Musculoskeletal Diseases


Osteoporosis is often considered a "silent disease" because patients may have few symptoms or may not recognize its symptoms. Osteoporosis can remain asymptomatic even after a fracture occurs. Once a fragility fracture has occurred, there is an increased risk for future fracture. The strategy should be to prevent the first fracture. If a fracture does occur, treatment of osteoporosis may reduce the risk of additional fractures.

Osteoporosis is a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture. Bone strength primarily reflects the integration of bone quality and bone density.

Skeletal disorder

The only certain way to determine a patient´s bone mineral density (BMD) and osteoporotic fracture risk is to perform a BMD test. The National Osteoporosis Foundation (NOF) recommends that all postmenopausal women be evaluated clinically for osteoporosis risk in order to determine the need for BMD testing.

While BMD measurements at any skeletal site are of value in predicting future fracture risk, hip BMD is the best predictor of fractures of the hip and other sites.

Bone density exams known as DXA (often pronounced – dexa II) are an enhanced radiology (x-ray) technique that is used to measure BMD. It is considered the most accurate test for measuring BMD. DXA test results are reported as two separate scores, which are known as the T-score and the Z-score.

X ray absorptiometry

The National Osteoporosis Risk Assessment (NORA) study is the largest study of osteoporosis ever conducted to date in the United States. The NORA study revealed that nearly half (about 47%) of the postmenopausal women age 50 and older had either low bone mass (T-score range from −1 to −2.5) or osteoporosis (T-score below −2.5) and that these women all were at greater risk for fractures than women with normal bone density. Half of those who fractured had low bone mass, according to their T-scores. According to the NOF, 1 in 2 women and 1 in 4 men over age 50 will have a fracture caused by osteoporosis in her or his remaining lifetime.

Osteoporosis and related fractures can lead to disability, chronic pain, and premature death. Osteoporotic fracture can occur in any bone, but the three most common sites are the spine (30%), the wrist (19%), and the hip (14%). The vertebrae have more trabecular bone, with a higher surface area and a faster rate of metabolic activity than the bones in the hip. Hip bones have relatively more cortical bone material, which has a lower surface area and slower rate of metabolic activity. Vertebral fractures are of primary concern because they tend to occur in early menopause. More than 85% of patients with vertebral fractures will have additional fracture.

Bone Remodeling Process

Bone is living, metabolically active tissue that requires continual removal of existing bone with replacement of newly formed bone. This process is called the bone remodeling process, or —bone turnover and is required to maintain the structural integrity of the bone. After menopause, both bone formation and bone resorption rates are increased. The bone resorption rates (taking away existing bone) are faster than formation (adding new bone), resulting in a net loss of bone. Certain medications such as glucocorticoid steroids can cause an imbalance, resulting in a decrease in bone formation and an increase in resorption, which can lead to bone loss.

After menopause, the loss of estrogen removes the main restraint on bone remodeling present in premenopausal women, so that both bone formation and bone resorption rates are increased. The bone resorption rates are faster than formation, resulting in a net loss of bone. In other words, more bone is being removed than is being replaced.

Osteoclasts are cells that are responsible for bone resorption, or breakdown. They degrade existing bone by attaching to the surface and secreting acids and enzymes that dissolve the bone matrix and mineral.

Osteoblasts synthesize osteoid, the protein component of bone tissue made up of collagen that is not yet mineralized. Osteoblasts are present on the surfaces where bone is undergoing new formation. They migrate to regions where the osteoclasts are actively involved in bone resorption, thereby laying down new bone after the existing bone has been removed.

The bone remodeling process involves the following steps:

  1. Activation:
    Osteoclast precursors are attracted to a localized area of quiescent bone surface or an area of existing bone. The single-celled osteoclast precursors fuse to form osteoclasts.
  2. Resorption:
    The osteoclasts begin to resorb the bone mineral and matrix, leaving a cavity. This takes about 1 to 2 weeks.
  3. Reversal:
    The osteoclasts disappear from the cavity and there is a delay during which time a reversal occurs. Bone resorption no longer occurs. A signal is emitted that recruits osteoblast precursors to the site, in preparation for bone formation.
  4. Formation:
    The osteoblast precursors then divide and convert into active osteoblasts, and the stage of bone formation begins. The mature osteoblasts secrete unmineralized bone matrix, or osteoid, which gradually fills the cavity. While the matrix is still being laid down, deposition of mineral salts begins. The entire cavity fills with osteoid over a period of a few weeks, although complete mineralization may take several months.
  5. Resting:
    Bone remodeling and mineralization is complete.
Bone formation

In a healthy body, osteoclasts and osteoblasts work together in a highly regulated process to maintain the balance between bone loss and bone formation. The average life span of osteoclasts is approximately 2 weeks, at which point they all undergo apoptosis, or programmed cell death. The average life span for osteoblasts is 3 months. Osteoporosis results from an imbalance between bone resorption and bone formation, with bone resorption occurring at a faster rate than bone formation. This imbalance between osteoclasts and osteoblasts within trabecular bone leads to more bone loss. Trabecular bone is therefore more vulnerable to fractures due to its structure.

Significant remodeling occurs at trabecular sites. Trabecular bone is affected to a greater extent than cortical bone early in the postmenopausal process, and as a result, trabecular bone is lost at a more rapid rate.

Like women, men can experience a dramatic loss of bone mass with aging, which significantly increases their risk of developing osteoporosis. This reduction in bone mass may be due to declining levels of testosterone as men age, similar to the bone loss that occurs in women due to declining estrogen levels associated with menopause. Estrogen may also play a key role in maintaining bone health in men. In fact, the changes in estrogen levels that occur with age in men may be as critical, if not more so, to bone loss as the changes in testosterone levels.

Bone Strength

The quality and density of the bone determine its overall strength. The bone´s material properties and mechanical characteristics also contribute to its strength. Bone strength is determined by the following formula: Bone Strength = Bone Density x Bone Quality.

Bone turnover must be within the physiological range to maintain optimal bone strength. If bone turnover is too low or too high, bone strength is compromised.

Bone strength

The term bone quality describes multiple elements contributing to bone strength. There are four known components that affect bone quality:
bone turnover rate (remodeling)
damage accumulation
bone architecture
bone mineralization

Bone architecture

How Is Osteoporosis Prevented And Treated?

Your doctor will use a risk fracture algorithm to determine the risk factors as well as run tests such as the BMD to understand which treatment will suit you best. Lifestyle modifications can be made to reduce risk of osteoporosis such as smoking cessation, reduce alcohol consumption, initiate calcium supplements and exercise.

Find out more about osteoporosis by speaking to your doctor.

Reference :
  1. National Osteoporosis Foundation (NOF) web site. Accessed January 4. 2008