment depends on the child's age, dysplasia severity, and duration.
• Earlier treatment yields better results.
• In children under 4-6 months, a Pavlik harness abducts and flexes the hip, remodeling the acetabulum.
• Up to 98% of children achieve excellent results with this treatment.
• A "closed" reduction followed by spica casting for up to 3 months can be done up to 12 months of age.
• After 12 months, surgical intervention, including opening the joint and realigning the femur and/or acetabulum, may be required.
• Good outcomes decrease with age.
• Up to 70% of children treated surgically after age 3 develop early osteoarthritis.
• Early intervention before age 1 improves outcome.
• Imaging studies (ultrasound) before 6 months are supported in infants with risk factors.

Congenital Foot Deformity

• Congenital foot deformity is found in approximately 4% of all newborns; metatarsus adductus accounts for 75% of these deformities.
• Metatarsus adductus is forefoot adduction with a normal hindfoot, believed to be from intrauterine positioning.
• It is associated with DDH in up to 20% of cases, so hips should be carefully evaluated.
• Metatarsus adductus is classified by flexibility (passively correctable vs. rigid) and deformity degree.
• The heel bisection line determines the deformity: mild (medial to 3rd toe), moderate (through 3rd or 4th toes), and severe (lateral to 4th toe).
• Serial casts are suggested for moderate to severe deformities during the first 6 months of life.
• 87% of children usually correct spontaneously by 6 years of age, and 95% by 15 years of age.
• Functional symptoms are rare even with residual deformity.

Clubfoot

• Clubfoot includes various foot deformities where the foot turns inward and downward.
• Technically called equinovarus, the heel is varus (inwardly deviated) and equinus (plantar flexed).
• Clubfoot can be positional (correctable passively), idiopathic, or teratologic (due to another syndrome).
• Positional equinovarus deformity lends itself to rapid correction by stretching or serial casts.
• Idiopathic variety is treated with weekly cast correction, Achilles tenotomy, and abduction bracing.
• Teratologic equinovarus deformities often require surgical correction or muscle-balancing procedures, or both.

Positional Equinovarus

• The foot is in equinovarus position but has flexibility without deep creases.
• The Achilles tendon is flexible; the foot can be passively brought to a plantigrade position.
• Conservative therapy corrects the foot without surgery or lengthy bracing.

Idiopathic Congenital Equinovarus

• The etiology of idiopathic equinovarus (clubfoot) is unknown.
• Human fetal studies show all clubfeet associated with anterior horn cell changes in L5 and S1.
• Muscle biopsies reveal decreased muscle fibers and/or abnormal fiber histology in at least 50% of cases.
• Genetics is unclear and studies are ongoing.
• Idiopathic equinovarus is also known as Clubfoot, occurs in about 0.3 to 7.8 per 1000 newborns.
• Males are affected twice as often as females.
• Since 1998 the casting technique developed by Ignacio Ponseti has been used.
• The technique involves six to eight above-knee casts, left on for 5 to 7 days each, followed by Achilles lengthening.
• Special braces are used at night until 3 to 4 years of age, requiring strict adherence.
• Around the age of 3, up to 30% of children may need anterior tibialis transfer.
• Ponseti techniques show better long-term results than operative posteromedial release.

Ponseti Casting

• Ponseti casting involves toe-to-groin casts changed weekly for 6 weeks.
• Casting begins as early as possible after birth, culminating in percutaneous Achilles lengthening, followed by a final cast for 3 weeks.
• In recalcitrant cases, a full surgical posteromedial release (PMR) still may be required.
• The need for PMR in idiopathic clubfoot has decreased when this casting technique is used.
• Long-term flexibility is better with Ponseti casting than with PMR.

Teratologic Equinovarus

• The most common causes of Teratologic Equinovarus are neuromuscular (spina bifida) or syndromic (arthrogryposis).
• Teratologic clubfoot fails to be corrected with Ponseti casting and may require operative intervention.
• The surgery is often more extensive than for idiopathic clubfoot, and revision surgery is also more common.

Pes Planus (Flatfoot) Deformity

• Most babies are born with flat (or "fat") feet, with the arch becoming more apparent with age.
• Diagnosing possible occult Achilles contracture is done by holding the hindfoot in varus position when dorsiflexing the ankle.
• Evaluation of the hindfoot by having the child stand on his or her toes, reveals that in flexible pes planus, the hindfoot swings into a varus position as the planter fascia tightens in toe raise.
• In rigid pes planus, the hindfoot stays in valgus.
• Custom orthotics, Helfet heel cups, and corrective orthopedic shoes do not have any influence over the natural history. Surgical or orthotic treatment of asymptomatic flexible pes planus is unnecessary.

Subset of Children with Painful, Flexible Flat Feet

• Occult Achilles contracture or tarsal coalition must me made in this subset of children
• Inexpensive shoe inserts and careful monitoring are suggested
• Achillies contracture can by surgically lengthened
• This group of children is best treated with inexpensive shoe inserts and then expectantly watched.
• Calcaneal lengthening may be performed if the pain continues into adolescence.
• Rigid flat feet often involves a coalition that may be resected with surgery; heel cord contractures can also by lengthened surgically if stretching alone is inadequate
• If a foot is flat but nonpainful, treatment is not required.

Osteogenesis Imperfecta (OI)

• OI is a collagen-related bone dysplasia.
• Collagen is the main component of bone and blood vessels.
• The Sillence classification is based on inheritance models and clinical findings.
• Newer classifications identify the defective gene, protein, or mechanism.
• In the severest cases, the child is usually stillborn or dies soon after birth.
• The less severe forms may not become evident until the child begins to walk.
• The prevalence rate of the most common form is about 1 in 30,000.
• Inheritance is usually autosomal dominant but can be autosomal recessive.
• At least four syndromes are been identified with various clinical manifestations and prognoses.

OI Pathophysiology

• Errors in OI lie in the synthesis of collagen.
• Number of metabolic abnormalities are associated with OI.
• Some individuals have increased serum thyroxine levels, suggesting hyperthyroidism.

Clinical Manifestations of OI

• Classic clinical manifestations are osteoporosis, increased rate of fractures, bony deformation, triangular facies, vascular weakness (i.e., aortic aneurysm), possible blue sclerae, and poor dentition.
• Sillence classificatio, designated types I through IV, are based on severity.
• Types II and III are most severe, can cause stillbirth or severe neonatal deformity, and have a short life expectancy.
• Type I is slightly more common than types II and III, and type IV is quite rare.
• Types I and IV vary onset from birth to adulthood.
• Type IV, especially when the sclerae are white, is the least deforming

Evaluation and Treatment of OI

• Evaluation is primarily on clinical manifestations.
• Serum alkaline phosphatase level is elevated in all forms of the disease.
• May be prenatally diagnosed by ultrasound or chorionic villi sampling
• Genetic disorders and inherited traits are diagnosed though electrophoresis.
• For other types of OI, careful positioning and handling of the newborn help prevent fractures.
• Beyond the neonatal period, various orthopedic measures are applied, such as prompt splinting of fractures and intramedullary rodding of the bones.
• Scoliosis can be present and often requires surgery.
• Bisphosphonate therapy showed improvements of bone density; however, may interfere with healing after surgery.

Rickets

• The disorder in which the bone fails to become mineralized (ossified).
• Results in "soft" bones and skeletal deformity.
• Most common form is X-linked hypophospatemic rickets in industrialized nations.
• Insufficient Vitamin D, over reliance on sunscreen, poor nutrition, and metabolic conditions are causes of metabolic rickets.
• Severe metabolic rickets in the immature skeleton leads to short stature; bowing of the limbs; and broad, irregular growth plates.
• Medical management of calcium, phosporous, and vitamin D levels must be optimized before surgical intervention.

Scoliosis

• Scoliosis is a rotational curvature of the spine most obvious in the AnteroPosterior plane
• May be classified as NonStructural and Structural
• Nonstructural scoliosis results from: posture; leg length discrepancy; or pain.
• Structural scoliosis results from: congenital scoliosis; neuromuscular disease; trauma.
• Most cases of structural scoliosis have no known cause
• Idiopathic scoliosis is classified as infantile, juvenile, or adolescent, depending on the child’s age at the time of onset.

Scoliosis Pathophysiology

• In individuals with adolescent idiopathic scoliosis, there may be an abnormality of the central nervous system involving the balance mechanism (reticular system) in the midbrain
• Earliest pathologic changes occur in the soft tissues.
• The curves increase most rapidly during periods of rapid skeletal growth.
• In curves greater than 50 degrees, the spine is biomechanically unstable, and the curve progresses even after the cessation of growth.
• Curves in the thoracic spine greater than 80 degrees result in decreased pulmonary function. The most common complication of large curves in the lumbar spine is back pain.

Clinical Manifestations of Scoliosis

• Nonstructural scoliosis is: mild spinal curvature with prominence of one hip or rounded shoulders
• Structural scoliosis includes: asymmetry of hip height; asymmetry of shoulder height; shoulder and scapular (shoulder blade) prominence; and rib prominence

Evaluation and Treatment of Scoliosis

• Diagnosis is made by roentgenographic examinations.
• Brace treatment is indicated for children with curves of 25 to 40 degrees who have at least 2 years of growth remaining.
• Braces will only prevent progression of the curve; it will not correct the curvature.
• Surgical treatment using spinal fusion with instrumentation is recommended for curves greater than 40 to 50 degrees.

Osteomyelitis

• Osteomyelitis is an infection of the bone
• Occurs twice as often in males as females.
• Occurs most often between 3 and 12 years of age.
• Bacteria enters the bone through the bloodstream and lodge in the medullary cavity.
• In some cases, the bacteria may lodge at the end of the venous loops beneath the epiphyseal plate

Causative Microorganisms of Osteomyelitis

• Newborns: Staphylococcus aureus; Group B Streptococcus; Gram-negative enteric rods.
• Infants: S. aureus (MRSA 70, MRSA 30); Haemophilus influenzae.
• Older Children: Staphylococcus aureus; Pseudomonas; Salmonella; Neisseria gonorrhoeae.
• Adolescents and Adults: Pseudomonas; Mycobacterium tuberculosis.
• Factors that predispose an individual to the can be as simple as breaking the skin through such things as: impentigo; chicken pocks; drug addiction; and injury to the area.

Pathophysiology of Osteomyelitis

• Usually begins as a bloody abscess in the metaphysis of the bone.
• Abscess ruptures under the periosteum and spreads along the bone shaft or into the bone marrow cavity if untreated.
• The periosteum may separate and form a shell of new bone around the infected portion of the shaft.
• Sections of the bone die which are called sequestra.
• The periosteum that maintains a blood supply generates new bone called the involucrum.
• Accumulation of debris caused by the infection can cause disruption between bones
• Osteomyelitis and septic arthritis in combination happens higher than 50% of the time.

Clinical Manifestiations of Osteomyelitis

• Clinical manifestations are age dependent.
• Three Types: Infants younger than 1 year; Children from 1 year of age to puberty; Adolescents after cessation of Bone Growth and Adults.
• Infants: May be characterized by fever and failure to move the affected limb (pseudoparalysis). Involvement of the adjacent growth plate can result in growth arrest.
• Children: characterized by fever and systemic signs of toxicity. Level of C-reactive protein (CRP) is elevated.
• Adolescents and Adults: may involve the vertebrae. Infection may develop in any part of a bone, and abscesses spread slowly.

Evaluation and Treatment of Osteomyelitis

• Monitor erythrocyte sedimentation rates as an indication of response to management but can be delayed.
• Should be prescribed anitbiotics for 6 weeks
• Death is rare, but growth arrest and osseous necrosis is possible.

Rheumatologic Disorders

• The rheumatic diseases are a group of diverse conditions having in common the inflammation of connective tissues.
• Includes juvenile idiopathic arthritis (JIA), systemic lupus erythematosus, dermatomyositis, and progressive systemic sclerosis.
• Juvenile idiopathic arthritis (JIA) is the most common rheumatologic disorder in childhood.
• The basic pathophysiology of JIA is the same as that of adult RA.

JIA Differs From Adult RA

• Predominantly the large joints are affected.
• Subluxation and ankylosis of the cervical spine are common if the disease progresses.
• Joint pain may not be severe because of the adult type
• Treatment is aimed to control inflammaton and minimize deformity.

Avascular Diseases of the Bone

• Caused by insufficient blood supply to growing bones.
• The cause is unknown, but vascular impairment and trauma, coupled with an underlying developmental or genetic predisposition, have been identified as possible.

Legg-Calvé-Perthes (LCP) Disease

• LCP disease is presumably produced by recurrent interruption of the blood supply to the femoral head with ossification center first becoming necrotic then collapses, and is then gradually remodeled by live bone.
• Occurring in Children between 3-10 years with peak incidence at 6. Usually more common in males that females. In the initial stage the soft tissues of the hip are swollen and hyperemic, often with fluid present in the joint Joint space widens, and the joint capsule bulges

Clinical Manifestations of LCPD

In some children, pain may be absent or minimal. If pain is present, it is usually aggravated by activity and relieved by rest. Typical physical findings include spasm on inward rotation of the hip and a limitation of internal rotation flexion and abduction. An abnormal gait, termed a Trendelenburg gait or abductor lurch, is apparent. Recent studies have shown that girls, despite earlier skeletal maturity, do as well as boys.

Osgood-Schlatter Disease

• Osgood-Schlatter disease consists of tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia.
• Occurs most often in preadolescents and adolescents who participate in sports.
• Causes pain and swelling in the region of the patellar tendon and tibial tubercle.
• Sudden onset of pain can represent a pathologic fracture through an area of ischemic necrosis.
• The goal of treatment is to decrease the stress at the tubercle.

Cerebral Palsy (CP)

• CP is a general term that refers to nonprogressive disorders of movement and posture resulting from injury or malformation of the developing central nervous system.
• Overall incidence is 3% to 5%; this number has stayed approximately the same.
• The diagnosis of CP is often made after failure to meet gross motor milestones at predicted ages.
• Can also be treated with physical therapy.

Neuromuscular Disorders

• The disorders are a group of inherited disorders that cause progressive muscle fiber loss leading to weakness, mostly of the voluntary muscles.
• Duchenne muscular dystrophy (DMD) and spinal muscular atrophy (SMA) are the most prevalent muscle diseases.
• Increasing genetic testing is used for diagnosis/ classifications
• Current paradigms follow the traditional approach with respect to the clinical history, physical examination, and family history to narrow the differential diagnosis to one or a few disorders that can then be tested directly with a genetic test.

Duchenne Muscular Dystrophy (DMD)

• DMD is the most common of the muscular dystrophies, affecting approximately 1 in 3500 male births.
• DMD occurs primarily in boys because of an X-linked inheritance.
• Caused by deletion of one or more exons of the DMD gene on the X chromosome, or more rarely, by a nonsense mutation resulting in premature termination of translation.
• Lacking in DMD means poorly anchored fibers torn apart under repeated contraction
• Genetic counseling is recommended for all families who have children with DMD.
• Maintain function in unaffected muscle groups for as long as possible.
• An exon-skipping approach to gene modification was recently accepted as the first FDA-approved treatment for DMD.

Clinical Manifestions of DMD

• Identical at approximately 3- 4 years of age.
• Children develop gait abnormalities, including toe walking, difficulty getting up from the ground, and frequent falls.
• Muscular Weakness begins in the pelvic girdle.
• Can progressively lead to respiratory insuffiency, cardiomyopathy and orthopedic complications.

Spinal Muscular Atrophy (SMA)

• SMA is a common, autosomal recessive disorder characterized by degeneration of motor neurons in the spinal cord leading to progressive muscle atrophy.
• Children have progressive weakness and loss of motor skills.
• Caused by a mutation in the SMN1 gene.
• The severity of SMA is variable from the child never achieving sitting or never walking

Facioscapulohumeral Muscular Dystrophy (FSHD)

• Facescapulohumeral Muscular Dystreophy - mild form of progressive, autosomal dominant muscular dystrophy.
• Age at onset from early childhood to adult hood, and the disease affects males and females equally.
• Begins with weakness of face and shoulders and atrophy of facial and shoulder girdle.
• Is rare compared to the others in that manifests asymmetrically.

Benign Bone Tumors

• Make up a majority of childhood tumors.
• Includes: Nonossifying Fibroma, Osteochondroma, Simple Bone Cyst, Aneurysmal Bone Cyst, Osteoid Osteoma, and Fibrous Dysplasia.
• Nonossifying fibromas constitues 50% of benign bone tumors and not treated until after a Fracture.

Malignant Bone Tumors

• Osteosarcoma; Ewing Sarcoma- most common
• Less than 5% of tumors in children are bone.
• Osteosarcoma is the most common malignant bone tumor
• Most tumors araise in Knee.
• The treatment is surgery and multiagent Chemotherapy

Overview of musculoskeletal alterations in children, including congenital, hereditary, and acquired conditions. Focus on bone formation processes, including intramembranous and endochondral formation. Understanding these processes is crucial for optimal care.