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What Is Causing My Hip Pain?


Understanding how your hip works

Your hip is one of the largest weight-bearing joints in your body. When it's working properly, it lets you walk, sit, bend, and turn without pain. To keep it moving smoothly, a complex network of bones, cartilage, muscles, ligaments, and tendons must all work in harmony.

The hip is a very stable ball-and-socket joint: A ball (femoral head) at the top of the thighbone (femur) fits into a rounded socket or cup-like cavity (acetabulum) in your pelvis. Bands of tissues called ligaments form a capsule connecting the ball to the socket and holding the bones in place.

A layer of smooth tissue called cartilage cushions the surface of the bones, helping the ball to rotate easily in the socket. Fluid-filled sacs (bursae) cushion the area where muscles or tendons glide across bone. The capsule surrounding the joint also has a lining (synovium) that secretes a clear liquid called synovial fluid. This fluid lubricates the joint, further reducing friction and making movement easier.

Injury or disease can damage your hip in several ways, resulting in a broken or deteriorated bone, irritated bursae, or worn cartilage. The most common cause of hip pain is osteoarthritis (OA). Other causes of hip pain include rheumatoid arthritis, osteoporosis, osteonecrosis (death of bone caused by insufficient blood supply), injury, infection, and bone tumors.

Osteoarthritis (OA)

The most common cause of hip pain is OA, a degenerative joint disease that causes the cartilage in your joints to break down. When that layer of cartilage—which is meant to cushion the joints and protect the surface of the bones—is damaged or worn away, your bones grind against one another, and that grinding hurts. You can feel it walking, sitting, or even lying down trying to sleep.


Rheumatoid arthritis


Traumatic arthritis/avascular necrosis

A serious hip injury or fracture can sometimes lead to a condition called avascular necrosis (osteonecrosis). In avascular necrosis, the blood supply to the ball portion (the femoral head) of the thighbone is cut off and the bone begins to wither. As a result, the surrounding cartilage begins to deteriorate, producing pain and other symptoms.


Age, disease, and being a woman increase your chances of fracturing a hip. Once you reach age 50, the odds increase significantly and double every five to six years thereafter. Falls are responsible for 90% of all hip fractures. A woman is two to three times more likely than a man to suffer a fractured hip. And the risk for women 5'8" or taller is twice that of women who are under 5'2".1


The bone in your hip is living tissue and is continuously being absorbed into your body and then replaced. When bone is no longer replaced as quickly as it is absorbed, the density or mass of the bone is reduced—resulting in porous bone, or osteoporosis. Osteoporosis causes the bone to become progressively weaker, increasing the risk that it may break. Bones begin to weaken with age, particularly among women. It’s estimated that osteoporosis, the disease that renders bones brittle and easy to break, affects more than 200 million women worldwide.2 With osteoporosis, your chances of breaking a bone in a fall increase dramatically.

The good news about arthritis and osteoporosis is that they can be treated. These are both diseases that typically worsen over the years, so it is common for treatment to involve more than one approach and to change over time. For some people, nonsurgical treatments such as lifestyle changes, medications, and walking aids help alleviate the pain. For others, correcting the alignment of the bones with an osteotomy restores normal function. And for many, hip replacement surgery may be the only long-term solution. You and your doctor can determine the best treatment options for you.


  1. Falls and Hip Fractures [Internet]. American Academy of Orthopaedic Surgeons; 2007 July [cited 2011 Nov 16]. Available from:
  2. Facts and statistics about osteoporosis and its impact [internet]. International Osteoporosis Foundation [updated 2011 Jan; cited 2011 Nov 16]. Available from: