About Pathogenesis in Osteoporosis

General considerations

Osteoporosis is a disease of diverse etiology that cause a reduction in the mass of bone per unit volume. The reduction in mass is not accompanied by a significant decrease in the ratio of the mineral to theorganic phase, nor by any known abnormality in bone mineral or organic matrix.

Histologically, the disorder is characterized by a decrease in cortical thickness and in number and size of the trabeculae of cancellous bone. Individual trabecular connectivity is reduced.

The osteoid seams, however, are of normal width. Osteoporosis is the most common of the metabolic bone disease (disorders in which all the skeleton is involved) and is an important cause of morbidity in the elderly.


The remodeling of bone (its formation and resorption) is a continuous process. In osteoporosis, the bone mass is decrease, indicating that the rate of bone resorption must exceed that of bone formation.

Bone formation is higher in cortical than in cancellous bone. This differences is exaggerated further in patients with osteoporosis because because rates of formation of cancellous bone tend to be lower in patients with osteoporosis.

Particular in women after the menopause. The fact that about a third of postmenopausal women have high skeletal turnover, assessed by whole-body retention of tc-methylene diphosphonate and by other biochemical markers, could reflect the greater relative contribution of cortical remodeling in this group.

After closure of epiphyses and cessation of longitudinal growth, there is a period of consolidation with a decrease in cortical porosity. When peak adult bone mass is reached at about age 30 to35 for cortical bone and probably earlier for trabecular bone, rates of bone formation and resorption are relatively low(compared with the period of growth spurt) and approximately equal.

The normal balance between bone formation and resorption result in maintaince of skeletal mass. The rates of remodeling differ, however, not only in cortical compared with trabecular bone but also in individual bones or portions of bones.

Most of the bone surfaces are “inactive” and not involved at any given time either in formation or resorption. Active surface may be distributed randomly, but formation or resorptions are locally coupled as units.

Resorption areas are covered by osteoclasts in active: bone formation surfaces are characterized by the presence of osteoid seams and are covered by active osteoblasters. Resorption precedes formation and is probably more intense, but it does not last as long formation.

As a consequence, there are normally more sites of active formation than of resorption. Bone turnover is high when there are many units active and low when there are few.

Unless formation compensates for resorption, bone mass decreases. In both sexes after age 40 to 50 there is a slow rate of loss cortical bone of about 0.3 to 0.5 percent per year. In women around the menopause, an accelerated loss of cortical bone is superimposed on the age-related loss.

Loss of trabecular bone begins at an earlier age in both sexes but is probably greater in degree in women. The rate of bone loss in women also may be accelerated around the time of menopause.

The cumulative losses of bone mass range from 20 to 30 percent in men and 40 to 50 percent for some women. In general, the bone loss involves predominantly trabecular bone in the spine and distal radius in women and the spine and hip in both women and men.

The fact that loss is not uniform has been documented with techniques such as single and dual-photon absorptiometery, quantitative computed tomography, x-ray-based dual-energy densitometry, and neutron activation analysis of total body calcium.

For example, the rate of loss is greater in the metacarpals, the femoral neck, and the vertebral bodies than in the airshaft of the femur, the tibia, and the skull.

Although, as noted, skeletal turnover may be increased, turnover is usually normal or low. Bone formation is low in the majority, but the degree of reduction varies with the different bone surface.

The major remodeling abnormalities in patients with vertebral crush fractures are a reduced frequency of activation of remodeling units and a decrease in the function of osteoblasts.

Even in those individuals with increased bone resorption, however, bone formation does not compensate. At some critical point if the difference between rate of formation and resorption is maintained, loss of bone substance may become so marked that the bone can no longer resist the normal mechanical forces to which it is subjected, and fracture results.

This problem is most evident following perforation of bony trabecular plates. The template for formation of new bone is lost, and loss of bone is rapid as bone resorption continues and is even more uncoupled from resorption.

Osteoporosis usually becomes a clinical problem following fracture. Although the level of reduction in bone mass sufficient to result in fracture after minimal trauma is variable, the bone mineral density as measured by x-ray-based dual-energy absorptiometery (DEXA) is an excellent predictor of fracture risk.

The strength of bone such as vertebrae depends on “quality” as well as mineral density.The age-related loss of bone begins earlier and proceeds more rapidly in women, and there is a trend toward acceleration of bone loss before the menopause.

All the reasons for this age-associated bone loss are not known, although several risk factors have been identified. In general, white women have a greater risk than black women. , and white men have a greater risk than black men.

One explanation for these population difference is that the bone mass at skeletal maturity is one determinant of the bone man at subsequent ages.

The lower incidence of osteoporosis and hip fracture in back men and women has been attributed to a higher bone mineral content in blacks than in whites despite the fact that bone formation is lower in blacks.

Since formation and resorption are usually coupled, and since bone mass is increased, bone resorption (and turnover) also must to reduced. Osteoporotic subjects are frequently less muscular and have lower average body weight.

Patients who are kept at complete bed rest and astronauts in microgravity can lose approximately I percent of their bone mass month. Exercise may have a beneficial effect in maintaining bone mass.

The fact that accelerated bone loss accompanies the menopause in some women and that premature osteoporosis occurs after premature surgical menopause suggests that estrogens play a major role in preventing bone loss.

Furthermore, Osteoporotic women as a group may have an earlier menopause than age-matched nonosteoporotic women. Osteoporotic women also have a higher incidence of smoking; cigarette smoking might directly affect bone remodeling or have secondary effects on ovarian function.

Excessive alcohol consumption, which can result in decreased bone formation, also is a risk factor for osteoporosis. Dietary calcium intake during the first three decades of life influences the ultimate peak bone mass.

Calcium intake during adult life has a small effect on bone mass and risk of fracture. Inability to synthesize adequate amounts of 1 A ( Alfa), 25-dihydroxyvitamin D ( 1,25[OH]2 D) may play a rile in the decreased calcium absorption, possibly because of decreased sensitivity of the 25(OH)D-1 ALFA- hydroxylase to parathyroid hormone or impaired activity of the renal 25(OH)D-1 ALFA- hydroxylase.

| Investigation, diagnosis and treatment of Osteoporosis | Various symptoms and other risk factors associated with the Osteoporosis |


Main Menu



Disclaimer : All the material contained on this page is been just provided for educational and informational purposes only and not intended to any type of consultation. Please consult with your physician or appropriate healthcare personal for any kind of opinions or recommendations with respect to your symptoms or medical condition. The author is not responsible to any person or entity with respect to any kind of damage, loss, or injuries, caused or alleged to be caused directly or indirectly by the information contained in this report. Also, the logos, trademarks, and brand names, if any, depicted on this site are exclusive property of their respective companies.

Copyright - © 2004 - 2022 - All Rights Reserved.

|Privacy Policy | Disclosure | Contact |