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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 55:M487-M488 (2000)
© 2000 The Gerontological Society of America

Editorial

Facets of Femoral Fracture

Horace M. Perry, IIIa

a Geriatric Research, Education, and Clinical Center, Saint Louis VA Medical Center, and Division of Geriatrics, Saint Louis University Medical School, Missouri

Horace M. Perry, III, 1402 South Grand Avenue, Saint Louis, MO 63104.

Decision Editor: John E. Morley, MB, BCh

HIP fracture remains the most feared of the so-called fragility fractures in older adults. It is the result of trauma (frequently from falling) and osteoporotic bone. A decade ago, only prolonged estrogen replacement in early menopause was accepted as diminishing femoral fracture incidence. Later, a French study reported that vitamin D and calcium replacement significantly decreased fracture incidence in older women (mean age of 88 years) in nursing homes (1). A large study of free-living individuals, however, did not replicate this finding (2). These individuals, however, were younger, and there was a tendency to reduce fractures with vitamin D supplementation. Because it is clear that vitamin D levels decrease with age (3), this difference in age may account for the difference in findings. These results suggest that calcium and vitamin D supplementation should be provided for all older individuals living in nursing homes.

More recently, a series of reports have documented that alendronate decreases fracture incidence (including femoral fracture) in vitamin D- and calcium-replete postmenopausal women across a wide range of ages and bone densities (4)(5)(6). This therapy increases bone mass. Other biophosphonates seem likely to offer similar benefits when they become available (7). Selective estrogen receptor modulators like tamoxifen and raloxifene also hold promise to reduce hip fracture incidence (8). In addition, they may also reduce breast cancer incidence or recurrence.

Other modalities, such as exercise, may also reduce fracture incidence in older women. A report in this issue demonstrates an increase in femoral bone mineral density (BMD) in women wearing weighted vests and performing weight-bearing exercise on a regular schedule (9). A much shorter study published recently failed to demonstrate any significant change in markers of bone formation and resorption (10). The major difference in the two studies is length of time of follow-up, which is considerable. Interventions that effect bone mass frequently require at least 6 months to begin to alter bone mass. Similarly, exercise protocols require a finite length of time to have effects. Effects of resistance exercise are frequently said to be maximal at 6 months, although some report improvement up to 12 months (11). The short-term study did not specify or mandate exercise. No effects on strength were noted. Not surprisingly, no effect on bone metabolism was noted either. Specific weight-bearing exercise (jumping) was mandated in the longer study. The study was carried out long enough to see effects. Thus, it should not be surprising that the short-term study had minimal results, and the long-term study, published in this issue, had more demonstrable effects.

As information accumulates about successful prevention of femoral fracture in women, attention is bound to shift to other aspects of this problem. Osteoporosis and hip fracture remain poorly studied in men. Thus, there is no widely promulgated definition of osteoporosis/osteopenia for men, such as the World Health Organization has done for women. Reports suggest that accepting similar population-based definitions describe a group of men with increased risk for fracture (12). Thus, a BMD of more than 2.5 standard deviations below the mean for young men would be pathologic bone loss in older men. Other measurements may be better identifiers of fracture risk, however. The most tantalizing of these in men is low bioavailable testosterone. Serum testosterone declines with age in longitudinal studies, and sex hormone binding globulin rises with age (13). Therefore, testosterone available to tissues, or bioavailable testosterone, declines with age more than the apparent decline in total testosterone.

In case control studies, men with hip fractures are commonly reported to have very low (i.e., hypogonadal) serum levels of testosterone (14). Kenney and her colleagues report bone density results in men over the age of 65 with low levels of bioavailable testosterone (15). This study examines only men with low bioavailable testosterone. Despite this, they showed a significant positive relationship between bioavailable testosterone and femoral neck BMD. Serum estrogen levels were not good predictors of BMD. This finding stands in distinction to several recent reports (16)(17) that suggest serum estrogen levels are better predictors of bone density in men than serum androgens. This finding, as Kenney and colleagues point out, is not consistent (15)(18)(19). It is possible, for example, that serum estrogen in older men is an excellent proxy for tissue-available testosterone. The precise relative importance of serum androgens and estrogens and age-related bone loss remain to be clearly worked out. In view of earlier reports of morbidity associated with low-dose estrogen therapy in men (20), however, such therapy would not appear to be very promising in men. It is hard to argue with the conclusion that testosterone replacement in hypogonadal men needs to be evaluated as the next step for prevention of hip fracture.

One other major aspect of hip fracture is addressed in this issue—recovery. Magaziner and associates carefully document a series of steps in eight domains in recovery from hip fracture (21). Of some interest is the finding that social activities actually increase post hip fracture, as the authors note, presumably because of interactions between patients and caregivers. Cognition—delirium—in the hospital resolves by 2 months, as does depression, and the patient apparently gets on with recovery. All these steps appear to occur in a relatively constant order and at a reasonably constant rate. The report has significance to physicians in that it allows the physician to ascertain whether an individual patient is progressing at the expected rate. The report also allows a physician to predict when a patient might expect to recover certain functions or interactions after a fracture. The report should provide comfort to a large number of individuals with hip fracture.

A fourth study, by Michel and colleagues, describes who is likely to recover how much function (22). Again, this study provides important information to practicing physicians. It identifies individuals who are likely to recover well, permitting the physician to reassure such individuals and actively pursue remedial interventions, if necessary. On the other hand, the report identifies groups of individuals who are not likely to do well. Again, this is useful to the physician, allowing him or her, in consultation with the family or other caregivers, to predict and plan for outcomes. Similarly, they can determine how strenuously to intervene.

Hip fracture is a major cause of morbidity and mortality in older persons. The four articles in this issue address major clinical issues vis-à-vis (i) the putative role of testosterone in the loss of bone in men, (ii) the effect of weighted vest exercise on osteoporosis, and (iii) the predictors and time course of recovery from hip fracture in older persons.

Received May 5, 2000

Accepted May 8, 2000


    References
 Top
 References
 

  1. Chapuy MC, Arlot ME, Duboeuf F, et al. 1992. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med 327:1637-1642. [Abstract]
  2. Lips P, Graafmans WC, Ooms ME, Bezemer PD, Bouter LM, 1996. Vitamin D supplementation and fracture incidence in elderly persons. A randomized, placebo-controlled clinical trial. Ann Intern Med 124:400-406. [Abstract/Free Full Text]
  3. Perry HM, III Horowitz M, Morley JE, Patrick P, Vellas B, Baumgartner R, Garry PJ, 1999. Longitudinal changes in serum 25 hydroxyvitamin D in older people. Metabolism 48:1028-1032. [Medline]
  4. Ensrud KE, Black DM, Palermo L, et al. 1997. Treatment with alendronate prevents fractures in women at highest risk: results from the Fracture Intervention Trial. Arch Intern Med 157:2617-2624. [Abstract]
  5. Cummings SR, Black DM, Thompson DE, et al. 1998. Effect of alendronate on risk of fracture in women with low bone density but without vertebral fractures: results from the Fracture Intervention Trial. JAMA 280:2077-2082. [Abstract/Free Full Text]
  6. Black DM, Cummings SR, Karpf DB, et al. 1996. Randomized trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Fracture Intervention Trial research group. Lancet 348:1535-1541. [Medline]
  7. Harris ST, Watts NB, Genant HK, et al. 1999. Effects of risedronate treatment on vertebral and nonvertebral fractures in women with postmenopausal osteoporosis. A randomized controlled trial. JAMA 282:1344-1352. [Abstract/Free Full Text]
  8. Delmas PD, Bjarnason NH, Mitlak BH, et al. 1997. Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women. N Engl J Med 337:1641-1647. [Abstract/Free Full Text]
  9. Snow CM, Shaw JM, Winters KM, Witzke KA, 2000. Long-term exercise using weighted vests prevents hip bone loss in postmenopausal women. J Gerontol Med Sci 55A:M489-M491. [Abstract/Free Full Text]
  10. Greendale GA, Salem GJ, Young JT, et al. 2000. A randomized trial of weighted vest use in ambulatory older adults: strength, performance, and quality of life outcomes. J Am Geriatr Soc. 48:305-311. [Medline]
  11. Morganti CM, Nelson ME, Fiatarone MA, et al. 1996. Strength improvements with 1 year of progressive resistance training in older women. Med Sci Sports Exerc 27:906-912.
  12. Melton LJ, III Atkinson EJ, O'Connor MK, O'Fallon WM, Riggs BL, 1998. Bone density and fracture risk in men. J Bone Miner Res 13:1915-1923. [Medline]
  13. Morley JE, Kaiser FE, Perry HM, III et al. 1997. Longitudinal changes in testosterone, luteinizing hormone, and follicle-stimulating hormone in healthy older men. Metabolism 46:410-413. [Medline]
  14. Jackson JA, Riggs MW, Spiekerman AM, 1992. Testosterone deficiency as a risk factor for hip fracture in men: a case control study. Am J Med Sci 304:4-8. [Medline]
  15. Kenny AM, Prestwood KM, Marcello KM, Raisz LG, 2000. Determinants of bone density in healthy older men with low testosterone levels. J Gerontol Med Sci 55A:M492-M497. [Abstract/Free Full Text]
  16. Center JR, Nguyen TV, White CP, Eisman JA, 1997. Male osteoporosis predictors: sex hormones and calcitropic hormones. J Bone Miner Res 12:S368
  17. Johnston C, 1997. Sex steroids and bone mass in older men: positive associations with serum estrogens and negative associations with androgens. J Clin Invest 100:1755-1759. [Medline]
  18. Greendale GA, Edelstein S, Barrett-Connor E, 1997. Endogenous sex steroids and bone mineral density in older women and men: the Rancho Bernardo study. J Bone Miner Res 12:1833-1843. [Medline]
  19. Wishart JM, Need AG, Horowitz M, Morris HA, Nordin BEC, 1995. Effect of age on bone density and bone turnover in men. Clin Endocrinol 42:141-146. [Medline]
  20. The Coronary Drug Project Research Group1973. The coronary drug project. Findings leading to discontinuation of the 25-mg/day estrogen group. JAMA 226:652-657. [Medline]
  21. Magaziner J, Hawkes W, Hebel JR, et al. 2000. Recovery from hip fracture in eight areas of function. J Gerontol Med Sci 55A:M498-M507. [Abstract/Free Full Text]
  22. Michel J-P, Hoffmeyer P, Klopfenstein C, et al. 2000. Prognosis of functional recovery 1 year after hip fracture: typical patient profiles through cluster analysis. J Gerontol Med Sci 55A:M508-M515. [Abstract/Free Full Text]



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