March/April 2008
Volume 3, Issue 2

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Osteoporosis and Vertebral Compression Fractures

An Original Contribution by Frank J.E. Falco, M.D.

Osteoporosis is the most common metabolic bone disease in the United States and is a chronic progressive disease that can affect almost the entire skeleton. It is characterized by low bone mass and bone weakening (Fig. 1) that increases the risk for bone fractures. Osteoporosis often does not become clinically evident until a complication occurs such as a bone fracture that can lead to severe pain, disability and a poor quality of life.

Figure 1: Normal bone structure (l) Abnormal bone structure low bone mass (r)

About 10 million people in the U.S. have osteoporosis and 14 to 18 million that have osteopenia – low bone mass. Osteoporosis affects 1 in every 3 women and 1 in every 8 men worldwide.

Osteoblasts are specialized cells that make bone and osteoclasts are unique cells that resorb bone. These cells are constantly remodeling the skeletal system with bone resorption followed by bone formation known as coupling. Osteoporosis occurs when there is a disruption in the coupling process that leads to a reduction in skeletal mass. During the post menopausal state bone loss is due to excessive osteoclast activity whereas the loss of osteoblasts leads to skeletal mass loss in the elderly.

Osteoporosis can be divided into primary and secondary disorders. Primary osteoporosis can be categorized as juvenile, postmenopausal, age related or senile. Juvenile osteoporosis occurs in children or young adults with an onset of 8 to 14 years of age. The characteristic finding in juvenile osteoporosis is the abrupt commencement of bone pain or a trauma related fracture. Post menopausal (type I) osteoporosis occurs in women from the age of 50 to 65 years old. This form of osteoporosis is exemplified by accelerated bone loss. The skeletal loss occurs primarily from trabecular bone leading to distal forearm and vertebral body fractures. Senile osteoporosis (type II) occurs in both men and women over the age of 70 years and is due to the loss of cortical as well as trabecular bone. Fractures of the wrist, spine and hip are often seen with type II osteoporosis.

Secondary causes of osteoporosis are due to disorders classified as genetic (congenital), endocrine, hypogonadal states, deficiency states, drug-induced, inflammatory states, hematologic, neoplastic and miscellaneous.

Risk factors for the development of osteoporosis include advanced age, alcohol use, androgen or estrogen deficiency, amenorrhea, body weight less than 127 pounds, Caucasian or Asian ethnicity, calcium deficiency, early menopause, family history of osteoporosis, female gender, fragility fracture, late menarche, physical inactivity and tobacco use.

The most common method of diagnosing osteoporosis is via a DEXA (Dual Energy X-ray Absorptiometry) scan. Osteopenia, osteoporosis and severe osteoporosis are respectively defined as DEXA scan T scores of -1 to -2.5, less than -2.5 and less than -2.5 with a fragility fracture.

Figure 2: Example of a Wedge Fracture

Vertebral compression fractures are the most common complication of osteoporosis at a cost of 10 to 15 billion dollars every year. There are approximately 700,000 vertebral compression fractures per year in the United States that result in spinal deformity (kyphosis/lordosis), acute/ chronic pain, disability and reduced vital respiratory capacity. An osteoporotic vertebral compression fracture should be considered in anyone over the age of fifty with a complaint of acute or chronic back pain. The most common location for vertebral compression fractures are at the T7-8 and T12-L1 levels which correspond to the most mechanically compromised spine regions. The diagnostic work up for someone suspected of having a spinal compression fracture includes spine x-rays looking for wedged shaped vertebral fractures (Fig. 2) as well as MRI imaging with T2 and STIR sequences to evaluate the acuity of the fracture. Nuclear bone scans and CT can also be helpful in evaluating vertebral compression fractures.

Vertebral compression fractures lead to decreased physical function, restricted activities of daily living, sleep disturbances, early satiety, psychological disturbances and reduced pulmonary function. The subsequent risk of additional vertebral fractures increased after the first fracture. Women with a vertebral fracture had a >20% higher mortality rate adjusted for age. Patients with vertebral fractures are 2-3 times more likely to die of pulmonary causes typically due to COPD and pneumonia complications.

Figure 3: Examples of the Kyphoplasty procedure: A) Balloon catheter insertion, B) Cavity creation and vertebral height restoration, C) Balloon catheter removal, and D) Cement injection

Kyphoplasty is a minimally invasive percutaneous procedure that restores vertebral body height (Fig. 3), provides fracture stability and reduces pain associated with vertebral compression fractures. The procedure involves the placement of a balloon catheter through a needle introducer into the vertebral fracture, inflation of the balloon (which creates a cavity and restores vertebral body height) and injection of cement into the cavity. The indications for kyphoplasty include an osteoporotic or malignant spinal compression fracture, persistent back pain, progressive vertebral collapse, spinal deformity and a correct diagnosis from imaging studies. Contraindications consist of bone retropulsion with neurological complications, infection and greater than 80% loss of vertebral body height. Clinical studies have demonstrated that kyphoplasty is a highly effective treatment for compression fractures and provides correction of spinal deformities with significant pain relief, improved quality of life and increased physical function.§