Varus deformity is an angulation of a bone or joint in which the distal segment tilts medially toward the midline of the body, resulting in an inward deviation from normal alignment.[1] This condition can affect various joints and bones, leading to abnormal limb posture and potential functional impairments if severe.[2]Common manifestations of varus deformity include genu varum (bowlegs) at the knee, where the knees remain apart when the ankles are together, often resolving spontaneously in young children but persisting or worsening in cases of underlying pathology.[3] Other notable types are coxa vara at the hip, characterized by a decreased neck-shaft angle; cubitus varus at the elbow, typically a complication of supracondylar fractures; and hallux varus at the first metatarsophalangeal joint of the foot, involving medial deviation of the great toe.[1] Ankle involvement may present as talipes varus, contributing to clubfoot deformities.[1] These deformities can be congenital or acquired, with the knee being the most frequently affected site in clinical practice.[2]Causes of varus deformity vary by location and age of onset but commonly include congenital factors such as skeletal dysplasias (e.g., achondroplasia), developmental anomalies, or intrauterine positioning in infants.[3] Acquired forms arise from trauma (e.g., fractures leading to malunion), infections (e.g., osteomyelitis), nutritional deficiencies like rickets due to vitamin D shortfall, metabolic disorders (e.g., Blount's disease in adolescents), or degenerative conditions such as osteoarthritis that unevenly load joint compartments.[2] In adults, biomechanical stresses or prior injuries can exacerbate varus alignment, particularly around the knee, shifting weight to the medial compartment and accelerating joint wear.[3]Symptoms often depend on severity and location but may encompass a painless limp, altered gait (e.g., waddling in bilateral knee varus), knee or hip pain, joint instability, reduced range of motion, and progressive arthritis in untreated cases.[3] Leg length discrepancies or shin splints can also occur with lower limb involvement.[2]Diagnosis typically involves clinical evaluation, including measurement of limb alignment during stance, supplemented by imaging such as standing X-rays or full-length radiographs to quantify the deformity angle.[3]Treatment is tailored to the etiology, degree of deformity, and patient age, with conservative approaches preferred initially for mild or physiologic cases. Observation suffices for infantile bowlegs that self-correct by age 2β3 years, while bracing or orthotics may address nutritional or early pathologic causes.[3] Surgical interventions, such as osteotomy (e.g., high tibial osteotomy to realign the knee) or guided growth procedures in children, are indicated for progressive or symptomatic deformities to restore mechanical axis, alleviate pain, and prevent complications like early osteoarthritis.[2]
Definition and Terminology
Definition
Varus deformity is characterized by an excessive medial angulation of the distal segment of a bone or joint relative to the body's midline, resulting in the distal portion pointing inward toward the midline.[4] This inward deviation contrasts with valgus deformity, which involves an excessive lateral angulation where the distal segment points outward away from the midline.[4]The condition can manifest at various anatomical sites, including major joints such as the knee or elbow, or involve specific bones like the tibia following fractures.[5] In these contexts, varus alignment alters the normal mechanical axis, often leading to abnormal positioning during weight-bearing activities.[5]Biomechanically, varus deformity shifts the load-bearing axis medially, which increases compressive forces on the inner (medial) compartments of affected joints while reducing loads on the outer (lateral) aspects. This redistribution of stress can contribute to accelerated wear in medial structures, such as cartilage and menisci, over time.
Terminology and Etymology
The term varus derives from Latin, where it originally denoted a condition of being "bent inward" or knock-kneed, referring to an outward angulation of the distal segment of the lower limb.[6] In ancient medical descriptions, such as those by the Roman physician Aulus Cornelius Celsus in the 1st century AD, varus was applied to what is now classified as valgus deformity (knock-knees), while valgus described bow-leggedness; this inverted usage relative to modern conventions arose from early linguistic and descriptive ambiguities in Latin texts.[7][8]The evolution of the term in medicine reflects broader historical shifts in orthopedic nomenclature. By the 19th and 20th centuries, standardization in English-language orthopedic literature reversed the ancient meanings, establishing varus to describe excessive medial (inward) angulation of the distal bone segment toward the body's midline, as seen in bow-legged alignment.[7] This convention, now universally adopted in orthopedics, resolved persistent confusions noted in dictionaries and early anatomical works, ensuring precise communication in clinical and surgical contexts.[8]Joint-specific variants of the term include genu varum for varus deformity at the kneejoint, characterized by medial angulation of the tibia relative to the femur, and coxa vara for similar inward deviation at the hip, where the femoral neck angles decrease below normal. These designations highlight distinctions between static bone or joint deformities and dynamic instabilities, such as varus thrust, which involves medial knee collapse during weight-bearing.In orthopedic specialties, varus deformity is categorized as an angular deformity within the coronal plane, encompassing both congenital and acquired forms addressed in pediatric and adult practices.[9] This classification aids in systematic evaluation and intervention, emphasizing the term's role in describing deviations from neutral alignment across the lower extremities.[10]
Anatomy and Pathophysiology
Normal Alignment
In normal lower limb alignment, the mechanical axis extends from the center of the femoral head through the center of the knee joint to the center of the ankle joint, typically passing near the medial compartment of the knee to facilitate even load distribution across the joint surfaces.[11] This alignment results in a tibiofemoral angle of approximately 5-7 degrees of valgus in adults, where the anatomic axis of the femur and tibia form a slight outward angulation at the knee, promoting balanced weight-bearing during gait and standing.[11]At the hip, the normal cervico-diaphyseal angle, also known as the neck-shaft angle, measures 120-135 degrees, allowing optimal positioning of the femoral head within the acetabulum for efficient force transmission from the trunk to the lower extremity.[12] In the knee, alignment evolves developmentally: infants exhibit physiologic varus up to 15 degrees at birth due to intrauterine positioning, which gradually resolves to neutral by age 2-3 years as the child grows, transitioning to the adult pattern of neutral to slight valgus.[13]The elbow maintains a normal carrying angle of 5-15 degrees valgus, formed by the long axis of the humerus and ulna in full extension, which positions the forearm laterally to avoid contact with the iliac crest during arm swing.[14] For the ankle and foot, neutralalignment is characterized by the tibia being perpendicular to the ground in the coronal plane, with the talus and calcaneus aligned to support the body's weight evenly across the hindfoot and forefoot.Biomechanically, this normal joint alignment ensures even distribution of compressive forces and shear stresses across articular surfaces and surrounding soft tissues, minimizing localized overload in any single compartment and supporting efficient locomotion without excessive strain on ligaments or cartilage.[15]
Pathological Mechanisms
Varus deformity arises from an altered mechanical axis of the lower limb, where the load-bearing line shifts medially relative to the kneejoint center. In varus deformity, the load-bearing line shifts further medially beyond the normal 4β8 mm medial position of the ground reaction force vector, increasing compressive forces on the medial tibiofemoral compartment by approximately 6β10% per degree of varus, corresponding to elevated knee adduction moments during gait, while simultaneously stretching the lateral capsular and ligamentous structures, leading to relative laxity on that side.[16]In pediatric cases, pathological mechanisms often involve disruption of the proximal tibial growth plate (physis), where asymmetric closure or inhibition of medial physeal overgrowth occurs due to excessive compressive forces or injury. This medial growth suppression, as seen in conditions like Blount disease, disrupts endochondral ossification and causes progressive angular deviation toward varus, with the medial physis experiencing delayed or arrested growth relative to the lateral side.[17][18]In adults, joint degeneration plays a central role, characterized by progressive cartilage loss in the medial compartment due to sustained overload, followed by subchondral bone remodeling and attrition that culminates in varus collapse. Bone remodeling manifests as medial tibial plateau flattening and sclerosis, exacerbating the deformity through a cycle of mechanical overload and structural failure.[19][16]Soft tissue alterations contribute significantly to the instability and progression of varus deformity, with medial structures such as the superficial medial collateral ligament and posterior oblique ligament undergoing contracture and tightening, while lateral soft tissues develop laxity. This imbalance promotes medial compartment compression and lateral subluxation, further destabilizing the joint.[20]The uneven stress distribution in varus deformity elevates medial compartment pressure, accelerating osteoarthritis through heightened knee adduction moments during gait, with each degree of varus increasing the odds of medial osteoarthritis progression by approximately 1.3-fold. The tibiofemoral angle, measured on anteroposterior radiographs as the angle between the femoral and tibial anatomic axes, normally averages 5β7Β° of valgus; values less than 3Β° of valgus indicate varus deformity and correlate with this pathological loading.[21][11]
Causes and Risk Factors
Congenital Causes
Congenital varus deformity encompasses a range of developmental anomalies present at birth that result in inward angulation of the lower extremities, primarily affecting the knee (genu varum) or foot (talipes varus). Physiologic genu varum represents the most common form, observed in nearly all infants due to fetal positioning in utero, where the legs assume a bowed posture to accommodate the confined space; this condition typically self-resolves spontaneously by 18 to 24 months of age as the child grows and weight-bearing aligns the limbs without requiring intervention.[22][23] In contrast, pathologic congenital variants arise from disrupted growth or structural development and persist beyond early childhood.Blount's disease, also known as tibia vara, is a developmental growth disorder of the medial proximal tibial physis that leads to progressive varus angulation of the tibia, often presenting bilaterally in toddlers under 3 years of age in its infantile form. This condition disrupts normal endochondral ossification, resulting in medial tibial beaking and metaphyseal irregularities, distinguishing it from physiologic bowing; the adolescent form emerges later (ages 10-15) and is typically unilateral, influenced by mechanical stresses on the growth plate. Infantile Blount's disease is rare, with prevalence not well-established in the general population, though higher rates have been reported in populations of African descent particularly for the adolescent form, with a female predominance of approximately 1.6:1.[23][24][25]Genetic syndromes frequently underlie congenital varus deformities through inherited disruptions in skeletal development. Achondroplasia, the most common form of skeletal dysplasia, is caused by a gain-of-function mutation in the FGFR3 gene and follows an autosomal dominant inheritance pattern with nearly complete penetrance; it manifests with rhizomelic shortening of the limbs and progressive genu varum due to disproportionate growth of the lower extremities. Similarly, metaphyseal chondrodysplasias, such as the Schmid type, result from mutations in the COL10A1 gene (also autosomal dominant) and feature irregular metaphyseal widening, coxa vara, and genu varum, leading to short stature and waddling gait. These dysplasias collectively account for a small but significant proportion of persistent varus cases in pediatric populations.[26][27]Intrauterine constraints can contribute to congenital varus deformities, particularly talipes equinovarus (clubfoot), where reduced fetal mobility leads to fixed inversion and adduction of the foot. Oligohydramnios, characterized by diminished amniotic fluid volume, restricts joint movement and increases the risk of talipes varus by up to 60-80%, while breech presentation further elevates this risk by 30-40% through abnormal uterine compression on the lower limbs. These positional factors affect approximately 1 in 1,000 live births for clubfoot overall, with varus components resolving less readily in constrained environments compared to physiologic knee bowing.[28][29]Overall, while physiologic genu varum is a common transient finding in young children under 2 yearsβresolving without sequelaeβpathologic congenital forms like Blount's disease or those tied to genetic syndromes remain rare, necessitating early differentiation through clinical and radiographic evaluation.[22][30]
Acquired Causes
Acquired causes of varus deformity arise from environmental, traumatic, degenerative, infectious, inflammatory, or iatrogenic factors occurring after birth, leading to progressive angular misalignment primarily in the lower extremities.[31] These etiologies contrast with congenital origins by involving modifiable or external influences that disrupt normal bone growth, joint loading, or structural integrity postnatally.Nutritional deficiencies, particularly vitamin D deficiency, can cause rickets, a condition characterized by defective mineralization of the growth plates, resulting in softened bones and varus bowing of the legs.[32] In rickets, inadequate vitamin D impairs calcium and phosphate absorption, leading to widened and irregular epiphyseal plates, especially at the distal femur and proximal tibia, which promotes medial angulation.[33] Historically, rickets was highly prevalent in industrialized nations before the widespread fortification of foods with vitamin D in the 1930s, with nutritional rickets remaining a significant public health issue in the United States until the late 1920s.[34]Trauma represents a key acquired cause, where post-fracture malunion, such as in the distal femur or tibia, heals in a varus position due to improper alignment during recovery.[35] Growth plate injuries, classified under the Salter-Harris system (particularly types III, IV, and V), can damage the physeal cartilage, leading to premature closure on one side and resultant angular deformity like varus.[36] For instance, a Salter-Harris V fracture of the proximal tibial metaphysis may cause asymmetric growth arrest, manifesting as progressive varus angulation over time.[36]Degenerative processes, notably osteoarthritis in adults, contribute to varus deformity through uneven wear of the medial knee compartment, exacerbating medial joint space narrowing and varus alignment.[19] This progression is driven by increased mechanical stress on the medial tibiofemoral joint, often beginning after age 50, where varus malalignment correlates with accelerated cartilage loss and subchondral bone changes.[37] In osteoarthritic knees, varus alignment amplifies load distribution imbalances, promoting further deformity and functional impairment.[19]Infections and inflammatory conditions can induce varus deformity by damaging joint structures or growth plates. Septic arthritis or osteomyelitis in children may lead to physeal destruction, causing partial growth arrest and angular deformities such as varus.[38] In adults, rheumatoid arthritis rarely contributes to varus alignment through chronic synovial inflammation and bone erosion, though it more commonly results in other deformities; when present, it correlates with tibial bone loss and overall joint instability.[39]Iatrogenic causes occur as complications of prior interventions, such as overcorrection during valgus osteotomy for limb realignment, which can result in rebound varus deformity due to excessive medial shift or soft tissue imbalance.[40]Risk factors for acquired varus deformity, particularly in osteoarthritis-related cases, include obesity, which increases biomechanical load on the knee joint, thereby accelerating medial compartment stress and varus progression.[41] Female sex also elevates the risk, potentially due to hormonal influences, wider pelvic geometry, and higher rates of obesity, leading to greater susceptibility to varus malalignment in degenerative contexts.[42]
Clinical Presentation
Symptoms
Varus deformity manifests primarily through patient-reported symptoms that vary by the affected joint, severity, and age of onset, often involving pain, instability, and functional impairments.In the knee (genu varum), the most common site, patients frequently experience medial compartment pain that intensifies during weight-bearing activities such as walking or standing, described as an inner knee ache in adults due to increased stress on the medial joint structures. This pain is often exacerbated in degenerative cases associated with osteoarthritis, where varus alignment accelerates medial joint loading and cartilage wear.[21] A sensation of instability or "giving way" may occur, particularly during dynamic movements, resulting from varus thrust, which is linked to heightened knee symptoms during weight-bearing.[43]Functional limitations are prominent across varus deformities, including a waddling or awkward gait pattern due to altered biomechanics, difficulty with running or prolonged standing, and leg fatigue from compensatory muscle overuse.[22] In children, cosmetic concerns about leg appearance can lead to self-consciousness, while unilateral deformities may cause limping to offload the affected side.[3] Associated symptoms in advanced or degenerative presentations include joint swelling, morning stiffness, and audible crepitus during motion, reflecting underlying inflammation or cartilage degradation.Age-specific variations are notable; physiologic varus in infants and toddlers is typically asymptomatic, resolving naturally without discomfort by age 2-3 years.[31] However, in pathologic cases like untreated Blount's disease, progressive medial knee pain and instability emerge in late childhood or adolescence, worsening if unaddressed, often accompanied by knee discomfort during physical activity.[44]For ankle varus deformity, symptoms center on lateral foot and hindfoot pain from overload, with medial ankle gutter discomfort that may radiate proximally, alongside instability during uneven terrain due to peroneal tendon strain.[45]
Physical Examination Findings
Physical examination of varus deformity begins with visual inspection of the lower extremities while the patient stands with feet together and weight evenly distributed. In genu varum, a characteristic medial angulation at the knee is observed, resulting in an intercondylar gap between the knees when the ankles are approximated; this gap increases with severity and is typically symmetric in bilateral cases but asymmetric in unilateral presentations.[46][47]Gait analysis reveals dynamic instability, notably the varus thrust, where the knee demonstrates medial collapse or lateral bowing during the weight-bearing stance phase, often indicating posterolateral corner or lateral collateral ligament insufficiency. In hip varus (coxa vara), a Trendelenburg gait pattern may be evident, characterized by pelvic drop on the contralateral side during single-leg stance due to weak abductors.[48][49]Range of motion assessment typically shows limitations in knee flexion and extension secondary to joint contractures, with tenderness elicited upon medial palpation along the joint line. Alignment is quantified clinically using a goniometer to measure the tibiofemoral angle, where a varus deviation exceeding 5 degrees (compared to the normal 5-7 degrees of valgus) is considered pathologic in adults; the thigh-foot angle, normally 0-20 degrees of external rotation, helps evaluate associated tibial torsion. Associated findings include quadriceps muscle atrophy visible as reduced bulk compared to the contralateral side, and ligament laxity assessed via varus stress testing at 0 and 30 degrees of knee flexion, where increased lateral gapping suggests lateral collateral ligament compromise.[50][48]
Diagnosis
Clinical Assessment
The clinical assessment of varus deformity initiates with a thorough patient history to elucidate the onset, which is typically gradual in physiologic or developmental cases but may be acute following trauma or infection.[51] Family history is systematically reviewed to detect hereditary patterns, such as those associated with genetic syndromes including skeletal dysplasias like achondroplasia or pseudoachondroplasia, which can contribute to varus alignment abnormalities.[22] Nutritional status is evaluated concurrently, with particular attention to deficiencies in vitamin D or calcium that heighten the risk of rickets, a metabolic condition leading to varus deformities through impaired bone mineralization.[18]Age plays a pivotal role in interpretation; physiologic varus alignment is common in children younger than 2 years, often resolving spontaneously as the lower limbs shift toward neutral or valgus by age 3 to 4, but persistence beyond this period or worsening deformity warrants pathologic consideration.[51] In adults, varus often emerges later due to degenerative processes or prior injuries, with progression tracked through serial clinical examinations to monitor alignment changes and functional impact over time.[10]Differential diagnosis during assessment aims to exclude alternative angular deformities such as genu valgum, rotational malalignments like tibial torsion, or neuromuscular etiologies including cerebral palsy, which may mimic or coexist with varus.[47]Screening tools enhance the evaluation; in pediatric cases, particularly for suspected Blount disease, standardized growth charts such as CDC stature-for-age percentiles are utilized to correlate varus severity with overall development and obesity risk, as excessive weight can exacerbate medial tibial compression.[51] For adults with varus-related osteoarthritis, patient-reported functional questionnaires like the Knee Injury and Osteoarthritis Outcome Score (KOOS) assess pain, symptoms, and activity limitations to quantify disease burden.[52]Multidisciplinary input is integral, with referrals to orthopedic specialists for deformity analysis and to endocrinologists for investigation of underlying metabolic causes such as rickets or other bone disorders.[18] Physical examination findings, such as medial knee prominence or gait deviations, inform this process but are integrated holistically without standalone emphasis.[47]
Imaging and Diagnostic Tests
Diagnosis of varus deformity primarily relies on radiographic imaging to confirm the presence and quantify the extent of angular deviation in the lower extremity. Weight-bearing anteroposterior (AP) radiographs of the full lower limb are the cornerstone for assessing mechanical axis deviation, allowing visualization of the overall alignment from the hip to the ankle. These images enable measurement of the anatomic tibiofemoral angle, normally approximately 6Β° of valgus; varus alignment is indicated when this angle is 0Β° or less (i.e., neutral or varus).[53] In cases of suspected Blount's disease, the metaphyseal-diaphyseal angle, measured on AP views of the proximal tibia, exceeding 11 degrees suggests pathological tibia vara rather than physiologic bowing.[54]Advanced imaging modalities complement plain radiographs when soft tissue involvement or complex bony abnormalities are suspected. Magnetic resonance imaging (MRI) is particularly valuable for evaluating ligamentous integrity, cartilage damage, and physeal bar formation in conditions like Blount's disease, providing detailed assessment of the medial collateral ligament and medial compartment degeneration.[55] Computed tomography (CT) scans offer three-dimensional reconstruction for precise evaluation of rotational and coronal alignment in complex deformities, aiding in preoperative planning for corrective osteotomies.[56]Bone scintigraphy, or bone scans, is employed to investigate underlying etiologies such as infection or neoplastic processes contributing to varus deformity, revealing areas of increased uptake indicative of metabolic activity or inflammation.[57] Quantitative metrics derived from full-leg standing radiographs, such as the hip-knee-ankle (HKA) angle, further characterize the deformity; a normal HKA angle is approximately 0 degrees, with varus defined as less than -3 degrees, helping to determine the center of the knee joint relative to the mechanical axis.[58]Specific diagnostic criteria for Blount's disease utilize the LangenskiΓΆld staging system, based on progressive radiographic changes observed on AP and lateral knee views, including medial beaking of the metaphysis and physeal irregularities across six stages to guide treatment decisions.[59]
Treatment
Conservative Management
Conservative management of varus deformity focuses on non-invasive strategies to monitor progression, alleviate symptoms, or promote correction in mild or early cases, particularly in pediatric patients with physiologic bowing or early pathologic conditions like Blount's disease. These approaches are most effective when initiated promptly and tailored to the underlying etiology, such as nutritional deficiencies contributing to acquired varus.[18]Observation is the primary approach for physiologic genu varum in infants and toddlers under 2 years of age, as this bowing is a normal developmental variant that typically resolves spontaneously without intervention. Serial clinical examinations every 6-12 months are recommended until age 3 to track alignment and distinguish physiologic from pathologic progression, such as in rickets or Blount's disease. Radiographs are indicated only if there are signs of pathology, such as progressive deformity, asymmetry, or lack of improvement by age 2. In most cases, the tibiofemoral angle improves naturally by age 2-3, with physiologic genu varum resolving spontaneously in nearly all (over 95%) cases with observation alone by age 3-4, and parental reassurance emphasizing the benign nature of the condition.[60][23][61][62]Bracing and splinting are indicated for early pathologic varus, such as LangenskiΓΆld stages I-II of Blount's disease in children under 3 years, using knee-ankle-foot orthoses (KAFO) to unload the medial proximal tibia and promote symmetric growth. These devices, often worn full-time initially and transitioned to nighttime use, incorporate pelvic bands to control rotation and are most successful in non-obese patients. For isolated hallux varus, custom night splints can maintain alignment and prevent progression in mild cases. Compliance is critical, with regular adjustments to accommodate growth.[63][18][64]Physical therapy plays a supportive role in managing symptoms and improving biomechanics, particularly for acquired varus in adolescents or adults with osteoarthritis. Programs emphasize quadriceps and hamstring strengthening exercises, such as straight-leg raises and hamstring curls, alongside gait training to reduce medial compartment loading and enhance knee stability. Stretching of hip external rotators and adductors can address compensatory patterns, with evidence showing reduced pain and improved function after 8-12 weeks of supervised sessions. These interventions are often combined with home exercises for sustained benefits.[65][66][67]Medical management targets reversible causes, such as nutritional deficiencies leading to rickets-associated varus, with vitamin D and calcium supplementation to restore bone mineralization and support deformity correction. In obesity-related varus knee osteoarthritis, structured weight loss programsβaiming for 5-10% body weight reduction through diet and low-impact exerciseβalleviate joint stress and slow progression. Referral to endocrinologists or metabolic specialists is advised for underlying metabolic disorders.[60][68][69]Success rates vary by etiology and severity; physiologic genu varum resolves in nearly all cases with observation alone by age 3-4. Bracing achieves correction in 50-90% of early infantile Blount's disease when started before age 3, though efficacy drops below 30% in severe or late-stage cases. Physical therapy and medical interventions yield symptom relief in 60-80% of mild osteoarthritis-related varus, with greater improvements tied to adherence and weight management.[61][64][63]
Surgical Options
Surgical options are considered for varus deformity when conservative measures fail to correct persistent or severe alignment issues, particularly in cases involving joint degeneration or growth disturbances. These interventions aim to restore mechanical alignment, alleviate pain, and prevent further deterioration, with selection based on patient age, deformity severity, and location (e.g., knee, ankle, or foot). Common procedures include osteotomies for angular correction in the knee, guided growth techniques in children, joint replacement in older adults, and soft tissue balancing for lower extremity varus.[70]High tibial osteotomy (HTO) is a primary surgical approach for knee varus deformity, typically indicated for patients under 60 years with medial compartment osteoarthritis and varus alignment exceeding 10 degrees. The medial opening wedge technique involves creating a cut in the proximal tibia, opening the wedge to shift the mechanical axis laterally toward neutral (0 degrees), and stabilizing with a locking plate, often without bone grafting. Alternatively, the lateral closing wedge HTO removes a bone wedge from the lateral tibia to achieve similar realignment, though it may require fibular osteotomy. For deformities involving the femur, distal femoral osteotomy corrects varus by adjusting the distal femoral alignment, ensuring the overall lower limb mechanical axis passes through the knee center. These procedures unload the medial compartment, improving joint stability and function.[70][71]In growing children with conditions like Blount's disease, temporary hemiepiphysiodesis employs guided growth to correct varus by tethering one side of the proximal tibial physis. This minimally invasive procedure uses reversible implants such as eight-plate constructs or staples on the medial physis to slow growth there, allowing lateral overgrowth to gradually realign the knee toward neutral, typically over 12-18 months. It is suitable for patients under 10 years with mild to moderate deformity and significant growth remaining (e.g., Langenskiold stages I-II), avoiding the need for immediate osteotomy. Hardware removal follows correction to resume symmetric growth.[72][73]For adults over 60 with advanced arthritis and severe varus, total knee arthroplasty (TKA) provides comprehensive correction and joint resurfacing. The procedure involves selective posteromedial soft tissue releases, reduction osteotomy of the tibial flare, and preservation of the medial collateral ligament to achieve balanced alignment, shifting the tibiofemoral angle from profound varus (e.g., >20 degrees) to slight valgus (4-10 degrees). This restores knee stability, motion, and pain relief, with high success in patients with comorbid osteoarthritis.[74][75]Soft tissue procedures address varus in the foot and ankle, such as in clubfoot (congenital talipes equinovarus), where tendon transfers and releases correct residual deformities after initial casting. The split anterior tibial tendon transfer (SPLATT) reroutes part of the tibialis anterior to the lateral foot (e.g., cuboid) to counter supination and adduction, while Achilles tendon lengthening relieves equinus. Medial or plantar releases address fixed contractures, often combined in revision surgery for dynamic or residual varus. These are indicated for correctable deformities in children post-Ponseti method.[76][77]Outcomes for osteotomies demonstrate high patient satisfaction, ranging from 88% to 97% with good-to-excellent results, and joint survival rates of 95% at 10-12 years, effectively delaying arthroplasty. Complications occur in 10-15% of cases, including cortical hinge fractures (up to 29%), infections (2%), and non-union (1-5%), with reoperation rates around 10% for hardware issues or loss of correction. Epiphysiodesis achieves over 75% angular correction but carries a 30% reoperation risk for hardware adjustment. TKA yields Knee Society scores improving from 23 to 91 points, with low recurrence (1.7%), though profound varus increases technical demands. Soft tissue procedures for clubfoot result in 62% good-to-excellent outcomes, with 16% requiring further surgery. Preoperative imaging guides planning to optimize alignment.[70][78][79]
Specific Examples
Genu Varum
Genu varum, commonly known as bowlegs, is characterized by a varus deformity of the knee where the legs curve outward. This condition manifests as a common normal physiologic variant in infants under 2 years of age, typically resolving spontaneously by age 3-4 without intervention. Pathologic genu varum, however, is rare, occurring in a small percentage of persistent cases beyond this period, often due to underlying disorders such as Blount disease, leading to progressive deformity if untreated.[60][80][18]The pathophysiology of genu varum at the knee involves unique mechanisms centered on the proximal tibia, particularly in pathologic forms like Blount disease, where excessive compressive forces on the medial aspect inhibit growth of the proximal tibial physis. This leads to cartilage damage, delayed ossification, and progressive varus angulation as the lateral physis grows unchecked. In adults, varus alignment exceeding 5 degrees accelerates medial compartment osteoarthritis (OA) progression by increasing load on the medial knee, exacerbating cartilage loss and subchondral bone changes.[18][81]Diagnosis of pathologic genu varum relies on clinical assessment combined with radiographic evaluation, with the metaphyseal-diaphyseal angle (Drennan's angle) serving as a key metric; an angle greater than 11 degrees on anteroposterior knee radiographs indicates early Blount disease and differentiates it from physiologic bowing. Full-length standing radiographs measure the mechanicalaxis deviation, while advanced staging (e.g., LangenskiΓΆld classification) assesses physeal involvement.[82][23]Tailored treatment for genu varum varies by age and severity: in children under 4 years with early-stage Blount disease, knee-ankle-foot orthoses (KAFO) bracing can correct deformity by redistributing medial forces. For adolescents with progressive deformity, high tibial osteotomy realigns the mechanical axis, often combined with guided growth techniques. In adults with symptomatic medial OA, unicompartmental knee arthroplasty preserves bone stock and addresses isolated compartment degeneration effectively.[18][60][83]If untreated, pathologic genu varum leads to complications such as early medial compartment OA, typically manifesting 10-20 years post-onset due to chronic overload, resulting in pain, instability, and functional decline. Additional risks include limb length discrepancy and contralateral joint strain from compensatory gait alterations.[18][3][84]
Untreated varus deformity imposes uneven mechanical loads on affected joints, particularly accelerating osteoarthritis in the medial compartment of the knee. Varus alignment has been associated with a fourfold increased risk of medial tibiofemoral osteoarthritis progression compared to neutral alignment.[81] In severe cases of genu varum, the medial joint space narrowing and cartilage loss can lead to significant joint degeneration over time.[93]Functional impairments from varus deformity often manifest as chronic pain in the affected joint and surrounding areas, such as the hips, knees, and ankles, due to abnormal stress distribution. This pain can progress to reduced mobility and an awkward gait pattern, increasing the likelihood of falls and secondary musculoskeletal strain on the lower back and contralateral hip.[60] Persistent gait abnormalities further exacerbate compensatory overload on adjacent joints, potentially leading to broader lower extremity dysfunction.[94]In pediatric cases, varus deformity disrupts normal growth plate function, resulting in disturbances such as progressive worsening of the bowing and leg length discrepancy, especially if unilateral or associated with conditions like Blount disease. Contralateral limb compensation may also occur, where the unaffected leg develops adaptive deformities to maintain balance.[95] Failure to address these issues early can lead to permanent growth asymmetry and heightened risk of early-onset joint issues in adulthood.[18]Secondary complications arise from the altered biomechanics, including an elevated risk of fractures due to imbalanced loading; for instance, cubitus varus increases susceptibility to lateral condylar fractures of the distal humerus. Additionally, cubitus varus can lead to tardy ulnar nerve palsy due to chronic nerve compression.[96][97] Skin breakdown over bony prominences, such as the medial knee or ankle, can also develop from chronic pressure and friction in severe deformities.Surgical interventions for varus deformity correction, such as osteotomies, carry specific risks including postoperative infection rates of 2-5%, hardware failure leading to loss of correction, and overcorrection resulting in iatrogenic valgus alignment. These complications can necessitate revision surgery and prolong recovery.[98][99]
Prognosis
The prognosis of varus deformity varies significantly depending on its etiology, the patient's age at diagnosis, and the timeliness of intervention. In physiologic genu varum, which is a common variant in infants and toddlers, the deformity typically resolves spontaneously without treatment in the vast majority of cases by age 2 to 3 years, as lower limb alignment naturally corrects with growth and weight-bearing activities.[31] For early-stage infantile Blount's disease, bracing initiated before age 3 years in non-obese children with metaphyseal-diaphyseal angles less than 16 degrees achieves correction in up to 90% of cases, often within 12 to 24 months of consistent use.[100]In contrast, untreated varus deformity associated with adult knee osteoarthritis, particularly in severe cases with Kellgren-Lawrence grade 4 changes and varus alignment greater than 5 degrees, demonstrates rapid progression, with approximately 30% of patients requiring total knee arthroplasty within 1 year and a substantial proportion advancing to surgery within 10 years due to worsening pain and joint degeneration.[101] Late-stage Blount's disease, diagnosed after age 4 years, carries a poor prognosis with bracing failure in over 50% of cases, necessitating surgical intervention in nearly all instances to prevent permanent deformity and secondary osteoarthritis.[102]Key factors influencing outcomes include early diagnosis before age 4 years in pediatric cases, which markedly improves correction rates; adherence to orthotic regimens, where non-compliance doubles failure risk; and the absence of comorbidities such as obesity, which exacerbates progression by 2- to 3-fold through increased medial compartment loading.[100] Post-treatment follow-up with annual radiographic monitoring is essential, as recurrence rates after surgical correction range from 18% to 40%, particularly in younger children or those with residual growth potential.[103]Successful correction generally leads to favorable quality-of-life outcomes in pediatric patients, with many achieving full functional restoration and normal gait after bracing or early surgery for Blount's disease, minimizing long-term disability. In adults undergoing high tibial osteotomy for varus knee osteoarthritis, significant pain relief and high patient satisfaction are reported at 5-year follow-up, with many appropriately selected individuals delaying the need for arthroplasty.[104]