Introduction
Developmental dysplasia of the hip develops when the hip joint does not form normally during fetal life or early infancy, leaving the ball of the femur and the socket of the pelvis poorly matched, unstable, or partially or fully displaced. The condition is not caused by a single event in most cases. Instead, it arises through a combination of biological and mechanical processes that interfere with normal hip development. The main influences include fetal positioning, inherited connective tissue traits, sex-related hormonal effects, family history, and other conditions that affect joint stability or fetal growth.
Biological Mechanisms Behind the Condition
The normal hip is a ball-and-socket joint. The femoral head should sit deeply within the acetabulum, and repeated movement during fetal development helps the socket deepen and the surrounding soft tissues mature. This development depends on a stable relationship between the two joint surfaces. When that relationship is disturbed, the socket may remain shallow, the cartilage may not mold properly, and the ligaments supporting the joint may be too loose to hold the femoral head in place.
One of the central mechanisms in developmental dysplasia of the hip is abnormal mechanical loading. The fetal hip responds to pressure and movement. If the femoral head is not centered in the socket, the acetabulum receives less of the normal shaping stimulus. As a result, the socket may remain underdeveloped. This can create a cycle in which instability leads to poorer joint shaping, and poorer shaping leads to more instability.
Another important mechanism is ligamentous laxity. The capsule and ligaments around the hip must provide enough restraint to keep the joint aligned while still allowing movement. If these structures are unusually loose, the femoral head can shift excessively. In newborns, the tissues may also be influenced by maternal and fetal hormones that temporarily increase laxity. This makes the joint more vulnerable to displacement during late pregnancy and after birth.
Cartilage and bone development are also affected. The acetabulum in early life contains a large amount of cartilage that gradually ossifies and deepens with normal contact and pressure. When the femoral head is not positioned correctly, the cartilage model may develop into a shallower socket. Over time, this anatomical mismatch becomes the structural basis of dysplasia.
Primary Causes of Developmental dysplasia of the hip
Breech positioning is one of the strongest associations with developmental dysplasia of the hip. In a breech presentation, the fetus is positioned with the buttocks or feet toward the birth canal rather than the head. This posture often leaves the hips flexed and the knees extended, which can place abnormal force on the developing joint. Because the hip is held in an unstable position for a prolonged period, the femoral head may not remain centered in the acetabulum. The socket then receives less of the shaping pressure needed for normal development, increasing the risk of dysplasia.
Female sex is another major factor. Girls are affected more often than boys, likely because of increased sensitivity of connective tissue to hormones such as relaxin and estrogen-related influences on ligament laxity. These hormonal effects may make the hip capsule more compliant, allowing greater movement of the femoral head. In a hip that is already vulnerable because of fetal positioning or genetic predisposition, this increased laxity can make instability more likely.
Family history strongly suggests a genetic contribution. Developmental dysplasia of the hip tends to run in families, indicating that inherited traits influence how the acetabulum forms and how tight or loose the supporting tissues are. Genes affecting collagen structure, connective tissue strength, and joint morphology may contribute to a hip that is shallower or less stable from the outset. Genetic influence does not usually cause the condition by itself, but it can lower the threshold at which mechanical stress produces dysplasia.
Firstborn status is another recognized contributor. In first pregnancies, the uterine environment may be relatively tighter, and the fetal hips may have less room to move freely. Limited intrauterine space can promote sustained hip flexion and adduction, increasing the chance that the femoral head will not remain centered. This does not create dysplasia directly, but it changes the mechanical environment in a way that favors instability.
Multiple gestation or crowded uterine conditions can have a similar effect. If there is reduced space in the uterus because of twins, fibroids, low amniotic fluid, or fetal size relative to the womb, the fetus may be constrained in positions that stress the hip. Prolonged constraint during critical periods of skeletal development can prevent the acetabulum from molding around the femoral head in the usual way.
Contributing Risk Factors
Several additional factors increase the likelihood of developmental dysplasia of the hip by altering fetal growth, connective tissue behavior, or postnatal joint stability. These are not always direct causes, but they modify the biological setting in which the hip develops.
Genetic influences extend beyond family history. Some children may inherit a combination of subtle anatomical traits, such as a shallow acetabulum or generalized joint laxity, that predispose the hip to instability. The condition may reflect polygenic inheritance, meaning that multiple genes each contribute a small amount to risk rather than one gene determining the outcome alone.
Hormonal changes during pregnancy also contribute. Maternal hormones such as relaxin and other pregnancy-related signals increase laxity in pelvic and connective tissues. This is adaptive for childbirth, but in the fetus it may also influence joint stability. If the hip capsule becomes too loose at the stage when the socket is supposed to deepen, the femoral head may shift repeatedly and fail to guide normal socket formation.
Environmental and positional factors matter because the fetal hip is highly sensitive to mechanical forces. Swaddling practices that keep the legs tightly extended and adducted after birth can worsen an already unstable hip by reducing the flexed, abducted position that helps maintain centering of the femoral head. While this is not the original cause in many infants, it can influence whether a mild instability persists and becomes a more established dysplasia.
Low amniotic fluid, uterine constraint, or abnormal fetal positioning can expose the hip to prolonged deformation. These conditions reduce the space available for normal movement, which limits the stimulus needed for proper acetabular development. Infections are not a common direct cause of developmental dysplasia of the hip, but severe fetal illness or conditions that restrict growth may indirectly alter intrauterine mechanics and tissue development.
Generalized connective tissue disorders can increase risk as well. When collagen or elastin is abnormal, the ligaments and joint capsule may be more compliant than normal, allowing the femoral head to slip more easily from the socket. This increased mobility becomes problematic during the period when the joint depends on stable contact for normal shaping.
How Multiple Factors May Interact
Developmental dysplasia of the hip usually develops through the interaction of more than one influence. A fetus with a genetic tendency toward ligament laxity may have a hip that is already less stable. If that fetus is also in a breech position, the mechanical stress on the joint increases. Together, these factors can prevent the femoral head from remaining centered long enough for the acetabulum to deepen normally.
The interaction is best understood as a feedback loop. Instability reduces the normal pressure on the socket, which slows acetabular development. A shallower socket then offers even less containment, allowing more displacement. Over time, the relationship between the femoral head and acetabulum becomes progressively less normal. In this sense, the condition is both a developmental problem and a mechanical problem, with each reinforcing the other.
Hormonal laxity, positional constraint, and inherited tissue characteristics can all act at the same time. A small degree of instability may be harmless in isolation, but if it occurs during a period of rapid skeletal growth or in the presence of restricted intrauterine space, it becomes more likely to produce permanent dysplasia. This is why the same exposure does not cause the condition in every infant; the outcome depends on the full biological context.
Variations in Causes Between Individuals
The causes of developmental dysplasia of the hip vary because the condition reflects the balance between anatomy, biology, and mechanical forces in a particular individual. Some infants are born with relatively shallow acetabula due to inherited morphology, while others have normal structure but excessive laxity. In some cases, the main issue is fetal position; in others, the problem is a combination of minor influences that together exceed the hip’s ability to stabilize itself.
Genetics can determine how sensitive the joint is to stress. A child with a family tendency toward hypermobility may develop dysplasia after a relatively modest positional constraint, while another child with stronger connective tissue may not. Age also matters because the younger the child, the more the joint is shaped by ongoing movement and contact. The fetus and newborn are in a critical window when the hip is still forming its final structure.
Health status influences the body’s ability to grow normally. Conditions that affect fetal growth, muscle tone, or connective tissue integrity can change the mechanical forces acting on the joint. Environmental exposure adds another layer, particularly when postnatal positioning either supports or undermines stability. For this reason, developmental dysplasia of the hip can appear mild in one child and severe in another even when the same broad risk factor is present.
Conditions or Disorders That Can Lead to Developmental dysplasia of the hip
Several medical conditions may contribute to or resemble developmental dysplasia of the hip by altering the anatomy or stability of the joint. Generalized joint hypermobility is one of the most important. In disorders that affect connective tissue, the hip capsule and surrounding ligaments may be unusually elastic, making it harder for the femoral head to stay centered. Over time, repeated partial displacement can prevent normal acetabular molding.
Connective tissue disorders such as Ehlers-Danlos syndrome can weaken the structural framework that supports joint stability. If collagen is abnormal, the capsule and ligaments may stretch excessively under normal fetal forces. The hip is particularly vulnerable because it depends on a tight balance between mobility and containment during development.
Neuromuscular disorders may also contribute indirectly. If muscle tone is reduced, the muscles that help stabilize the hip may not maintain the femoral head in a centered position. When active stabilization is impaired, the joint relies more heavily on static structures such as the capsule and acetabulum, which may not be enough to ensure proper development.
Congenital postural abnormalities can create similar mechanical effects. Conditions that restrict fetal movement or alter limb posture can keep the hip in a persistently abnormal alignment. Since the developing socket responds to pressure and motion, prolonged abnormal posture can lead to underdevelopment of the acetabulum.
Conclusion
Developmental dysplasia of the hip arises when normal hip formation is disrupted by a combination of mechanical, genetic, hormonal, and positional influences. The core biological problem is failure of the femoral head and acetabulum to maintain the stable contact needed for proper joint molding. Breech position, female sex, family history, uterine constraint, and connective tissue laxity are among the most important contributors, but the condition often reflects multiple factors acting together.
Understanding these mechanisms explains why developmental dysplasia of the hip occurs. The condition is not simply a matter of a bone being out of place; it is a developmental failure in which early instability interferes with the shaping of the joint itself. The final anatomy is therefore the result of how the hip responded to its biological environment during a critical period of growth.