INTRODUCTION — Osteoporosis is a leading cause of morbidity and mortality in older people. While less common in men than women, over 8 million men in the United States have low bone mass or osteoporosis [1,2]. The mortality rate associated with hip fractures [3,4], as well as vertebral and other major fractures [5], is higher in men than in women; in part, this is related to older age and a greater number of comorbid conditions at the time of fracture. In addition, men are even less likely than women to be evaluated or receive antiresorptive therapy after a hip fracture (4.5 versus 49.5 percent, respectively) [6-8].
The treatment of osteoporosis in men consists of lifestyle measures, hormonal therapy (when indicated), and/or drug therapy. An overview of the approach to therapy of osteoporosis in men will be presented here. The diagnosis, evaluation, and epidemiology of osteoporosis in men are discussed separately. (See "Clinical manifestations, diagnosis, and evaluation of osteoporosis in men" and "Etiology of osteoporosis in men".)
LIFESTYLE MEASURES — In general, lifestyle modifications should be encouraged for all men with osteoporosis. A weight-bearing exercise regimen may be modestly beneficial, given the association of reduced physical activity with bone loss and fracture in older men and the positive effect of exercise in women with osteoporosis (see "Overview of the management of osteoporosis in postmenopausal women", section on 'Exercise' and "Etiology of osteoporosis in men", section on 'Lifestyle factors'). In addition, smoking and excessive alcohol intake should be avoided.
The Recommended Daily Allowance for total calcium intake (from diet and supplements) in men is 1000 mg per day for men age 19 to 70 years and 1200 mg per day for men age 71 years and older. The Recommended Daily Allowance for vitamin D is 600 international units (15 mcg) per day for men age 19 to 70 years and 800 international units (20 mcg) per day for men age 71 years and older. Older persons confined indoors and other high-risk groups may have low serum 25-hydroxyvitamin D (25[OH]D) concentrations at this intake level and may require higher intakes of vitamin D. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Groups at high risk'.)
In some trials, vitamin D has been shown to reduce fracture risk in men and women when administered at a dose of at least 700 international units/day and when given with calcium supplements (see "Calcium and vitamin D supplementation in osteoporosis"). However, in most cases, the addition of pharmacologic therapy is necessary for the treatment of osteoporosis in men [9].
MANAGEMENT OF UNDERLYING CONDITIONS — If osteoporosis is due to another condition (eg, testosterone deficiency), the underlying cause should be treated. Potential offending agents (eg, glucocorticoids, alcohol, tobacco, etc) should be eliminated whenever possible. There are many conditions that may cause osteoporosis in men (table 1). Some of the more common underlying causes are reviewed below. (See "Etiology of osteoporosis in men".)
Hypogonadism — Men with symptomatic hypogonadism, or a clear etiology for hypogonadism (eg, pituitary tumor, Klinefelter syndrome), and a distinctly subnormal serum testosterone concentration are typically treated with testosterone therapy regardless of fracture risk. For hypogonadal men who have a high risk for fracture, we suggest the addition of nonhormonal pharmacologic therapy to testosterone therapy. (See 'Candidates for therapy' below and 'Choice of therapy' below.)
Hypogonadism is among the most commonly identified causes of osteoporosis in men. The diagnosis of hypogonadism and details of testosterone therapy, including a discussion of contraindications and possible increases in cardiovascular risk with testosterone therapy, are discussed elsewhere. (See "Clinical features and diagnosis of male hypogonadism" and "Testosterone treatment of male hypogonadism".)
Testosterone therapy has skeletal benefits in men with serum testosterone levels below the normal range, as illustrated by the studies described below. In one physiologic study, declines in bone mineral density (BMD) due to testosterone deficiency generally did not occur until testosterone levels approached 200 ng/dL [10]. (See "Etiology of osteoporosis in men".)
●Young and middle-aged men – Several studies have demonstrated that testosterone replacement increases BMD in young and middle-aged men with hypogonadism associated with a clear etiology (eg, pituitary tumors, Klinefelter syndrome, gonadotropin-releasing hormone [GnRH] deficiency, etc) [11-14]. For example, in one report of 36 men with previously untreated acquired hypogonadism, most of whom had pituitary tumors, spinal BMD increased (5 percent by dual-energy x-ray absorptiometry [DXA] and 14 percent by computed tomography [CT]) during 12 to 18 months of intramuscular testosterone replacement therapy [11]. The response was greatest in previously untreated men with the lowest BMD at baseline [12] and in skeletally immature men with hypogonadotropic hypogonadism, although, even with prolonged therapy, BMD failed to normalize in men with open epiphyses at the time of testosterone therapy [13]. (See "Testosterone treatment of male hypogonadism".)
●Older men – Only a few randomized controlled trials have examined the effects of testosterone on BMD in older men with low serum testosterone levels.
•Two small trials (n = 70 and n = 48) in men at least 60 or 65 years of age with testosterone levels below the reference range reported improvement in spine BMD by DXA with testosterone supplementation [15,16]. In men whose mean baseline testosterone concentration was in the normal range (367 ng/dL), however, changes in BMD were similar in men treated with testosterone or placebo, probably because the testosterone concentration at baseline was too high to demonstrate a beneficial effect on BMD [17].
•In the Testosterone Trials, a 12-month placebo-controlled randomized controlled trial designed to assess the effects of testosterone administration on a variety of outcomes in men ≥65 years whose serum testosterone level was <275 ng/dL (9.5 nmol/L), there was a greater increase in mean lumbar spine trabecular volumetric BMD (7.5 versus 0.8 percent) (figure 1), as well as lumbar peripheral and hip trabecular and peripheral volumetric BMD (as measured by quantitative CT) in men treated with testosterone [18]. There was also a significant but less impressive increase in areal BMD (DXA) of the lumbar spine. (See "Approach to older men with low testosterone", section on 'Previous efficacy data'.)
One area of uncertainty is when hypogonadal men should be treated with a medication for osteoporosis in addition to testosterone. There are no clinical trial data that address this question, and in particular, the effect of testosterone therapy on fracture risk has not been evaluated. We agree with the recommendation from the Endocrine Society to add a pharmacologic agent with proven antifracture efficacy (eg, a bisphosphonate or teriparatide) in testosterone-treated hypogonadal men whose risk of fracture is felt to remain high [2]. (See 'Hypogonadal men' below.)
Glucocorticoid-induced osteoporosis — Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur at higher BMD values than occur in postmenopausal osteoporosis. The increased risk of fracture has been reported with doses of prednisone or its equivalent as low as 2.5 to 7.5 mg daily. (See "Clinical features and evaluation of glucocorticoid-induced osteoporosis", section on 'Epidemiology and risk factors'.)
Glucocorticoid-induced bone loss should be treated aggressively, particularly in those already at high risk for fracture (older, prior fragility fracture). In other individuals, clinical risk factor and BMD assessment may help guide therapy. The prevention and treatment of glucocorticoid-induced bone loss in men and women is reviewed in detail separately. (See "Prevention and treatment of glucocorticoid-induced osteoporosis".)
Androgen deprivation therapy — Androgen deprivation therapy (bilateral orchiectomy or GnRH agonist administration) reduces BMD in men with prostate cancer and increases the risk of clinical fractures. The management of osteoporosis in men treated with androgen deprivation therapy is reviewed in detail separately. (See "Side effects of androgen deprivation therapy", section on 'Osteoporosis and bone fractures'.)
Gastrointestinal disorders — Osteoporosis is common in malabsorptive disorders (eg, celiac disease) and in inflammatory bowel diseases (eg, Crohn disease, ulcerative colitis).
In celiac disease, osteoporosis is due, in part, to secondary hyperparathyroidism related to vitamin D deficiency. In such patients with severely low vitamin D levels (and particularly if the serum parathyroid hormone [PTH] is high), the need for osteoporosis therapy should be re-evaluated after vitamin D repletion. In severely vitamin D-deficient patients, there can be marked increases in BMD after treatment of osteomalacia with calcium and vitamin D supplementation, such that treatment for "osteoporosis" is not necessary. Similarly, treatment of celiac disease with a gluten-free diet can result in significant improvement in bone mineral density. (See "Management of celiac disease in adults", section on 'Dietary counseling' and "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Vitamin D replacement'.)
In patients with inflammatory bowel disease, there are multiple potential causes of osteoporosis, including disease-related inflammatory activity, glucocorticoid therapy, hypogonadism, and nutritional deficiencies. The treatment of osteoporosis in patients with inflammatory bowel disease is reviewed separately. (See "Metabolic bone disease in inflammatory bowel disease".)
NONHORMONAL PHARMACOTHERAPY
Candidates for therapy — Men with the highest risk of fracture are the ones most likely to benefit from osteoporosis drug therapy; therefore, selection of patients based upon fracture risk, as determined by a combination of bone mineral density (BMD) and clinical risk factors, is desirable. The following approach is largely in agreement with guidelines from The National Osteoporosis Foundation (NOF) (table 2) and the Endocrine Society [2,19]. Although these guidelines are useful, osteoporosis treatment should remain individualized through shared decision-making between patient and clinician.
Eugonadal men — For men who do not have hypogonadism (or in hypogonadal men in whom testosterone therapy is contraindicated), we advise nonhormonal pharmacotherapy in the following groups:
●For men with osteoporosis (history of fragility fracture, or a T-score below -2.5 in men ≥50 years), we recommend nonhormonal pharmacologic therapy. This recommendation is widely accepted, though largely based on the proven efficacy of pharmacologic therapy in women with osteoporosis. (See 'Choice of therapy' below and "Clinical manifestations, diagnosis, and evaluation of osteoporosis in men", section on 'Diagnosis'.)
●For men ≥50 years with T-scores between -1.0 and -2.5 who are at high risk for fracture, we suggest nonhormonal pharmacologic therapy. A reasonable threshold for high risk that may be cost effective in some settings is a 10-year probability (using the Fracture Risk Assessment Tool [FRAX]) of hip fracture or combined major osteoporotic fracture of ≥3.0 or ≥20 percent, respectively.
The FRAX criteria for pharmacologic intervention were chosen on the basis of a United States-specific economic analysis. The treatment of men with BMD T-scores between -1 and -2.5 using FRAX-calculated absolute risk of fracture has not been assessed in clinical trials. Intervention thresholds have been estimated for other countries based upon assessment of absolute fracture risk and country-specific analyses. As examples:
•The 2010 Osteoporosis Canada guidelines recommend pharmacologic therapy to men (and women) at high 10-year absolute risk (>20 percent probability for major osteoporotic fracture) and to individuals over age 50 who have a fragility fracture [20]. For those at moderate risk (10 to 20 percent), the decision to treat should be based upon the presence of additional risk factors not considered in the risk assessment system and upon individual preference.
•In the United Kingdom, the National Osteoporosis Guideline Group recommends an age-dependent intervention threshold for men (and women), which ranges from 7.5 to 30 percent for ages 50 to 80 years [21]. For clinicians in the United Kingdom, intervention thresholds may be accessed directly from the FRAX website.
In an analysis of data from a population-based cohort of 5880 older men (mean age 73.6 years), the proportion of men identified for osteoporosis treatment varied from 2.2 to 25.3 percent, depending upon the different criteria used to assess osteoporosis and risk for fracture [22]. Use of the BMD criteria proposed by the World Health Organization (WHO; femoral neck T-score ≤-2.5 derived from female reference database) identified the fewest men for osteoporosis treatment (2.2 percent), whereas use of the FRAX intervention thresholds set by the NOF for men with BMD T-scores between -1 and -2.5 identified the most men for treatment (25.3 percent). During the 10-year follow-up period, 177 (3 percent) men had a hip fracture. The observed 10-year fracture probabilities were highest among the men identified as having osteoporosis by the WHO BMD criteria (20.6 versus 9.5 percent using FRAX thresholds set by the NOF). (See "Clinical manifestations, diagnosis, and evaluation of osteoporosis in men", section on 'Diagnosis'.)
The FRAX intervention thresholds as proposed by the NOF increase the proportion of older men who are candidates for therapy, whereas restricting treatment only to men who meet the WHO BMD criteria reduces the total number of men treated, but may exclude some men who might benefit from treatment. Of note, the use of a male reference database (rather than a female reference database as proposed by the WHO) to calculate T-scores leads to the identification of many more men for treatment (see "Overview of dual-energy x-ray absorptiometry", section on 'Reference databases'). Even with the FRAX-NOF thresholds, some high-risk patients with secondary causes of osteoporosis, such as men receiving high-dose glucocorticoids, gonadotropin-releasing hormone (GnRH) agonists, or who have undergone organ transplantation, should often be treated even if they fail to meet the criteria listed above.
Hypogonadal men — Most symptomatic hypogonadal men will be on testosterone replacement therapy. For testosterone-treated hypogonadal men who have a high risk for fracture, we suggest the addition of nonhormonal pharmacologic therapy to testosterone therapy. In the absence of definitive data upon which to objectively classify fracture risk in hypogonadal men (see 'Hypogonadism' above), we consider high risk to include the following:
●High-dose glucocorticoids
●Frequent falls
●History of a recent fragility fracture, particularly with a BMD T-score below -2.5 at any skeletal site
●BMD T-scores below -3.5 or even below -3.0 if they have other risk factors for fracture
●BMD T-score <-2.5 (or fragility fracture) even after receiving adequate testosterone replacement therapy for two years (based upon clinical trial data in men showing that testosterone continues to improve BMD for at least two years [15])
For hypogonadal men who are not taking testosterone, the approach is the same as for eugonadal men. (See 'Eugonadal men' above.)
Choice of therapy — Men seem to respond to available nonhormonal osteoporosis pharmacologic therapies in the same way that women respond so that, for the most part, the approach to treating men and women with osteoporosis is quite similar. There are few trials evaluating the effect of pharmacologic agents to reduce fracture risk in men [23,24]. In the absence of high-quality, head-to-head drug comparison trials to determine the relative efficacy of the individual drugs, choice of therapy should be based upon efficacy, safety, cost, convenience, and other patient-related factors.
Bisphosphonates — For most men who require pharmacologic therapy, we suggest oral bisphosphonates as initial therapy because of their efficacy, favorable cost, and the availability of long-term safety data. In a meta-analysis of trials in men with osteoporosis, bisphosphonates reduced the risk of vertebral (six trials, relative risk [RR] 0.37, 95% CI 0.25-0.54) and nonvertebral (four trials, RR 0.60, 95% CI 0.40-0.90) fracture [25].
Among the available oral bisphosphonates, we (and others) suggest weekly alendronate or risedronate [2,20,26,27]. In randomized trials, alendronate and risedronate improved BMD and significantly reduced the risk of vertebral fracture [28-33]. As an example, in a two-year, open-label trial of 316 men with osteoporosis who were randomly assigned to risedronate (5 mg daily) or an active comparator group (alfacalcidol or vitamin D), the incidence of vertebral fractures was significantly lower in the risedronate group (9.2 versus 23.6 percent) [32]. In a meta-analysis of trials evaluating individual osteoporosis drugs in men with osteoporosis, there was a significant reduction in the risk of vertebral fractures with alendronate (two trials, RR 0.33, 95% CI 0.16–0.69) and risedronate (two trials, RR 0.43, 95% CI 0.24–0.75) [25].
The dosing, adverse effects, and the prescribing instructions designed to minimize gastrointestinal side effects of oral bisphosphonates are reviewed in detail elsewhere. (See "Bisphosphonate therapy for the treatment of osteoporosis", section on 'General Principles' and "Risks of bisphosphonate therapy in patients with osteoporosis", section on 'Risks specific to oral bisphosphonates'.)
Bisphosphonates are generally not recommended for those with estimated glomerular filtration rate (eGFR) below 30 to 35 mL/min, although the evidence upon which this practice is based is limited. Management of osteoporosis in people with chronic kidney disease is reviewed separately. (See "Osteoporosis in patients with chronic kidney disease: Diagnosis and evaluation" and "Osteoporosis in patients with chronic kidney disease: Management".)
Contraindications or intolerance to oral bisphosphonates — Intravenous (IV) bisphosphonates, zoledronic acid (ZA) and ibandronate, offer an alternative for individuals who cannot tolerate oral bisphosphonates or who find the dosing regimen more convenient. ZA is the only IV bisphosphonate that has demonstrated efficacy for fracture prevention in men [34,35], and it is therefore our agent of choice.
Men who have esophageal disorders (achalasia, scleroderma involving the esophagus, esophageal strictures, varices), gastrointestinal intolerance to oral bisphosphonates, or an inability to follow the dosing requirements of oral bisphosphonates (including an inability to sit upright for 30 to 60 minutes and/or to swallow a pill) should not be treated with oral bisphosphonates. Oral bisphosphonates should also be avoided after certain types of bariatric surgery (eg, Roux-en-Y gastric bypass) due to uncertainty about medication absorption/bioavailability and theoretical risk for damage to surgical anastomoses within the gastrointestinal tract.
In the absence of direct fracture efficacy data for IV ibandronate, we prefer ZA based upon the following trials:
●In the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) Recurrent Fracture Trial, 2127 men and women with hip fracture were randomly assigned to receive yearly ZA (5 mg) or placebo within three months of surgical repair [34]. Patients also received vitamin D, if the 25-hydroxyvitamin D [25(OH)D] concentration was <15 mg/dL or unknown, and calcium. After a median follow-up of 1.9 years, new fractures occurred in 8.6 and 13.9 percent of individuals in the ZA and placebo groups, respectively, representing a relative risk (RR) reduction of 35 percent (hazard ratio [HR] 0.65, 95% CI 0.50-0.84). All-cause mortality, a secondary safety endpoint, was lower in the ZA group compared with placebo group (HR 0.72, 95% CI 0.56-0.93).
●In a separate trial, 1199 men with primary or hypogonadism-associated osteoporosis (mean T-score femoral neck -2.23, approximately 30 percent with prevalent vertebral fractures) were randomly assigned to ZA (5 mg IV) or placebo at baseline and 12 months [35]. All patients received calcium and vitamin D supplementation. After two years, there were fewer morphometric vertebral fractures in the ZA group (1.6 versus 4.9 percent in the placebo group, RR 0.33, 95% CI 0.16-0.70).
Prior to receiving IV bisphosphonates, patients should be assessed for hypocalcemia, vitamin D deficiency, and renal impairment by measuring serum calcium, creatinine, and 25(OH)D. It is unclear what level of 25(OH)D is desirable prior to IV bisphosphonate infusion, although many experts recommend levels of at least 20 to 25 ng/mL (50 to 62 nmol/L). Additional information regarding dosing, adverse effects, and the prescribing instructions designed to minimize adverse effects is reviewed elsewhere. (See "Bisphosphonate therapy for the treatment of osteoporosis", section on 'IV regimen' and "Risks of bisphosphonate therapy in patients with osteoporosis".)
Contraindications/intolerance to any bisphosphonates — For men who cannot tolerate oral or IV bisphosphonates or who have difficulty with the dosing requirements, options include teriparatide (PTH 1-34) or denosumab. For men with severe osteoporosis (low BMD [T-score <-2.5] and at least one fragility fracture) who are unable to tolerate any of the available bisphosphonates, we suggest teriparatide.
●Teriparatide – Teriparatide, an anabolic agent, is generally reserved for men with severe osteoporosis (low BMD [T-score <-2.5] and at least one fragility fracture), or men who have failed previous therapy (eg, continue to fracture after one year of bisphosphonate therapy).
In the largest trial to date, 437 men with osteoporosis were randomly assigned to receive teriparatide (20 or 40 mcg/day by subcutaneous injection) or placebo. After 11 months of treatment, teriparatide increased spine and femoral neck BMD more than placebo (5.9 and 9 percent in the low- and high-dose groups at the spine; 1.5 and 2.9 percent in the low- and high-dose groups at the femoral neck) [36]. The study was stopped early due to occurrence of osteosarcomas in rats, which limited the assessment of fracture reduction efficacy in these men. (See "Parathyroid hormone/parathyroid hormone-related protein analog therapy for osteoporosis", section on 'Choice of therapy'.)
Contraindications, dosing, adverse effects, monitoring, and duration of therapy are reviewed separately. (See "Parathyroid hormone/parathyroid hormone-related protein analog therapy for osteoporosis".)
●Denosumab – Denosumab may have a role for the treatment of osteoporosis in men who are intolerant of or unresponsive to other therapies and in those with impaired renal function. Denosumab increases BMD in men with low bone mass [37], but it has not yet been shown to reduce fracture risk in men, except for men with prostate cancer receiving androgen deprivation therapy. (See "Side effects of androgen deprivation therapy", section on 'Osteoporosis and bone fractures'.)
Delaying or discontinuing denosumab therapy increases the risk of multiple rebound vertebral fractures, a phenomenon documented primarily in women but also reported in men [38]. This problem is reviewed in more detail separately. (See "Denosumab for osteoporosis", section on 'Discontinuation or delay of denosumab'.)
●Other – Other agents, including romosozumab and abaloparatide, are being evaluated for the treatment of men with osteoporosis [39-41]. In a randomized trial of 245 men with T-score ≤-2.5 or ≤-1.5 plus history of fragility fracture, romosozumab increased BMD at the lumbar spine and total hip more than placebo over 12 months [39]. However, there were more serious cardiovascular adverse events in men receiving romosozumab (4.9 versus 2.5 percent in the placebo group), although the increase was not statistically significant. Neither abaloparatide nor romosozumab have yet been approved by the United States Food and Drug Administration (FDA) for the treatment of osteoporosis in men.
Combination therapy — Concurrent treatment with alendronate and teriparatide attenuates the ability of teriparatide to increase spine and hip BMD in men [42]. Thus, we do not recommend concurrent use of bisphosphonates with teriparatide for the management of osteoporosis. However, the immediate use of bisphosphonates after teriparatide is withdrawn may maintain or even increase BMD in men further [43]. (See "Parathyroid hormone/parathyroid hormone-related protein analog therapy for osteoporosis", section on 'Management after teriparatide'.)
MONITORING THE RESPONSE TO THERAPY — While there are a number of approaches to monitoring therapy, there is no consensus on the optimal approach. For patients starting on therapy, we typically obtain a follow-up dual-energy x-ray absorptiometry (DXA) of hip and spine after one or two years and, if bone mineral density (BMD) is stable or improved, we monitor less frequently thereafter. There may be limitations to the use of spine DXA in aging men due to interference from osteophytes and vascular calcifications on the spine measurement. The use of biochemical markers of bone turnover to monitor response to therapy is not well studied in men and is not routinely recommended.
Monitoring for the identification of patients who may require a change in therapy is reviewed elsewhere. (See "Overview of the management of osteoporosis in postmenopausal women", section on 'Response to therapy'.)
DURATION OF THERAPY — There is currently no consensus on how long to continue bisphosphonate therapy in men. In postmenopausal women with osteoporosis, alendronate, risedronate, and zoledronic acid (ZA) have been shown to reduce fracture risk for up to 10, 7, and 6 years, respectively. Due to concerns about possible long-term risks of bisphosphonates (see "Risks of bisphosphonate therapy in patients with osteoporosis"), many experts recommend a "drug holiday" in selected groups of women and in men. We suggest suspending bisphosphonate treatment for men who have taken alendronate for five years or who have received ZA once yearly for three years if their BMD is stable, they have not had previous fragility fractures, and they are at low risk for fracture in the near future. Bone mineral density (BMD) should be monitored approximately every two years after suspending therapy, and therapy should generally be resumed if BMD declines significantly or if the patient develops a new fragility fracture.
This topic is reviewed in detail separately. (See "Bisphosphonate therapy for the treatment of osteoporosis", section on 'Duration of therapy'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Osteoporosis" and "Society guideline links: Clinical densitometry".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Osteoporosis (The Basics)" and "Patient education: Calcium and vitamin D for bone health (The Basics)")
●Beyond the Basics topics (see "Patient education: Osteoporosis prevention and treatment (Beyond the Basics)" and "Patient education: Calcium and vitamin D for bone health (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS — The treatment of osteoporosis in men includes lifestyle measures, calcium and vitamin D supplementation, and hormonal or nonhormonal pharmacotherapy.
●Important lifestyle measures include exercise, smoking cessation, counseling on fall prevention, and avoidance of heavy alcohol use for all men with osteoporosis. (See 'Lifestyle measures' above.)
●In men with osteoporosis (T-score below -2.5), we suggest calcium and vitamin D supplementation (Grade 2B). Although the optimal intake (diet plus supplement) has not been clearly established in men with osteoporosis, approximately 1000 to 1200 mg of calcium (total diet plus supplement) and 600 to 800 international units of vitamin D daily are generally suggested. (See "Calcium and vitamin D supplementation in osteoporosis".)
The dose of calcium and vitamin D may vary in individuals with coexisting medical conditions. (See "Calcium and vitamin D supplementation in osteoporosis", section on 'Coexisting medical problems'.)
●If osteoporosis is due to another condition (eg, testosterone deficiency), the underlying cause should be treated. (See 'Management of underlying conditions' above.)
●For men with osteoporosis (history of fragility fracture, or in men ≥50 years, a T-score below -2.5) who do not have hypogonadism (or in hypogonadal men who are not receiving testosterone therapy), we recommend nonhormonal pharmacologic therapy (Grade 1B). (See 'Candidates for therapy' above.)
●For similar men ≥50 years with T-scores between -1.0 and -2.5 who are at high risk for fracture, we suggest nonhormonal pharmacologic therapy (Grade 2B). A reasonable threshold for high risk that may be cost effective in some settings is a 10-year probability (using the Fracture Risk Assessment Tool [FRAX]) of hip fracture or combined major osteoporotic fracture of ≥3.0 or ≥20 percent, respectively. (See 'Candidates for therapy' above.)
●For testosterone-treated hypogonadal men who have a high risk for fracture, we suggest the addition of nonhormonal pharmacologic therapy to testosterone therapy (Grade 2C). High-risk groups might include hypogonadal men whose bone mineral density (BMD) T-score is <-2.5 even after receiving adequate testosterone replacement therapy for two years; men on high-dose glucocorticoids; men with frequent falls; men who have had a recent fragility fracture, particularly if they have a BMD T-score below -2.5 at any skeletal site; or men with T-scores below -3.5 or even below -3.0 if they have other risk factors for fracture. (See 'Hypogonadal men' above.)
●For nonhormonal pharmacotherapy in men, we suggest bisphosphonates as first-line therapy (Grade 2B). We favor alendronate or risedronate over other available bisphosphonates because of clinical trial data demonstrating efficacy in men with osteoporosis. (See 'Bisphosphonates' above.)
Men who have esophageal disorders, gastrointestinal intolerance to oral bisphosphonates, certain types of bariatric surgery (eg, Roux-en-Y gastric bypass), or an inability to follow the dosing requirements of oral bisphosphonates should not be treated with oral bisphosphonates and can be treated instead with intravenous (IV) bisphosphonate therapy. Zoledronic acid (ZA) is the only IV bisphosphonate that has demonstrated efficacy for fracture prevention in men. (See 'Contraindications or intolerance to oral bisphosphonates' above.)
Teriparatide and denosumab may have a role in men who are intolerant of or unresponsive to any bisphosphonate. (See 'Contraindications/intolerance to any bisphosphonates' above.)
●For men with severe osteoporosis (low BMD [T-score <-2.5] and at least one fragility fracture) who are unable to tolerate any of the available bisphosphonates, we suggest teriparatide (Grade 2B). Denosumab is an alternative option. (See 'Contraindications/intolerance to any bisphosphonates' above and "Parathyroid hormone/parathyroid hormone-related protein analog therapy for osteoporosis" and "Denosumab for osteoporosis".)
●While there are a number of approaches to monitoring therapy, there is no consensus on the optimal approach. Patients can be monitored with BMD measurements, as is recommended for postmenopausal women. For patients starting on therapy, we typically obtain a follow-up dual-energy x-ray absorptiometry (DXA) of hip and spine after two years and, if BMD is stable or improved, less frequent monitoring thereafter. (See "Overview of the management of osteoporosis in postmenopausal women", section on 'Monitoring'.)
