Osteoporosis is a bone disorder that increases a person’s risk of fracture due to low bone mineral density (BMD), impaired bone microarchitecture/mineralization, and/or decreased bone strength. Osteoporotic fractures most commonly occur at the hip, spine and wrist.

Fracture prevalence increases dramatically with age. The majority of postmenopausal women with osteoporosis have bone loss related to estrogen deficiency and/or age. The incidence of these fracture rises steeply with age, such that most occur in people aged >65 years, where they are associated with excess mortality, substantial morbidity, and significant health and social services expenditure.

Treatment Options

Multiple therapeutic regimens have been designed to prevent or treat bone loss in postmenopausal women and older adults. The first step in the prevention or treatment of osteoporosis is ensuring adequate nutrition, particularly maintaining an adequate intake of calcium and vitamin D, physical exercise.

Effective pharmacological therapies for the prevention and treatment of osteoporosis have been developed, including bisphosphonates (alendronate, risedronate, zoledronic acid, ibandronate), denosumab, raloxifene, conjugated estrogens/bazedoxifene, parathyroid hormone analogues (abaloparatide, teriparatide) and calcium and vitamin D.

Role of calcium and vitamin D in bone and osteoporosis

Bone mass contains a high proportion of calcium. Peak bone mass is largely dependent on calcium intake during adolescence, and maintaining a high intake can slow age-related bone loss. Conversely, inadequate dietary calcium intake increases the prevalence of osteoporosis. The efficiency of calcium absorption decreases further in the presence of vitamin D insufficiency.

As people age, the skin's capability to synthesize vitamin D declines, whilst intestinal vitamin D absorption also becomes less efficient. These changes may be compounded by lower exposure to the sun, as a result of diminished physical activity, and reduced dietary vitamin D intake.

The presence of low calcium levels stimulates the secretion of PTH in order to increase production of vitamin D, i.e. causes secondary hyperparathyroidism.

Elevated PTH levels trigger bone metabolism, causing bone resorption and bone loss and releasing calcium ions in the blood. When bone resorption occurs at an elevated rate, fracture risk is increased regardless of the individual's BMD, as the bone is eroded, weakening the skeleton.

Target groups for calcium and vitamin D supplementation

Evidence has shown that calcium and vitamin D supplementation has a beneficial effect on the bone health and fracture risks of certain groups of individuals.

Calcium and vitamin D supplementation is most effective when targeted to those who:

(i)               are receiving ant-iresorptive or anabolic osteoporosis therapy;

(ii)             are being treated with glucocorticoids; and

(iii)           are likely to be calcium or vitamin D insufficient.

These benefits are most apparent when 800 IU day vitamin D is complemented with a dose of 1000–1200 mg day elemental calcium.

Conclusions:

In summary, the age-related increase in fracture risk is influenced by changes in bone remodelling and bone mineral density (BMD) and an increased propensity to falls, attributable in part to the loss of muscular strength. Adequate dietary calcium intake is critical in maintaining bone mass, whilst vitamin D plays a key role in modulating calcium homeostasis and maintaining muscular strength.