Osteoporosis

Essentials of Diagnosis

General Considerations

Osteoporosis is the most commonly seen metabolic bone disease in the USA. It is characterized by an absolute decrease in the amount of bone present to a level below which it is capable of maintaining the structural integrity of the skeleton. There is a greater loss of trabecular bone than compact bone, accounting for the primary features of the disease, ie, crush fractures of vertebrae, fractures of the neck of the femur, and fractures of the distal end of the radius. Whatever bone is present is normally mineralized. Osteoporosis may be produced secondarily by a number of disorders, but more commonly it is primary and of unknown cause.

Since the usual form of the disease is clinically evident in middle life and beyond and since women are more frequently affected than men it is often termed "postmenopausal and senile" osteoporosis. The serum calcium, phosphate, and alkaline phosphatase are normal, and the bone formation rate is usually normal whereas the bone resorption rate is increased. The inheritance of low skeletal mass in young adult life (especially in white females), loss of sex hormones at the time of the menopause, the effects of aging, lack of activity, inadequate dietary calcium intake, impaired intestinal calcium absorption, a high phosphate intake, acid ash diet, inappropriate secretion of parathyroid hormone or calcitonin, or some combination of these factors have been considered as possible contributing causes.

Etiology

A. Principal Causes:

  1. Lack of activity, eg, immobilization as in paraplegia or rheumatoid arthritis. (Osteoblasts depend upon strains and stresses for proper function.)
  2. Lack of estrogens ("postmenopausal osteoporosis"). (Females are deprived of estrogens relatively early in life. About 30 per cent of women over 60 years of age have clinical osteoporosis. Some degree of osteoporosis is almost always present in senility.)
  3. More recently a chronic low intake of calcium has been suggested as of etiologic importance. However, the evidence for this is still not conclusive.
  4. Intestinal lactase deficiency may be an impor-tant factor in elderly patients with osteoporosis.

B. Less Common Causes:

  1. Developmental disturbances (eg, osteogenesis imperfecta).
  2. Nutritional disturbances (eg, protein starvation and ascorbic acid deficiency).
  3. Chronic calcium depletion is claimed by some investigators to cause osteoporosis.
  4. Endocrine diseases- Lack of androgens (eu-nuchoidism, senility in men), hypopituitarism (causes secondary gonadal failure), acromegaly (cause un-known; possibly due to hypogonadism), thyrotoxicosis (not constant; causes excessive catabolism of protein tissue), excessive exogenous or endogenous ACTH or corticosteroids causing catabolism of bone (eg. Cushing's disease), and long-standing uncontrolled diabetes mellitus (rare).
  5. Bone marrow disorders- The presence of abnormal cells in the bone marrow, such as in myeloma or leukemia, may prevent osteoblastic activity and cause osteoporosis. This is in addition to the active replacement of the marrow with tumor cells. A bone marrow factor may also play an etiologic role in senile osteoporosis.
  6. Prolonged use of heparin may lead to osteoporosis.
  7. Idiopathic osteoporosis- The cause is undeter-mined. It is most common in young men and women but occasionally occurs in older people, and does not respond well to therapy.
  8. Idiopathic juvenile osteoporosis is a rare disorder which shows spontaneous remission after pu-berty.

Clinical Findings

A. Symptoms and Signs :

Osteoporosis may first be discovered accidentally on x-ray examination, or may present as backache of varying degrees of severity. On other occasions it presents as a spontaneous fracture or collapse of a vertebra.

B. Laboratory Findings :

Serum calcium, phosphate, and alkaline phosphatase are normal. The alka-line phosphatase may be slightly elevated in osteogenesis imperfecta and also in other forms of osteoporosis if there has been a recent fracture. Urinary calcium is high early, normal in chronic forms.

C. X-Ray Findings :

X-ray shows compression of vertebrae. The principal areas of demineralization are the spine and pelvis; demineralization is less marked in the skull and extremities. The lamina dura is preserved. Kidney stones may occasionally be seen in acute osteoporosis.

D. Bone densitometry measurements may be helpful.

Differential Diagnosis

It is important not to confuse this condition with other metabolic bone diseases, especially osteomalacia and hype rparathyroidism; or with myeloma and metastatic bone disease, especially of the breast and uterus, since estrogen therapy may aggravate them. Bone biopsy may be required, since these conditions may coexist in the postmenopausal patient.

A rare case of hypophosphatasia may appear as "osteoporosis."

Treatment

A. Specific Measures :

Specific treatment varies with the cause; combined hormone therapy is usually employed, although its effectiveness has not been proved.

  1. Postclimacteric (mostly in females) - Estrogens appear to decrease bone resorption. Before beginning estrogen therapy in a postmenopausal woman, perform a careful pelvic eamination to rule out neoplasm or other abnormality and warn the patient or a relative that vaginal bleeding may occur. Administer estrogen daily except for the first 5-7 calendar days of each month and then repeat the cycle. Any of the following may be used: (1) Diethylstilbestrol, 0.5-2 mg orally daily as tolerated (may produce nausea). (2) Ethinyl estradiol, 0.02-0.05 mg orally daily as tolerated. (3) Estrone sulfate and conjugated estrogenic substances (Premarin®, Amnestrogen®, ete) are well tolerated and widely used. The dosage is 1.25-2.5 mg orally daily. The long-acting injectable estrogen preparations may be more reliable. Testosterone may be used in addition to estrogen for its protein anabolic effect. Give methyltestosterone, 5-10 mg orally daily. Avoid overdosage in females since excessive use may cause the appearance of male secondary sex characteristics. While some of these regress if therapy is stopped, others (eg, hoarseness, hirsutism, clitoral enlargement) may persist. Some of the newer anabolic agents, eg, estradiol valerate and testosterone enanthate (Deladumone®), norethandrolone (Nilevar®), or methandrostenolone (Dianabol®), may be used.
  2. Old age and idiopathic- As for postclimacteric; both testosterone and estrogens may be used in both males and females. Use with caution in very old people.
  3. Patients with malnutrition- Adequate diet is of great importance. However, hormones may be used as above if response to diet alone is poor.
  4. Sodium fluoride in doses of 1 mg/kg has recently been tried in refractory osteoporotic patients, but it must be considered still an experimental procedure. Combined with calcium and vitamin D, it appears to enhance bone formation.
  5. Phosphate supplements may be of value in certain types of osteoporosis (eg, after fracture, mye-loma), especially if combined with calcium.
  6. Intravenous infusions of calcium have been advocated recently for refractory osteoporosis. This must be considered an experimental procedure and may act by stimulating calcitonin.
  7. Calcitonin therapy is under investigation but appears to have little effect in arresting osteoporosis. It may be helpful in osteogenesis imperfecta.

B. General Measures :

The diet should be high in protein and adequate in calcium (milk and milk products are desirable) and vitamin D. Increased calcium intake by use of supplementary calcium salts (eg, calcium lactate or carbonate), up to 1-2 gm calcium per day, may be warranted. Additional vitamin D (2000-5000 units/day) may be needed if there is associated malabsorption or osteomalacia. Patients should be kept active; bedridden patients should be given active or passive exercises. The spine must be adequately supported (eg, with a Taylor brace), but rigid or excessive immobilization must be avoided.

Prognosis

With proper and prolonged therapy the prognosis is good for postclimacteric osteoporosis. Spinal in-volvement is not reversible on x-ray, but progression of the disease is often halted. In general, osteoporosis is a crippling rather than a killing disease, and the prog-nosis is essentially that of the underlying disorder (eg, Cushing's syndrome). The idiopathic variety does not respond appreciably to any form of therapy. Careful periodic records of patient's height will indicate if the disease has become stabilized. In the future, periodic measurements of bone mass in a given individual with modern technics may alert the physician that progres-sive bone loss is occurring prior to clinical or x-ray evidence of osteoporosis. Measures to prevent progres-sive resorption of bone may be more effective than treatment of clinical disease.

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