Bone metabolism in adolescent girls

Bone metabolism in adolescent girls

J.J. Amy

Emeritus Professor, Vrije Universiteit Brussel, Brussels,


Bone mineral density (BMD) reflects the balance between the

continuous processes of bone formation and resorption. These are controlled by

intricate mechanisms wherein exercise, as well as nutritional and endocrine

factors, plays a very important role.

Moderate exercise helps to prevent bone loss, whereas strenuous

exercise may promote it. Body weight is a major determinant of BMD accrual in

postpubertal girls. Leptin, which is secreted by adipocytes, binds to its

receptors in the GnRH pulse generator located in the arcuate nucleus of the

hypothalamus. The pulsatile release of GnRH in turn elicits the production of

gonadotrophins that stimulate ovarian folliculogenesis and steroid production.

Normally, at least 40 % of bone mass is formed during

adolescence and early adulthood. During this phase of life, the dietary

requirement of calcium increases from about 900 mg/day to about 1500 mg/day.

Unfortunately, the calcium intake in that age group is often insufficient, which

adversely affects skeletal development. Women attain their peak bone mass around

25 years of age; bone loss starts normally after the age of 40, and accelerates

after menopause, unless this latter is treated.

Oestrogens, in particular oestradiol, inhibit the activity of

osteoclasts. Oral, vaginal and transdermal oestrogen/progestogen contraceptives

used by adolescents and young women presumably enhance the acquisition of a

satisfactory bone mass. Long-term users of depot-medroxyprogesterone acetate on

the contrary show a decrease in their bone density, which is reversible after

cessation of therapy. Hypooestrogenism as seen in hypothalamic amenorrhoea (e.g.,

GnRH deficiency) or ovarian failure (e.g., Turner’s syndrome) is associated with

a negative skeletal mineral balance, which can be corrected by hormone

replacement therapy (HRT).

This treatment is of limited benefit in anorexia nervosa.

Indeed, multiple interacting factors contribute to the development of

osteoporosis in anorectic patients : beside the decreased body fat and body

weight, and the deficient oestrogen production, one notes an inadequate dietary

calcium intake, vitamin D deficiency, elevated cortisol levels, and excessive

strenuous physical exercise. The only proven treatment for osteoporosis in

anorexia nervosa consists of regaining sufficient body weight and body fat,

leading to the resumption of menstrual cycles. Yet, HRT should be contemplated

if amenorrhoea has lasted for more than one year, and the patient is still

underweight. Bisphosphonates and recombinant insulin-like growth factor-1

(IGF-1) are presently being investigated but show little promise in terms of

clinical application in this entity.

BMD is decreased and stress fractures are more frequent in

athletes with exercise-associated amenorrhoea; this is due to delayed skeletal

maturation, accelerated bone loss, or both. These subjects often began endurance

training at an early age, and this interfered with their development of an

adequate bone mass. The bone loss is worsened by the nutritional disturbances so

common in amenorrhoeic athletes. Treatment consisting of a modification of the

exercise programme, an adjustment of diet and, possibly, the cyclic

administration of an oestrogen/progestogen preparation will partially or

completely reverse the observed skeletal anomalies.

Patients with a complete androgen insensitivity syndrome have

BMDs lower than those of unaffected women. The anomaly precedes gonadectomy; it

may be worsened by an inadequate oestrogen replacement following the procedure.

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