The Influence of Cigarette Smoking and Age on Bone Loss in Men

Sparrow, David; Beausoleil, Irene; Garvey, Arthur J.; Rosner, Bernard; Silbert, Jeremiah E.

doi:10.1080/00039896.1982.10667572

Cited by 26 publications

(7 citation statements)

References 6 publications

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“…In 341 male subjects aged between 40-80 yrs smoking added to the bone loss due to ageing [21]. In this wide range of ages, the current smokers had a lower per cent of bone cortical areas than those who never smoked.…”

Section: Epidemiologymentioning

confidence: 99%

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Osteoporosis in chronic obstructive pulmonary disease

Ionescu¹,

Schoon²

2003

Eur Respir J

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Osteoporosis is one of the systemic effects associated with chronic obstructive pulmonary disease (COPD). Potential risk factors of osteoporosis may be due to the lifestyle, genetics, treatment with corticosteroids, endocrine abnormalities or the impairment of the body composition and peripheral skeletal muscles. Evidence for the possible contribution of such factors is reviewed.The occurrence of fractures, as a consequence of osteoporosis, can contribute to the disability and mortality of patients with COPD and add to the economic burden of the disease. The treatment with corticosteroids for the lung disease is associated with increased prevalence of fractures, but other factors may contribute.There is a remarkable paucity of interventional studies targeting the osteoporosis in patients with COPD. The results of studies on the treatment of osteoporosis in chronic lung diseases, some including small numbers of patients with COPD, are reviewed in the paper.Prospective longitudinal studies on the incidence of osteoporosis in chronic obstructive pulmonary disease need to assess patients with various degrees of disease severity and investigate the possible contribution of etiological factors. Randomised placebo-controlled trials are required to assess the effect of intervention, such as bisphosphonates, hormone replacement, calcium supplementation, on the prevention and treatment of osteoporosis and fractures in chronic obstructive pulmonary disease.

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Section: Epidemiologymentioning

confidence: 99%

“…In this wide range of ages, the current smokers had a lower per cent of bone cortical areas than those who never smoked. In a multiple regression analysis, after adjustment for the initial percentage of cortical area, both age (p=0.005) and smoking (p=0.03) were inversely related to the per cent cortical area [21].…”

Section: Epidemiologymentioning

confidence: 99%

Osteoporosis in chronic obstructive pulmonary disease

Ionescu¹,

Schoon²

2003

Eur Respir J

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“…Excess ethanol intake may cause osteoporosis (5-7) by directly inhibiting osteoblast function and bone formation (8-1 1). Tobacco use has also been reported to have deleterious effects on bone mass (5,12,13) and osteoblast activity (8). Although studies on trabecular bone formation using dynamic bone histomorphometry have indicated that the recruitment and activity of osteoblasts may be altered in men with idiopathic osteoporosis (8,11,14), the cellular osteoblastic dysfunction responsible for the defective bone formation in these patients remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation.

Marie

Vernejoul²,

Connes³

et al. 1991

J. Clin. Invest.

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To determine the osteoblastic dysfunction that may be involved in the pathophysiology of osteoporosis in men we have compared histomorphometric indices of bone formation with in vitro characteristics of osteoblastic cells isolated from the trabecular bone surface in 23 untreated men with eugonadal osteoporosis. In most patients (n = 14), trabecular bone loss resulted from decreased bone formation evidenced by a lower than normal osteoblast surface, double tetracycline labeled surface, bone formation rate, and mean wall thickness. In these patients, DNA synthesis by cultured osteoblastic cells was altered. The peak of 1314thymidine incorporation into DNA, the maximal DNA synthesis, and the area under the curve of cell proliferation were lower than the values in normal bone cells from age-matched controls. Parameters of bone cell growth were decreased in correlation with the extent of actively bone forming surfaces. By contrast, in patients (n = 9) with normal histomorphometric indices ofbone formation, bone cell proliferation in vitro was not different from normal. Parameters of osteoblastic differentiation in vitro such as osteocalcin production and alkaline phosphatase activity were normal in the two groups of patients. This study shows that the trabecular bone loss resulting from defective bone formation in eugonadal osteoporotic men is associated with a lower than normal proliferative capacity of osteoblastic cells lining the trabecular bone surface.

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“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] Potential reasons for these differences include variations in bone sites examined and methods of bone density measurement, end points of interest, age and menopausal status of subjects, source of subjects, and adjustment for confounding variables. In addition, most studies ofbone density have been conducted only in women, and most have not examined the hip, the site of most serious fractures in the elderly.…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoking and bone mineral density in older men and women.

Hollenbach

Barrett‐Connor²,

Edelstein³

et al. 1993

Am J Public Health

189

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OBJECTIVES. The association between cigarette smoking and bone mineral density was examined prospectively in a population-based study of older Caucasian men and women. METHODS. Smoking patterns were determined at a 1972-1974 baseline evaluation and, again, 16 years later when 544 men and 822 women had bone mineral density measurements taken. RESULTS. Men and women who were cigarette smokers at baseline demonstrated significantly reduced bone mineral density of the hip compared with nonsmokers. Baseline smoking was not associated with significantly lower bone density at non-hip sites. Women demonstrated a significant dose-response relationship between baseline smoking status at all hip sites measured. Both sexes exhibited significant dose-response relationships between hip bone mineral density and change in smoking status between baseline and follow-up, demonstrating that smoking cessation in later life was beneficial in halting bone density loss associated with smoking. CONCLUSIONS. Smoking was positively and significantly associated with decreased hip bone mineral density in old age. Bone loss associated with smoking would be expected to predict an increased risk of hip fracture in those who do not succumb earlier to another complication of tobacco use.

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The Influence of Cigarette Smoking and Age on Bone Loss in Men

Cited by 26 publications

References 6 publications

Osteoporosis in chronic obstructive pulmonary disease

Osteoporosis in chronic obstructive pulmonary disease

Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation.

Cigarette smoking and bone mineral density in older men and women.

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