Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.     

Odontogenic focus as the etiology of cerebral ischemia]

Several authors have established a relationship between osteoporosis and periodontal disease. The ageing process is associated with a loss of both oral and total bone mass. It has been shown that a reduction of bone mineralization aggravates pathological periodontal changes, resulting in less support for the teeth. The present study investigates the nutritional influences that may condition the appearance of both pathological process. Insufficient dietary calcium and a reduction in the calcium: phosphorous ratio may favour the appearance of both these conditions by promoting bone reabsorption. Bone loss affects the following in descending order: jaw bones (especially alveolar bone), cranial bones, ribs, vertebrae and long bones. Alveolar bone which has the highest rate of renewal, is affected first and consequently is the most severely affected in the long term. The role of calcium in the etiology of osteoporosis is a controversial issue. Nevertheless, its implication has been proven in numerous investigations. The effect of adequate calcium intake on dental health has formed the basis of several recent studies. These investigations have demonstrated that increased calcium intake improves the suffering of inflammatory processes and tooth mobility in patients suffering from gingivitis with haemorrhaging. Based on the results of studies which link dietary calcium and phosphorous to the risk of osteoporosis and periodontal disease, and bearing in mind that in a large proportion of the Spanish population calcium intake is below that recommended, there is a need for a general improvement of the diet. It may be of special interest to increase the calcium intake of patients suffering periodontal disease. It may also help in the prevention of osteoporosis.     

Lithium carbonate therapy is not a risk factor for osteoporosis

Lithium carbonate is a widely used drug for affective disorders. It may effect calcium metabolism and alter parathyroid physiology by causing hypersecretion of parathyroid hormone. Patients treated with this medication might therefore be predisposed to osteoporosis. The purpose of this study was to evaluate the effect of either short- or long-term lithium carbonate therapy on parameters of bone metabolism. Parathyroid function and indices of bone metabolism were assessed in 23 patients treated for affective disorders. 10 patients were treated for 0.4-1.0 year (Group 1), and 13 patients were treated for more than 3 years (Group 2). In all subjects, bone mineral density measurements in the hip and lumbar spine regions were performed using dual energy X-ray absorptiometry. Serum thyroid hormone, PTH, LH, testosterone and urine OH-proline, free cortisol, calcium and phosphate excretion were measured. The two groups were well matched for sex, weight, calcium intake, lithium levels and smoking habits, although Group 2 was slightly older. No differences between the two groups were noted in either bone mineral density or other parameters that were assessed. Urinary OH-proline was elevated similarly in both groups. Our results did not detect any effect on bone density after short- or long-term lithium carbonate therapy, although the data does suggest an increase in bone turnover associated with this treatment. Thus, short- or long-term treatment with lithium is not associated with increased risk for osteoporosis.     

Glucocorticoid-induced osteoporosis: prevention and treatment

Glucocorticoid excess carries the risk of inducing secondary osteoporosis. In endogenous Cushing's syndrome, osteoporosis may be the presenting symptom of the underlying disease. Bone loss may reverse after the condition is cured, but often active treatment of established osteoporosis is necessary. In long-term glucocorticoid treatment at therapeutic doses, bone loss is likely and should be prevented; if prevention is ineffective, treatment is necessary. Hypercortisolism impairs calcium homeostasis and bone metabolism in a complex, multifactorial way: Glucocorticoids diminish calcium absorption and increase renal calcium excretion; this negative calcium balance leads to secondary hyperparathyroidism and osteoclast activation. Osteoblast activity is directly impaired by glucocorticoids, which lower activity of the gonadal hormone axis so that hypogonadism also contributes to bone loss. Glucocorticoids lead to muscle atrophy and decreased muscle strength with negative consequences for bone formation. For prevention and treatment, two different strategies have been used. The pathophysiological approach substitutes calcium and vitamin D in the first step; if bone loss nevertheless continues, bone formation is stimulated by fluorides. The alternative pharmaco-dynamic approach uses antiresorptives-calcitonin or, for preference, bisphosphonates. Clinically it is mandatory to monitor all patients in whom glucocorticoids are used (e.g., organ transplant recipients) before and after the initiation of treatment to stabilize bone metabolism as early as possible.     

A randomized, placebo-controlled trial of calcium supplementation for decreased bone density in corticosteroid-using patients with inflammatory bowel disease: a pilot study

BACKGROUND: Patients with inflammatory bowel disease (IBD) have a high prevalence of osteoporosis. A number of studies have found that corticosteroid use is associated with the development of osteoporosis in these patients. Calcium supplementation may be of benefit in corticosteroid-induced osteoporosis and calcium may be a nutrient that patients with IBD lack. AIM: To test the benefit of calcium supplementation on bone density in a pilot study over a 1-year period, in a group of corticosteroid-using patients with IBD, in a randomized, double-blind, placebo-controlled treatment study. METHODS: Corticosteroid-using patients with IBD including males over the age of 18 years and premenopausal females, were randomized to receive either calcium carbonate 1000 mg plus vitamin D 250 IU (Oscal) or an identically matched placebo. Dual energy X-ray absorptiometry measurements of bone density were obtained at entry and at 1 year. At entry, and every 3 months thereafter, serum was collected for the measurement of haemoglobin, biochemistry and bone hormones. Simultaneously a 24-h urine collection was analysed for calcium excretion and creatinine clearance, and a 4-day food record was collected to document dietary calcium and vitamin D ingestion. RESULTS: We found a high prevalence of moderately severe decreased bone density in corticosteroid-using patients with IBD. The dose of prednisone in the year prior to study entry was inversely correlated with bone density at the hip (R = -0.67, P = 0.004). At study entry serum osteocalcin was inversely correlated with corticosteroid dose in the year prior to the study (R = -0.64, P = 0.02) and at study end, directly correlated with the percentage change in spine bone density (R = 0.59, P = 0.01). The dietary calcium intake of these patients was close to the current RDA (recommended daily intake) for premenopausal, post-adolescent adults. Calcium supplementation with small extra doses of vitamin D conferred no obvious benefit to bone density at the end of 1 year. There was no correlation between oral calcium ingestion and bone mass measurements. Both the treatment and placebo groups' bone density remained relatively stable at 1 year, suggesting that bone loss in corticosteroid-using patients may peak early into the use of the corticosteroids. CONCLUSIONS: Calcium supplementation (1000 mg/day) conferred no significant benefit to bone density at 1 year in patients with corticosteroid-using IBD patients with osteoporosis. Future investigations should explore other therapeutic avenues that may have greater effects on increasing bone density in patients who already have considerable osteoporosis.     

Glucocorticoid-induced osteoporosis--mechanisms and preventions

It has been well known that patients with Cushing's syndrome have frequently osteoporosis or bone loss due to excess endogenous glucocorticoids and also osteopenia or osteoporosis is commonly observed in patients with long-term glucocorticoid therapy. In this paper, the mechanisms involved in bone loss in Cushing's syndrome and glucocorticoid-induced osteoporosis were demonstrated. In the patients with Cushing's syndrome, excess endogenous glucocorticoids increase bone resorption and decrease bone formation and also act to depress intestinal calcium absorption and increase urinary calcium excretion, leading to compensatory stimulation of parathyroid hormone secretion. Then, parathyroid hormone stimulates bone resorption. Thus, secondary osteoporosis is commonly observed due to excess glucocorticoid. Finally, preventions and managements for glucocorticoid-induced osteoporosis were discussed.     

Osteogenesis of electrically stimulated bone cells mediated in part by calcium ions

Culture selected and expanded osteoblastic cells may be able to be reintroduced into massive skeletal defects to accelerate cell mediated regeneration of skeletal tissues, especially in bone ingrowth in total joint replacement, fracture healing, and osteoporosis. In vitro osteogenic cell culture is a useful model in studying the mechanism of bone metabolism under direct current stimulation. In this study, an osteoblastlike cell line was isolated from newborn rat calvaria. The osteogenic processes of the in vitro cultured cell line were studied by cytochemical, electron microscopic, and energy dispersive x-ray analysis techniques that resembled those observed in membrane bone ossification centers in vivo. Direct current stimulation of 100 microA/cm2 accelerated greatly the proliferation and calcification of the in vitro cultured cells. Intracellular free calcium ion metabolism was measured with an Adherent Cell Analysis and Sorting Machine. Under direct current stimulation, intracellular free calcium ion concentration increased an average of 2.3 times of the original level, which may play a key role in regulating osteogenesis and bone metabolism.     

Osteoporosis in rheumatoid arthritis

In cases of rheumatoid arthritis, osteoporosis may be local or general. The aetiology is multifactorial. Reduced bodily function, synovial inflammation, steroids and menopause are important risk factors. Studies have shown that, in cases of primary osteoporosis, bone mineral density measurements in the distal radius may predict risk of fracture at other sites, such as the neck of the femur and the dorsal vertebrae. Such a connection is not found for rheumatoid arthritis. Bone density measurements in the distal radius may overestimate the risk of fractures due to localised periarticular osteoporosis. Overall bone quality is assumed to be poorer, however, in patients with rheumatoid arthritis, leading to higher risk of fracture than the bone mineral density measurements seem to show. Data are lacking on the effect of antiresorptive drugs on this condition. Treatment with oestrogen and the bisphosphonate pamidronate has been shown to increase bone mineral density. Data are lacking on fractures. As shown in the case of primary osteoporosis, decreased risk of fracture is to be expected also in patients with secondary osteoporosis.     

Osteoporosis in men. New insights into aetiology, pathogenesis, prevention and management

Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.     

Sustained response to intravenous alendronate in postmenopausal osteoporosis

We studied the effects of alendronate (amino-hydroxybutylidene bisphosphonate) on biochemical indices of bone turnover and on lumbar spinal bone mineral density in 15 postmenopausal women with vertebral osteoporosis. Alendronate 7.5 mg daily was administered intravenously as a slow infusion for four consecutive days. Treatment was associated with a significant decrease in serum calcium (p < 0.01), fasting urinary calcium excretion (p < 0.01) and hydroxyproline excretion within several days followed a later decrease in serum alkaline phosphatase activity that showed a significant reduction at two months after treatment (p < 0.05). Serum calcium reverted to pretreatment values by the second week after infusion, but the decrease in alkaline phosphatase, urinary calcium, and hydroxyproline excretion persisted to six months after infusion. There was a 3% mean increase in lumbar bone mineral density at six months (p < 0.01). A transient lymphopenia or leucopenia was noted in eight patients and a short-lived fever in six. No other side effects were observed. This study demonstrates that shortterm exposure to high intravenous doses of alendronate induces suppression of bone resorption in osteoporosis that persists for at least 6 months after infusion. We conclude that a short exposure to high intravenous doses induces sustained effects on bone turnover in much the same manner as that observed in Paget's disease of bone.     

Bisphosphonate therapy in osteoporosis. Inhibition of trabecular perforation by aminobisphosphonate

After many years of experience with bisophosphonates in the treatment of "tumor osteopathy" and Paget's disease, these substances have now also been approved for use in the treatment of osteoporosis. Owing to their high affinity for calcium hydroxyapatite, the bisphosphonates are deposited in the bony surface, and the aminobisphosphonates exert their effect at the site of active resorption via direct inhibition of active osteoclasts. As a result of this inhibition of the osteoclastic bone resorption, trabecular perforation is reduced and during the course of bone remodelling by the activity of the osteoblasts, boneformation occurs. In addition to an increase in bone density, both etidronate and alendronate have been shown to inhibit vertebral fractures in patients with osteoporosis. In addition, in patients with preexisting fractures, alendronate is able, at the same time, to lower the incidence of fractures of the femoral neck. With proper administration, the associated occasional gastrointestinal side effects can be avoided. The introduction of bisphosphonates into the treatment of osteoporosis is definitely an enrichment of the therapeutic spectrum in conjunction with the basic treatment comprising calcium, vitamin D, diet and physical measures.     

Inflammation and bone metabolism in rheumatoid arthritis. Pathogenetic viewpoints and therapeutic possibilities

BACKGROUND: Systemic osteoporosis is a common and pathogenetically heterogenous complication in rheumatoid arthritis. Various factors such as disease activity, dosage and duration of glucocorticoid treatment and immobilization are involved in pathogenesis of osteoporosis in rheumatoid arthritis. INFLAMMATION AND BONE METABOLISM: Proinflammatory cytokines secreted by immunocompetent cells have a role in the regulation of the activity of osteoblasts and osteoclasts. The effects of these proinflammatory cytokines include the inhibition of bone formation and an increase in bone resorption. Interleukin-6 and nitric oxide induced in osteoblasts by proinflammatory cytokines are likely to be important mediators between these cytokines and the function of osteoblasts and osteoclasts. Furthermore, disease activity dependent changes in the secretion of glucocorticoids and in vitamin D metabolism may be involved in the pathogenesis of osteoporosis in this disease. Alteration of bone remodeling associated with immobilization is an important factor of systemic bone loss in rheumatoid arthritis. CONCLUSION: The inflammatory process in rheumatoid arthritis may cause penarticular and systemic bone loss by various cytokine and hormone mediated mechanisms. Concluding from these pathogenetic mechanisms, bisphosphonates and active vitamin D metabolites are likely to be effective therapeutic options in osteoporosis associated with rheumatoid arthritis.     

The (-)-enantiomer of gossypol inhibits proliferation of stromal cells derived from human breast adipose tissues by enhancing transforming growth factor beta1 production

BACKGROUND: Age-related osteoporosis may be associated with inefficient intestinal calcium absorption and bone remodeling. OBJECTIVE: We investigated the pathogenesis of age-related osteoporosis in Chinese women with habitual low calcium intakes. DESIGN: We studied the response of intestinal calcium absorption, calcitropic hormones, and biochemical bone markers to graded dietary calcium deprivation. RESULTS: The osteoporotic subjects (n = 25) had higher urinary calcium excretion (P < 0.05) and lower plasma 1,25-dihydroxyvitamin D concentrations (P < 0.02) than did age-matched control women (n = 25). Parathyroid hormone was not significantly different from that in age-matched control women but was significantly higher than in young women (n = 15, P < 0.05). Fractional 45Ca absorption was approximately 61% in all 3 groups when the diet was unmodified and increased to 71%, 69%, and 68% in the osteoporotic subjects, age-matched control women, and young women, respectively, when dietary calcium was reduced to 300 mg/d. When the osteoporotic women were calcium deprived, serum 1,25-dihydroxyvitamin D failed to increase but urinary calcium excretion persisted. In contrast, supplementation with 1200 mg Ca resulted in a lowering of parathyroid hormone (P < 0.005 compared with the unmodified diet) and 1,25-dihydroxyvitamin D (P < 0.01) and decreased fractional 45Ca absorption (P < 0.01), suggesting that the increased calcium intake was associated with a potent compensatory ability of the intestine and calcitropic hormones to adapt. Calcium supplementation lowered osteocalcin (P < 0.05) but not alkaline phosphatase, which remained elevated in the osteoporotic subjects at all stages. CONCLUSIONS: Elderly osteoporotic women had reduced 1,25-dihydroxyvitamin D production, excessive urinary calcium loss, and high bone turnover. The Chinese women had exceptionally potent intestinal calcium absorption.     

Osteoporosis for the allergist

OBJECTIVE: This review is intended to be an authoritative summary of the pathogenesis of osteoporosis, a problem that may be encountered in allergy practice. It also provides an outline for identification of subjects at high risk and directions for their appropriate evaluation, management, and prevention of the disease. DATA SOURCES: References were obtained through a MEDLINE literature search as well as from previous reviews. Relevant articles were critically reviewed and their conclusions were included. RESULTS: Osteoporosis is a relatively common disease that is associated with significant morbidity and mortality. The management and prevention of osteoporosis have been improved by an increased awareness of the magnitude of the problem, a better understanding of the pathogenesis, development of a better technique for assessment of bone mineral density, and the availability of specific medications. With the increase in human life-span and the increasing use of glucocorticosteroids for a wide variety of diseases, the incidence of osteoporosis has been on the rise. CONCLUSION: Glucocorticosteroids are the most common medications that cause or contribute to the pathogenesis of osteoporosis and have been widely used in allergy practice. It is important for physicians to appreciate the current basic understanding of osteoporosis and to be able to identify patients at high risk for this serious disorder, and to initiate appropriate intervention at a sufficiently early time to be effective. Medications for treatment and prevention of osteoporosis include: calcium, vitamin D, estrogen, bisphosphonates, calcitonin, and others are reviewed in this article.     

Adverse effects of bisphosphonates. A comparative review

The bisphosphonates comprise a new class of drugs, and are increasingly being used to treat bone diseases characterised by increased osteoclastic bone resorption. These compounds are generally well tolerated, but toxicity may vary considerably from one compound to another. Dosages of etidronic acid above 800 mg/day impair the normal skeletal mineralisation and this may be associated with the appearance of fractures, but at the doses used for the treatment of osteoporosis, none of the bisphosphonates induce clinical or histological signs of impaired mineralisation. The skeletal half-life of bisphosphonates is of the order of several years, but this appears to be of little clinical consequence since the pharmacological effect is of relatively short duration. The mechanical properties of the skeleton of animals treated over long periods with high doses of various bisphosphonates have been shown to be perfectly preserved. However, in growing individuals, excess inhibition of bone remodelling might induce osteopetrotic-like alterations. When high doses of amino-bisphosphonates are given to patients who have never received bisphosphonate therapy, the patients may experience fevers up to 39 degrees C for 1 to 3 days, associated with transient haematological changes resembling a typical acute-phase response. Rapid intravenous injection of bisphosphonates at doses greater than 200 to 300 mg may cause severe renal failure; this can be prevented by slowing the rate of infusion (< 200 mg/h). Administration of high doses of bisphosphonates to patients with high bone turnover may induce a rapid and transient drop in serum calcium which is seldom symptomatic. The gastrointestinal absorption of bisphosphonates is low, and they must be taken without food. Oral amino derivatives may induce dose-related serious gastrointestinal lesions, with the sporadic appearance of erosive oesophagitis. Amino-bisphosphonate administration has been also associated with the sporadic occurrence of uveitis, scleritis and phlebitis and, in single cases, with irritative reactions at the skin, peritoneum and pericardium.     

Effect of measuring bone mineral density on calcium intake

The diet in Japan has improved, but calcium intake has not increased for the past ten years, and it remains insufficient. To prevent osteoporosis, instruction in nutrition is directed at increasing calcium intake. We studied the effect of measuring bone mineral density on calcium intake in people receiving nutrition education. Intake of other nutrients was also measured. The subjects were 87 healthy women living in an agricultural region (Yamanashi Prefecture). They were members of a group formed to improve the diet of people in their area. For three days in October 1992 and in August 1994 food-weight records were obtained. A total of 76 of the 87 women chose to have their bone mineral density measured. The measurements before the first nutrition assessment in 1992. The intake of almost all nutrients tended to be greater in 1994 than in 1992. Calcium intake exceeded the minimum daily requirement (600mg). Calcium intake increased between 1992 and 1994 only in the subjects whose bone mineral density had been measured. Calcium intake decreased in the other subjects. Therefore, nutrition education programs aimed at preventing osteoporosis may be more effective if bone mineral density is measured. In addition, an appropriate balance of other nutrients can be maintained as the intake of calcium is increased.     

Long-term effects of bisphosphonates on the growing skeleton. Studies of young patients with severe osteoporosis

Osteoporosis in children and adolescents is relatively uncommon and usually secondary to identifiable causal factors. There are no generally accepted therapies for patients with no treatable underlying cause of disease. Any treatment of young patients with bone-acting compounds should be not only effective but also devoid of adverse effects on bone growth and remodeling. For many years we have been studying the effects of bisphosphonates-an effective treatment of postmenopausal osteoporosis-on the growing skeleton. We review here our experience in the treatment of young patients with osteoporosis with special emphasis on issues of skeletal safety and effectiveness, and we discuss the available literature data. We studied 12 patients aged between 10.7 and 17.2 years with symptomatic osteoporosis and multiple fractures treated with the bisphosphonates pamidronate or olpadronate for periods between 2 and 8 years continuously. Linear growth continued normally on treatment; there was even a catch-up growth in prepubertal patients, and there was no excessive suppression of bone remodeling, assessed biochemically. Bone biopsies obtained at various stages during treatment showed bone of normal lamellar structure without mineralization defects. There was an increase in calcium balance, already evident within 10 days, the level of which was maintained for at least 3 years of treatment. This was associated with progressive increases in bone mineral density along a different slope from that of healthy peers as well as correction of vertebral deformities on X-rays in patients given bisphosphonates before puberty. Treatment was well tolerated and clinical improvement was remarkable. Our studies, supported by literature data, strongly suggest that bisphosphonate therapy can be beneficial to young patients with osteoporosis for whom no other options are currently available, and justify planning controlled studies in more common conditions for which no treatment is currently available, such as osteogenesis imperfecta.     

Effect of temperature on electrical resonance in leopard frog saccular hair cells

There has been increasing interest in the interrelationship between systemic osteoporosis, oral bone loss, tooth loss, and risk factors for these conditions. Because the severity of alveolar bone loss increases with age, it has long been hypothesized that it may, in part, be related to systemic conditions that also predispose the patient to osteoporosis/osteopenia. The purpose of this paper is to review the risk factors for osteoporosis and periodontitis, as well as the evidence that loss of oral bone mineral may be related to systemic osteopenia. There is also evidence that therapies designed to influence systemic bone mineral density, such as hormone replacement and bisphosphonate therapy, may be associated with less tooth loss and a slower loss of alveolar bone, respectively.     

Inflammatory bowel disease and osteoporosis

The relation between inflammatory bowel disease (IBD) and osteoporosis has received increasing attention during the past decade. The prevalence of low bone mass in patients with IBD has been reported to be more than 50%. The development of a quick non-invasive method to diagnose osteoporosis (dual-energy X-ray absorptiometry) provides a practical tool to identify the patient who needs special attention. The aetiology of the bone disease in patients with IBD has still not been elucidated, but corticosteroids may play a major role. Studies on the prevention/treatment of IBD-related osteoporosis are scarce. In a single uncontrolled study hormone replacement therapy proved effective in preventing bone loss in peri- and post-menopausal women with IBD. A placebo-controlled study showed that supplementation with calcium and vitamin D prevents bone loss in patients with Crohn's disease. The present paper reviews our current knowledge on the mechanisms and epidemiology of IBD-related bone disease.     

Calcium needs of adolescents

Adolescents grow at the greatest rate of any age group after infancy and accumulate 37% of their total bone mass during this growth spurt. Because maximum bone mass is acquired during adolescence, the calcium deposited during adolescence determines the risk of osteoporosis and fracture in adulthood. Bone mass is dependent on calcium intake, growth and pubertal development, exercise, and genetic and racial factors. Unfortunately, during this time of tremendous calcium need, most adolescents eat a diet that is very deficient in calcium. Girls are twice as likely to be deficient as boys (85% vs 43%). Other factors contributing to poor bone mineralization include adolescent pregnancy, anorexia nervosa, excessive exercise, and various chronic medical conditions. To avoid osteoporosis in later life, adequate dietary calcium intake should be recommended and calcium supplementation considered in all adolescent patients.