What Is the Femoral Neck? Anatomy, Function, and Conditions

The femoral neck is the short, angled bridge of bone connecting the ball-shaped head of your femur (thighbone) to its main shaft. It sits just below the hip joint and plays an outsized role in transmitting your body weight from the pelvis to the legs every time you stand, walk, or climb stairs. Despite being only a few centimeters long, the femoral neck is one of the most clinically significant pieces of bone in the human skeleton, largely because its architecture, blood supply, and position make it vulnerable to fractures, blood flow disruptions, and structural abnormalities that affect millions of people each year.

Where It Sits and How It Is Oriented

If you picture the upper end of the thighbone, it looks a bit like a bent walking stick. The round femoral head sits inside the hip socket (acetabulum), and the femoral neck angles away from it, connecting down to the shaft and the greater trochanter, the bony bump you can feel on the outside of your hip. The angle between the neck and the shaft, sometimes called the neck-shaft angle, is typically around 125 to 135 degrees in adults. That angle matters because it determines how efficiently forces travel from the hip joint into the leg.

The neck also has a twist relative to the shaft. When viewed from above, it points slightly forward rather than straight to the side. This forward rotation is called femoral anteversion, and it describes the degree of torsion of the femur as a whole.¹ In most adults, anteversion falls somewhere around 10 to 15 degrees. Too much or too little twist can change how the knee tracks during walking and may predispose someone to hip problems or an unusual gait.

The Internal Scaffolding

From the outside, the femoral neck looks like a simple column. Inside, it is anything but. The interior is filled with an intricate lattice of thin bony struts called trabeculae, arranged along the lines of force that travel through the hip. Two main trabecular systems have been identified: a medial system with vertical struts running from the inner shaft wall up into the femoral head, and a lateral system formed by secondary struts that cross-brace the neck near the greater trochanter. Where these groups intersect in the femoral head and neck, they create a balanced mesh that handles both compressive and tensile loads.²

This internal scaffolding is more complex than older textbook diagrams suggest. Dissection studies have shown that the trabecular columns blend intimately with the outer shell of cortical bone, behaving more like a composite structure than two separate layers stacked on top of each other.³ One of the trabecular columns even spirals through the neck rather than running in a straight line, and its exact orientation varies considerably between individuals. That variability helps explain why two people with similar bone density can have very different fracture risks.

This trabecular system does not arrive fully formed at birth. The primary compression trabeculae, the ones that handle most of the weight-bearing load, are present in infants as young as four months. But the tension-side trabeculae do not appear in all children until around age four, and the secondary compression trabeculae take until about age six to become universal. The system reaches full maturity around age seven, with scores stabilizing at their highest values.⁴ This developmental timeline is one reason pediatric femoral neck fractures, while rare, behave differently from adult ones.

How the Neck Handles Mechanical Loads

Every step you take sends a pulse of force through the femoral neck. The way that force is shared between the hard outer shell (cortical bone) and the inner lattice (trabecular bone) shifts depending on exactly where along the neck you look and what you are doing. Near the femoral head, the trabecular bone carries most of the load. Moving toward the shaft, cortical bone takes over, eventually shouldering the vast majority of the stress. In normal standing, cortical bone handles roughly 88% of the load in the mid-to-lower neck region; during a sideways fall, that share drops to about 64%, meaning the trabecular bone suddenly has to absorb much more force than usual.⁵ This explains why weakened trabeculae from osteoporosis are so dangerous in a fall scenario: the internal scaffolding is being asked to do more work precisely when it is least able to.

The type of activity also changes where the highest strains land on the neck. Walking loads the femoral neck mostly through the hip flexor muscles. Stair climbing and jumping shift the action to the gluteal muscles, which generate higher strains along the front and top of the neck.⁶ That finding has practical implications: activities involving the glutes and higher ground reaction forces are more effective at loading the femoral neck in ways that may help slow bone loss. It is one of the reasons exercise programs for osteoporosis favor things like stair climbing and controlled jumping over gentle flat walking.

A Vulnerable Blood Supply

The femoral neck has a blood supply that is elegant but fragile. The femoral head gets its oxygen primarily from a network of small arteries that run along the neck’s surface inside thin tissue folds called retinacular vessels. The most important of these is the inferior retinacular artery, which originates from the medial femoral circumflex artery and travels within a small ligament on the back of the neck.⁷ Inside the femoral head, an epiphyseal arterial network is the most widely distributed blood supply structure, with more connections in the center of the head and fewer near the periphery.⁸

This arrangement is a problem when the neck fractures. A displaced fracture can shear or kink the retinacular arteries, cutting off blood to the head. In nondisplaced fractures, the inferior retinacular artery system remained intact in all cases examined in one cadaver and patient study; in more severely displaced fractures, it survived only about 60% of the time.⁸ When blood supply is lost, the bone tissue of the femoral head starts to die, a condition called avascular necrosis.

Avascular Necrosis

Avascular necrosis (AVN) of the femoral head is caused by disruption of the blood supply to the proximal femur, and femoral neck fractures are the most common traumatic trigger.⁹ But trauma is not the only cause. Long-term corticosteroid use and heavy alcohol consumption are the leading nontraumatic risk factors. In traumatic AVN, two factors matter most: whether the fracture was displaced and how much time passed between the injury and surgery.⁹ A second mechanism, called the tamponade effect, also plays a role: bleeding inside the joint capsule raises pressure, which can further compress the already damaged vessels and choke off what little flow remains.¹⁰

Early AVN may cause no symptoms at all, appearing only on MRI. As the dead bone collapses, the joint surface becomes irregular and painful, eventually leading to arthritis if untreated. Treatment ranges from core decompression (drilling into the bone to relieve pressure and encourage new blood vessel growth) to total hip replacement in advanced cases.

Femoral Neck Fractures

Hip fractures in older adults are overwhelmingly femoral neck or intertrochanteric fractures, and the femoral neck variety carries special challenges because of that precarious blood supply. Clinicians have traditionally classified femoral neck fractures using the Garden system, which grades them from undisplaced incomplete breaks (Grade I) through fully displaced fractures (Grade IV). In practice, though, the four-grade system has proven unreliable, with low agreement between doctors reading the same X-rays. Classification improves when surgeons simply label fractures as “displaced” or “nondisplaced.”¹¹ One study found interobserver agreement for the full four-grade system averaged only moderate, reinforcing the value of the simplified approach.¹²

The displaced-versus-nondisplaced distinction drives treatment decisions. A nondisplaced fracture in a healthy patient can often be pinned in place with screws (internal fixation), preserving the natural hip. A displaced fracture, especially in an older patient, is far more likely to fail with screws alone. In a randomized trial of patients over 70, internal fixation of displaced fractures had a 46% failure rate at ten years, compared with only about 9% for hip replacement.¹³ Another trial found that at four years, the complication rate was 4% with total hip replacement versus 42% with internal fixation in elderly patients with displaced fractures, and hip function was consistently better after replacement.¹⁴

The picture is less clear for middle-aged patients. In people aged 40 to 59, internal fixation carried higher odds of reoperation at both one and three years compared with total hip replacement, with the gap widening over time.¹⁵ But hip replacements have a finite lifespan, and a 45-year-old may outlive the implant and need revision surgery. This age group is where the hardest trade-offs live, and decision-making often depends on the specific fracture pattern, the patient’s activity level, and how good the remaining blood supply appears.

Stress Fractures of the Femoral Neck

Not all femoral neck fractures happen suddenly in a fall. Repetitive loading without adequate recovery time can produce stress fractures, most commonly in runners, military recruits, and other athletes who ramp up activity quickly. Femoral neck stress fractures come in three main types: compression-sided, tension-sided, and displaced.¹⁶ Compression-sided fractures, on the lower part of the neck, tend to be more stable and are usually managed with rest and activity modification. Tension-sided fractures, on the upper part, are more worrisome because they are at higher risk for complete displacement and typically need surgical fixation. A displaced stress fracture is a surgical emergency for the same reasons a displaced traumatic fracture is: the blood supply is in jeopardy.

The tricky part is diagnosis. Early femoral neck stress fractures may produce only vague groin or thigh pain that gets worse with weight-bearing activity. Plain X-rays can look normal for weeks. MRI is the gold standard for catching them early, and there is a strong argument that anyone with unexplained groin pain worsened by running or marching should get one sooner rather than later, because a stress fracture that progresses to full displacement dramatically changes the prognosis.

Cam Impingement and the Head-Neck Junction

The junction between the femoral head and neck is supposed to have a smooth, concave transition that allows the head to rotate freely inside the hip socket. In some people, an extra bump of bone develops at this junction, reducing the normal offset between head and neck. This creates what is known as cam-type femoroacetabular impingement (FAI). As the hip flexes and rotates, the bump jams against the rim of the socket, progressively shearing and damaging the cartilage lining.¹⁷

Cam morphology is present in roughly 15% to 25% of people who have no symptoms at all, and it is far more common in males.¹⁸ Quantitative imaging studies have shown that normal femoral heads can deviate up to about 2.5 mm from an ideal sphere, while cam-type hips show deviations of 4 to 5 mm.¹⁹ The cam deformity is thought to develop during adolescence when the growth plate at the head-neck junction is still active. High-impact sports during that window appear to promote extra bone formation in the area, though the exact mechanism is still being worked out. When cam impingement causes persistent pain, limited range of motion, or progressive cartilage damage, arthroscopic surgery to reshape the bump is a common treatment.

How the Femoral Neck Changes With Age and Sex

The femoral neck remodels throughout life, and the pattern differs between men and women. In young adults, men and women have similar cortical thickness and bone density in the neck after adjusting for body size. The key difference is geometric: the cortex in young men sits farther from the center of the neck, which gives it roughly 13% greater bending strength even at the same thickness.²⁰ With aging, both sexes lose bone on the inner surface (endocortical resorption) and add small amounts on the outer surface (periosteal expansion). Men add more on the outside, which keeps the cortex displaced outward and partially maintains bending strength. Women do not compensate as effectively, and the cortex thins faster.²⁰ In older adults, men’s femoral necks can be roughly 46% stronger in bending and 23% stronger under direct compression than women’s, even after accounting for body size.²¹ This is a big piece of why hip fracture rates are substantially higher in women.

The thinning is not uniform around the neck’s cross-section. The upper and rear portions of the cortex thin the most, while the lower portion actually thickens somewhat with age in both sexes, as if the bone is trying to shore up the area under the greatest compressive load.²² Overall, cortical thickness can drop to barely half its young-adult value in the oldest age groups, and the ratio of diameter to wall thickness rises steeply, making the neck behave more like a thin-walled tube vulnerable to buckling under side impacts.²³

Measuring Bone Density at the Femoral Neck

There is a reason the femoral neck is the standard site for measuring bone density. Its mix of cortical and trabecular bone makes it a good barometer for overall skeletal health, and fractures here have among the worst consequences of any osteoporotic fracture. A DXA scan of the femoral neck produces a T-score that compares your bone density to a healthy young adult reference. The WHO’s FRAX tool uses the femoral neck T-score, along with clinical risk factors like age, smoking, and family history, to estimate your ten-year probability of a major osteoporotic fracture.²⁴ ²⁵

But DXA has real limitations. It gives a two-dimensional projection that averages bone density across the entire cross-section, so it can miss the regional cortical thinning described above. Two people with the same T-score can have very different distributions of cortical thickness around the neck, and therefore very different actual fracture risks. Research comparing 3D measurements (via high-resolution CT) to standard 2D analysis in postmenopausal women found that three-dimensional imaging detected substantially lower trabecular bone volume and connectivity loss in hip fracture patients compared with controls, along with regional cortical thinning at the back and bottom of the neck that a flat DXA image would not distinguish.²⁶ These advanced imaging tools are still largely research instruments, but they point toward a future where fracture risk assessment goes beyond a single density number.

A Condition Unique to Growing Hips

In adolescents, the femoral head is still attached to the neck through a growth plate made of cartilage. In slipped capital femoral epiphysis (SCFE), the head slips off the neck along this growth plate, almost always sliding backward and downward. The condition is most common in overweight adolescents during growth spurts, and modeling work has shown that steeper physeal sloping angles and increasing body weight both raise the probability of slippage.²⁷ Treatment involves pinning the head in place with a screw. Even after fixation, the growth plate continues to be active: one study documented significant ongoing growth of the proximal femoral physis over a mean follow-up of about two and a half years after screw placement, with the neck-shaft angle decreasing by an average of about 6.5 degrees as the bone remodeled.²⁸ That continued growth means follow-up imaging is important to make sure the hardware remains in a good position.

What the Femoral Neck Tells Us About Walking Upright

The femoral neck is one of the most studied bones in paleoanthropology because its shape records how a creature walked. The oldest fossil evidence of distinctive hip mechanics adapted for upright walking comes from Orrorin tugenensis, about six million years old, whose femoral morphology shows it shared key biomechanical features with later hominins called australopiths. That hip design persisted for nearly four million years before modifications appeared with the emergence of early Homo.²⁹

Early hominins had femoral necks that were longer and set at a lower angle than ours. Both the internal trabecular pattern and the external shape of their necks indicate adaptation to higher side-to-side bending loads, consistent with a gait that involved more lateral sway over the standing leg than modern humans use. Their femoral heads were also proportionally smaller.³⁰ Over millions of years, the neck shortened, the angle steepened, and the head enlarged, all changes that reflect a progressively more energy-efficient stride. The modern human femoral neck, for all its fracture vulnerability, is the product of a long optimization for endurance walking and running on two legs.