Osteoporosis is a skeletal disease characterized by an increased susceptibility of bones to fracture secondary to a loss in both bone quantity (bone mass) and quality (changes in the microarchitecture). This may result as a symptom of aging, poor lifestyle (decreased calcium intake, smoking, alcoholism, sedentary lifestyle), chronic steroid therapy, or as a symptom of an underlying disease state. Osteopenia is the term used to describe bones which are in the continuum between normal and osteoporotic states.
Diagnosis is established by determining bone mineral density (a measurement of bone mass) via DXA scanning. The T-score is used to determine the stage of disease. T-score values greater than –1 are considered normal. Osteopenia is diagnosed by a T-score between –1 to –2.5 standard deviations, and osteoporosis is diagnosed by a T-score below –2.5 standard deviations. While the diagnosis is established by DXA scanning, this form of evaluation only evaluates bone mass and not bony microarchitecture. Spontaneous vertebral compression fractures or fractures occurring from standing height or with minimal trauma suggest the diagnosis.
When the T score is below -2.5, the next step should be to determine the GFR. If the GFR is below 50 ml/hr, then adynamic bone disease of renal failure is a possible cause for the low T score. To establish the diagnosis, the serum parathyroid hormone (PTH) and vitamin D levels should be determined. If the PTH is elevated then adynamic renal bone disease is the underlying cause. This disorder is not treated with standard osteoporosis therapies but rather with either high dose vitamin D or a vitamin D analogue (rocaltrol or paricaltrol) in an attempt to normalize PTH levels and thus prevent further bone damage.
While most cases of osteoporosis are associated with “normal aging” (primary disease), certain risk factors increase an individual's risk of disease. These risks include smoking, excessive alcohol intake, poor lifetime dietary calcium intake, sedentary lifestyle, family history of disease, slight body habitus, early menopause, amenorrhea, certain medications (steroids, antiepileptic medications, DMARDs, etc.), and race (higher incidence of disease in Caucasian and Asian populations). More commonly, chronic vitamin D deficiency predisposes patients to poor bone health. When the level of disease seems premature or excessive or if the patient is male, a secondary cause should be suspected. A Z score of less than -1.0 is suggestive of an underlying secondary cause.
Prevention includes patient education about adequate calcium and vitamin D intake (premenopausal women: 1000 mg calcium and 2000 IU vitamin D and postmenopausal women: 1500 mg calcium with 2000 IU vitamin D per day) and strenuous exercise. Smoking cessation is important in this disease as well as for general good health.
Treatment includes calcium and vitamin D supplementation with follow-up until adequate vitamin D levels have been reached. The bisphosphonates are considered first line therapy in most cases. If they cannot be tolerated, raloxifene (60 mg PO Qday), intranasal miacalcin, or denosumab (60 mg injections twice a year) can be considered as second line agents. Severe cases may be treated with teriparatide subcutaneous injections to stimulate bone growth. It is important to screen and treat secondary causes especially vitamin D deficiency. Patients with osteoporosis warrant therapy. Patients with osteopenia may be candidates for therapy based on their risk factors. The FRAX score should be determined in patients with osteopenia. If the FRAX is equal to or greater than 20% for a major fracture or equal to or greater than 3% for a hip fracture, then antiresorptive therapy is indicated. Also, osteopenic patients with evidence of more severe disease (vertebral compression fractures or standing height falls with a fracture) should receive therapy. As stated above, adynamic renal bone disease is treated with high dose vitamin D or vitamin D analogues in an attempt to normalize the serum PTH level.
To follow a patient’s response to therapy, serial measurements of biochemical markers may be used. Typically, a measurement of the resorption marker urinary N-telopeptides of type 1 collagen is used at baseline and again in three months; however, this is not the current standard of care. Serial measurements of BMD do not accurately reflect the individual’s response to therapy as BMD measures only bone density and not the changes in microarchitexture that occur with therapy. Serial measurements of BMD only help determine that no further bone density is lost during treatment.