The anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) are the core stabilizing structures of the knee joint: the ACL restricts anterior tibial translation and rotational instability, while the PCL limits posterior tibial displacement, critical for knee kinematics during weight-bearing and movement.

• Etiology: ACL injuries are most commonly caused by low-energy sports trauma (e.g., basketball, football, skiing, sudden deceleration or pivot movements), while PCL injuries typically result from high-energy trauma (e.g., traffic accidents, falls from height, direct posterior impact to the tibia). Combined ACL/PCL injuries often occur with multi-ligament knee damage.
• Clinical Manifestations: Acute injury presents with an audible pop, immediate hemarthrosis, severe pain, and loss of joint mobility. Chronic injury is characterized by recurrent knee instability, "giving way" during movement, reduced athletic performance, and secondary meniscal or cartilage damage.
• Diagnosis: Definitive diagnosis is made via physical examination (Lachman test, anterior/posterior drawer test, pivot shift test), with magnetic resonance imaging (MRI) as the gold standard for assessing ligament tear severity. X-rays are used to rule out associated fractures.

• Conservative Management: Indicated for partial-thickness tears without objective instability, low-demand elderly patients, or those with contraindications to surgery. Core interventions include rest, ice, compression, elevation (RICE protocol), brace immobilization, non-steroidal anti-inflammatory drugs (NSAIDs) for pain control, and structured rehabilitation to strengthen the quadriceps and hamstring muscles for compensatory stability.
• Surgical Treatment: The gold standard for complete tears, symptomatic instability, or high-demand patients is arthroscopic ligament reconstruction. Autografts (hamstring tendon, patellar tendon, quadriceps tendon) are the first-line graft choice, with allografts or synthetic ligaments used for select cases. Complex multi-ligament injuries require simultaneous reconstruction, and revision surgery is performed for failed primary procedures. Postoperative structured rehabilitation is critical for functional recovery.

The rotator cuff is a tendinous structure composed of 4 muscles (supraspinatus, infraspinatus, teres minor, subscapularis) that surround the glenohumeral joint, providing shoulder stability and enabling overhead movement and rotation. A rotator cuff tear refers to a partial or full-thickness rupture of one or more of these tendons.

• Etiology: The primary causes are age-related degenerative changes (reduced tendon vascularity in patients over 40), acute trauma (e.g., fall on an outstretched hand, heavy lifting), and chronic repetitive overhead motion (e.g., badminton, tennis, swimming, occupational overhead work).
• Clinical Manifestations: Core symptoms include persistent shoulder pain (worse at night and with overhead movement), weakness in shoulder abduction and external rotation, limited glenohumeral mobility, and muscle atrophy of the supraspinatus/infraspinatus in chronic massive tears.
• Diagnosis: Physical examination (Neer test, Hawkins-Kennedy test, Jobe empty can test) is used for initial screening, with MRI or magnetic resonance arthrography (MRA) as the gold standard for assessing tear size, location, and retraction. X-rays rule out glenohumeral osteoarthritis, acromial spurs, or fractures, and ultrasound allows dynamic evaluation of tendon function.

Treatment is stratified based on tear size, symptom severity, patient age, and functional demand:

• Conservative Management: First-line treatment for small, partial-thickness tears, asymptomatic tears, or low-demand elderly patients. Interventions include activity modification, physical therapy to strengthen rotator cuff and periscapular muscles, NSAIDs for pain control, corticosteroid or hyaluronic acid intra-articular injections, and cryotherapy.
• Surgical Treatment: Indicated for full-thickness tears with persistent symptoms despite conservative treatment, massive tears, acute traumatic tears in young active patients, or tears with progressive weakness and functional loss. The gold standard is arthroscopic rotator cuff repair, with techniques including single-row, double-row, and suture-bridge fixation. For massive, irreparable tears, patch augmentation, tendon transfer, or reverse total shoulder arthroplasty (rTSA) may be performed. Structured postoperative rehabilitation is essential for tendon healing and functional recovery.

Femoral head necrosis is a progressive orthopedic disease caused by interruption or impairment of the blood supply to the femoral head, leading to osteocyte and bone marrow necrosis, subsequent structural damage, femoral head collapse, and eventual glenohumeral joint dysfunction. It is the leading cause of total hip arthroplasty (THA) in young and middle-aged adults.

• Etiology: Classified into two main categories: traumatic FHN (caused by femoral neck fracture, hip dislocation, or hip trauma that disrupts the femoral head blood supply) and non-traumatic FHN (most commonly associated with long-term excessive alcohol intake, prolonged glucocorticoid use, decompression sickness, autoimmune diseases, and idiopathic cases).
• Clinical Manifestations: Early-stage FHN is often asymptomatic. As the disease progresses, patients develop deep groin or gluteal pain exacerbated by weight-bearing, limited hip internal rotation and abduction, and antalgic gait. End-stage disease with femoral head collapse presents with persistent rest pain, severe hip dysfunction, and disability.
• Diagnosis: MRI is the gold standard for early-stage diagnosis, with a sensitivity and specificity of nearly 100%. X-rays and CT scans are used for middle and late-stage assessment of femoral head collapse, subchondral fracture, and joint space narrowing. The Association Research Circulation Osseous (ARCO) staging system is the most widely used classification for disease severity.

• Conservative Management: Indicated for early-stage FHN (ARCO 1-2) with small necrotic lesions. Core interventions include risk factor modification (alcohol cessation, glucocorticoid discontinuation), protected weight-bearing, pharmacotherapy (bisphosphonates, anticoagulants, lipid-lowering agents), extracorporeal shock wave therapy (ESWT), hyperbaric oxygen therapy, and structured rehabilitation.
• Joint-Preserving Surgical Treatment: The first-line option for young and middle-aged patients with early to mid-stage FHN (ARCO 2-3) without femoral head collapse. Procedures include core decompression, vascularized bone grafting (e.g., free vascularized fibular graft), osteotomy, stem cell transplantation, and porous tantalum rod implantation. These procedures aim to improve femoral head perfusion, prevent collapse, and avoid or delay total hip replacement.
• End-Stage Surgical Treatment: Total hip arthroplasty (THA) is indicated for patients with femoral head collapse, joint space obliteration, severe pain, and functional disability (ARCO 3-4).

Osteoarthritis is the most common chronic degenerative joint disease, characterized by progressive articular cartilage degradation, subchondral bone sclerosis, osteophyte formation, and synovial inflammation. It primarily affects weight-bearing joints (knee, hip), as well as the hand and spine, and is the leading cause of disability in middle-aged and elderly adults globally.

• Etiology: The primary risk factor is advancing age, with additional contributing factors including obesity, joint trauma, genetic predisposition, excessive joint use, chronic inflammation, and mechanical malalignment.
• Clinical Manifestations: Core symptoms include joint pain exacerbated by activity, morning stiffness lasting less than 30 minutes, joint swelling, crepitus with movement, progressive range of motion limitation, and joint deformity in end-stage disease. Severe cases present with persistent rest pain and loss of functional independence.
• Diagnosis: Diagnosis is based on clinical symptoms, physical examination, and weight-bearing X-rays, with the Kellgren-Lawrence grading system used to classify radiographic severity. MRI is used to assess early cartilage damage, meniscal lesions, and synovial inflammation.

• Foundational Non-Pharmacological Therapy: The cornerstone of all OA treatment, including patient education, weight management, low-impact aerobic exercise and muscle strengthening therapy, physical therapy, assistive devices (e.g., knee braces, canes), and activity modification.
• Pharmacological Therapy: Used for symptom control when foundational therapy is insufficient. Interventions include topical NSAIDs (first-line for knee OA), oral NSAIDs, intra-articular corticosteroid or hyaluronic acid injections, and symptomatic slow-acting drugs for OA (SYSADOA, e.g., glucosamine, chondroitin sulfate).
• Surgical Treatment: Indicated for patients with severe symptoms, progressive functional decline, and end-stage radiographic OA refractory to conservative treatment. Procedures include arthroscopic debridement, osteotomy (joint-preserving surgery for malalignment in young patients), unicompartmental knee arthroplasty (UKA), and total knee/hip arthroplasty (TKA/THA).

Lumbar disc herniation is a common spinal disorder caused by rupture of the annulus fibrosus of the intervertebral disc, with protrusion of the nucleus pulposus compressing or irritating the adjacent nerve roots or cauda equina, resulting in a spectrum of clinical symptoms. Over 90% of cases occur at the L4-L5 and L5-S1 spinal levels.

• Etiology: Intervertebral disc degeneration is the fundamental underlying cause, with precipitating factors including acute trauma, chronic repetitive bending and weight-bearing, pregnancy, genetic predisposition, and poor spinal posture.
• Clinical Manifestations: Core symptoms include low back pain, radicular lower extremity pain (sciatica), numbness, and muscle weakness in the corresponding dermatomal distribution. Severe cases present with cauda equina syndrome, including bowel/bladder dysfunction, saddle anesthesia, and progressive lower extremity paralysis, a surgical emergency.
• Diagnosis: Diagnosis is based on clinical symptoms, physical examination (straight leg raise test, femoral nerve stretch test, sensory/motor/reflex assessment), with lumbar MRI as the gold standard for confirming the level, size, and location of herniation, as well as nerve root compression. CT scans are used to assess bony spinal structure, and X-rays evaluate spinal alignment and stability.

Over 80% of LDH patients achieve symptom relief with conservative management, with surgery reserved for refractory or severe cases:

• Conservative Management: The first-line treatment for all patients without absolute surgical indications. Core interventions include bed rest in the acute phase, NSAIDs, dehydrating agents, neurotrophic medications, physical therapy, lumbar traction, acupuncture, tuina massage, and structured rehabilitation to strengthen the core spinal muscles.
• Surgical Treatment: Absolute indications include cauda equina syndrome, progressive motor weakness, and bowel/bladder dysfunction. Relative indications include persistent and disabling symptoms refractory to 6 weeks of conservative treatment, and recurrent radicular pain. Minimally invasive procedures are the first-line surgical choice, including percutaneous endoscopic lumbar discectomy (PELD), microendoscopic discectomy (MED), and open laminotomy discectomy. Lumbar fusion surgery is performed for patients with concurrent spinal instability or recurrent herniation.

Lumbar spinal stenosis is a degenerative spinal disorder characterized by narrowing of the spinal canal, neural foramen, or lateral recess due to bony or fibrous hypertrophy, resulting in compression of the cauda equina or nerve roots. It is the leading cause of neurogenic claudication and low back pain in elderly adults.

• Etiology: The most common cause is age-related degenerative changes, including ligamentum flavum hypertrophy, facet joint hyperplasia and medial migration, intervertebral disc herniation, and posterior vertebral body osteophyte formation. Secondary causes include congenital spinal stenosis, spondylolisthesis, trauma, and postoperative epidural adhesions. Multi-level stenosis is common in elderly patients, with the L3-L4 and L4-L5 levels most frequently affected.
• Clinical Manifestations: The hallmark symptom is neurogenic intermittent claudication—lower extremity pain, numbness, and weakness that develops with walking and is relieved by rest, spinal flexion, or sitting. Additional symptoms include chronic low back pain, radicular leg pain, and in severe cases, bowel/bladder dysfunction and progressive lower extremity weakness.
• Diagnosis: Diagnosis is based on clinical symptoms, physical examination, and lumbar MRI, which is the gold standard for assessing the level and severity of canal stenosis, nerve root compression, and soft tissue pathology. CT scans are used to evaluate bony stenosis, and standing X-rays assess spinal alignment, stability, and spondylolisthesis.

• Conservative Management: Indicated for patients with mild to moderate symptoms, no progressive neurological deficit, and high surgical risk. Interventions include NSAIDs, neurotrophic medications, physical therapy, core muscle strengthening rehabilitation, epidural steroid injections, and activity modification.
• Surgical Treatment: Indicated for patients with disabling symptoms refractory to conservative treatment, progressive neurogenic claudication, neurological deficits, or bowel/bladder dysfunction. The primary goal is adequate spinal canal decompression with preservation of spinal stability. Minimally invasive procedures are the first-line choice, including unilateral biportal endoscopic (UBE) decompression, percutaneous endoscopic decompression, and microscopic decompression. Open decompression with fusion and instrumentation is performed for patients with concurrent spinal instability, spondylolisthesis, or deformity.

Scoliosis is a three-dimensional spinal deformity defined by a lateral curvature of the spine with vertebral rotation, with a Cobb angle of ≥10° on standing full-spine X-rays as the diagnostic threshold. It is classified into four main types: idiopathic scoliosis (the most common, accounting for 80% of cases), congenital scoliosis (caused by vertebral malformation), neuromuscular scoliosis (secondary to cerebral palsy, spinal muscular atrophy, etc.), and syndromic scoliosis (associated with genetic syndromes).

• Etiology: The cause of adolescent idiopathic scoliosis (AIS), the most common form, remains unclear, with genetic, hormonal, biomechanical, and neuromuscular factors implicated. Congenital scoliosis is caused by embryonic vertebral developmental anomalies, while neuromuscular and syndromic scoliosis are secondary to underlying systemic conditions.
• Clinical Manifestations: Early-stage scoliosis is often asymptomatic, presenting only with cosmetic abnormalities such as shoulder height asymmetry, thoracic asymmetry, waistline asymmetry, and a rib hump (razorback deformity) upon forward bending. Severe progressive scoliosis can lead to chronic back pain, restrictive pulmonary dysfunction, cardiac impairment, neurological deficits, and substantial psychological distress in adolescents.
• Diagnosis: Standing full-spine anteroposterior and lateral X-rays are the gold standard for diagnosis, with Cobb angle measurement to assess curve severity and progression risk. MRI is used to rule out intraspinal pathology (e.g., syringomyelia, tethered cord), and pulmonary function testing evaluates cardiopulmonary impact in severe curves.

• Conservative Management: Indicated for patients with a Cobb angle of 10-25° and remaining skeletal growth potential. Core interventions include regular radiographic follow-up, bracing (the only evidence-based non-surgical treatment to prevent curve progression), and structured rehabilitation (e.g., Schroth method), physical therapy, and core muscle strengthening.
• Surgical Treatment: Indicated for patients with a Cobb angle ≥40°, rapidly progressive curves, curves with neurological deficits, severe deformity with cardiopulmonary impairment, or unacceptable cosmetic deformity. The standard procedure is spinal deformity correction with posterior spinal fusion and instrumentation using pedicle screw systems, to correct the three-dimensional spinal deformity, restore spinal balance, and prevent curve progression. For young children with remaining growth potential, growth-friendly procedures (e.g., growing rods, magnetically controlled growing rods) are used to correct deformity while preserving spinal growth.

Bone tumors are neoplasms arising from bone tissue or its附属 structures (vessels, nerves, bone marrow, fat, etc.), classified into three main categories: benign bone tumors, primary malignant bone tumors (e.g., osteosarcoma, chondrosarcoma, Ewing sarcoma), and metastatic bone tumors (the most common malignant bone lesions, originating from primary cancers of the lung, breast, prostate, thyroid, and kidney).

• Etiology: The pathogenesis of most bone tumors remains unclear, with implicated risk factors including genetic mutations, hereditary syndromes, radiation exposure, chronic inflammation, and prior bone trauma.
• Epidemiology: Benign bone tumors are significantly more common than malignant tumors, with an excellent prognosis. Primary malignant bone tumors are rare, with an annual global incidence of approximately 3-5 per 1 million people, most commonly affecting children and adolescents (osteosarcoma peaks at age 10-20). Metastatic bone tumors are far more prevalent, affecting 30-40% of patients with advanced solid tumors, most commonly in middle-aged and elderly adults.
• Clinical Manifestations: Benign bone tumors are often asymptomatic, presenting only as a slow-growing painless mass, with rare pathological fractures. Malignant bone tumors are characterized by progressive local pain (worse at night), a rapidly growing soft tissue mass, swelling, pathological fractures, and systemic symptoms (weight loss, anemia, fever) in advanced disease. Metastatic bone tumors most commonly present with intractable bone pain, pathological fractures, hypercalcemia, and spinal cord compression.
• Diagnosis: Diagnosis requires a combined clinical-radiological-pathological approach. Imaging studies include X-rays, CT, MRI, whole-body bone scan (ECT), and PET-CT to assess tumor extent, local invasion, and systemic metastasis. Histopathological biopsy is the gold standard for definitive diagnosis and tumor classification.

Treatment is personalized based on tumor type, grade, stage, location, and patient age, with a multidisciplinary team (MDT) approach as the standard of care:

• Benign Bone Tumors: Asymptomatic lesions with no malignant potential are managed with regular follow-up. Symptomatic lesions, aggressive benign tumors, or those with malignant potential are treated with surgical curettage or en bloc resection with bone grafting, with a near 100% cure rate.
• Primary Malignant Bone Tumors: A multidisciplinary comprehensive treatment approach is standard. For osteosarcoma and Ewing sarcoma, the standard protocol is neoadjuvant chemotherapy followed by definitive surgery and adjuvant chemotherapy. Limb-salvage surgery is the first-line surgical option for over 90% of patients, with amputation reserved for advanced, unresectable tumors with neurovascular invasion. Radiotherapy, targeted therapy, and immunotherapy are used for select tumor subtypes and advanced disease.
• Metastatic Bone Tumors: Treatment is palliative and multidisciplinary, with the goals of relieving pain, preventing skeletal-related events (pathological fractures, spinal cord compression), improving quality of life, and prolonging survival. Interventions include treatment of the primary tumor, radiotherapy, chemotherapy, targeted therapy, immunotherapy, bone-modifying agents (bisphosphonates, denosumab), and palliative surgery (pathological fracture fixation, spinal cord decompression, tumor resection).