USPSTF new osteoporosis screening guidelines

 the US Preventive Services Taskforce (USPSTF) recently published new guidelines regarding screening for osteoporosis to prevent fractures (see osteoporosis USPSTF recs JAMA2025 in dropbox, or doi:10.1001/jama.2024.27154)

 

Recommendations, for adults 40 years or older without known osteoporosis or history of fragility fractures, and without having secondary osteoporosis from cancer, metabolic bone diseases, hyperthyroidism, or chronic steroid use:

-- screen women 65 years or older for osteoporosis, moderate certainty of evidence, Grade B

-- screen postmenopausal women younger than 65 at increased risk for osteoporosis, moderate certainty of evidence, Grade B

-- men: insufficient evidence for screening for osteoporosis in the balance of benefits and harms, Grade I

 

--there are important caveats to these (and all USPSTF recommendations) noted in the document:

    -- "USPSTF recognizes that clinical decisions involve more considerations than evidence alone. clinicians should understand the evidence but individualize decision-making to the specific patient or situation"

    -- "USPSTF does not consider the costs of providing a service in this assessment"

 

Their comments/justifications, with my embedded critiques/additions italicized and in brackets

 

Definitions:

-- fragility fracture: a "low energy" or "low trauma" facture sustained from falling from standing height or lower that would not be expected to cause a broken bone

    -- [my comment: there is some play here: there clearly is a difference from a fracture associated with fall off a 40-foot ladder and a fracture from a height of a couple of feet. a pretty recent study found that in 66,874 women in the Women's Health Initiative Study, comparing those who self-reported a broken bone in many sites (hip, upper leg, pelvis, knee, lower leg or ankle, foot (not toes), coccyx, vertebrae, lower arm or wrist, hand (not finger), elbow, upper arm or shoulder) with those not experiencing a fracture, there was a 49% increased risk of a subsequent fracture. this all suggests from this prospective observational study that a traumatic fracture from an undefined relatively low height still seems to be a risk factor for more fractures. the baseline data in this study found no major difference between the groups on estrogen therapy, physical activity, vitamin D intake, calcium intake, physical function, diabetes, smoking, number of falls in past year, and BMI: see osteoporosis inc traumatic fx jamaintmed2021 in dropbox, or doi:10.1001/jamainternmed.2021.2617)]. unfortunately,  this study did not have data on the actual traumatic events and the level of the falls}

-- chronic corticosteroid use: [not defined more precisely by dose or length of exposure]

-- major osteoporotic fracture (MOF): fracture of the hip, spine, wrist, or shoulder

-- [and, as noted below, the recommendations exclude 4 items associated with secondary osteoporosis, but that is a small percentage of all of the secondary causes (more below). No explanation why these 4 were singled out}

 

Comments:

-- Osteoporotic fractures are associated with lots of collateral effects, including psychological distress, subsequent fractures, loss of independence, reduced ability to perform activities of daily living (ADLs), and death

--repair of fractures does not necessarily bring women back to normal:

    -- hip fractures: only 40-60% of people return to their prefracture level of mobility and ability to perform ADLs

    -- [hip fractures are still associated with significant mortality overall. There used to be about a 30% 1-year mortality, though now getting better. But with 1.4 million women getting total hip replacements, that’s still lots of people [my comment]]

    --[vertebral fractures: about 30% of women have chronic pain, even after the fracture heals]

 

 

-- for low bone mass, a frequent precursor for developing osteoporosis: 

 

 

-- [the above graphs on the prevalence of osteoporosis and osteopenia are from the feds and not in the USPSTF document]

-- of note, though BMD is a strong predictor of fragility fractures, age is a stronger determinant

-- older adults with the same low BMD as younger ones are still at higher risk because they have increased risk of falling (balance problems, vision/hearing problems, cognitive decline...)

 

Risk factors for osteoporosis [the document is really unclear: at different times in the document they include different risk factors. this list includes all of them included in the USPSTF text]

-- menopausal status, low body weight, parental history of hip fracture, cigarette smoking, excess alcohol intake [not defined specifically, though likely at least 3 drinks/d, per other guidelines. But are 1-2 drinks/day really okay, especially if drinking like that for years?? is there a cumulative effect? this amount of drinking is certainly bad for the heart or cancer prevention: see below]

-- “other medical conditions and medications”, which are also listed but not on the above list, include corticosteroids [no info on how high a dose, how often, or if a cumulative cutpoint], diabetes treated with insulin [again, no indication of dose/amount of insulin]

    -- [and, diabetes itself is associated with osteoporosis: https://pmc.ncbi.nlm.nih.gov/articles/PMC10515121/]

    -- [and in general, systemic inflammation is associated with increased osteoporosis: https://pmc.ncbi.nlm.nih.gov/articles/PMC1308846/]

-- [no note of other medications that can be associated with decreased bone density, such as some of the anti-seizure meds (valproate, carbamazepine, the older seizure meds such as phenytoin, phenobarbital, and some studies finding topiramate and lamotrigine), PPIs, SSRIs, medroxyprogesterone acetate, hormone deprivation therapy, warfarin, and several oncology agents: https://journals.sagepub.com/doi/10.1177/1759720X14546350]

--[there are also other conditions not mentioned above that are incorporated into the FRAX risk calculators below; the FRAX score, for example, includes previous fracture (not just parental history of hip fracture), rheumatoid arthritis, and alcohol consumption of at least 3 units/d, though not diabetes or meds other than glucocorticoids]           

 

Screening tests (the USPSTF does comment that there needs more research "to develop and validate new primary care-feasible risk assessment tools that accurately predict risk of hip and nonhip major fractures":

-- BMD alone is not the most useful predictor of fracture risk, especially in younger people

-- there are 3 fracture risk tools, including FRAX (the most studied), the Fracture Risk Calculator, and the Garvan Fracture Risk Calculator

-- here is a reproduction of the FRAX risk assessment that is included in the USPSTF documents:

 

 

 

    -- though BMD is not necessarily included in the risk evaluations, adding it does improve its accuracy

    -- the FRAX risk calculator predicts the 10-year probability of hip fracture or major osteoporotic fractures, which adds fractures in the spine, wrist or shoulder, as well as hip)

    -- there are several concerns about FRAX:

        -- [the above components of FRAX is not exactly what is in the standard FRAX calculator (frax.shef.ac.uk/FRAX/tool.aspx?country=9 ), which includes femoral neck BMD, though the USPTF document does not include this standard FRAX calculator for ??reason].

        -- FRAX also uses binary inputs (yes or no) for glucocorticoids and alcohol [though they specify at least 3 units of alcohol/day, unlike the USPSTF. However, we do know that men and women have different thresholds for alcohol ingestion. and 3 units is a lot. how was this derived? should it really be binary? are 2 units okay? does 8 units have the same risk as 3 units? should characterizing the alcohol consumption include for how long/what cumulative dose? unfortunately, the <3 unit cutpoint actually validates that as an okay amount to drink, which goes in the face of lots of data suggesting that the target needs to be zero to effectively decrease cardiovascular and cancer complications (http://gmodstmedblogs.blogspot.com/2025/01/alcohol-and-cancers.html)]

        -- [the standard FRAX calculator only includes femoral BMD and not lumbar spine BMD or evaluation of trabecular bone score, see below]

        -- [also, no inclusion of history of falls or frailty]

 

--[there was no information on the BMD screening interval, other than that we need more data]

    -- there are some data suggesting that for 10% of women to develop osteoporosis (https://www.e-enm.org/journal/view.php?doi=10.3803/EnM.2022.1429):

        -- if a woman has a normal BMD, it takes about 17 years

        -- if a woman has mild osteopenia (T-score between -1 and -1.5), it takes 13.2 years

        -- if a woman has moderate osteopenia (T-score between -15 to -2), it takes 15.0 years

        -- if a woman has severe osteopenia (T-score between -2 and -5.5), it takes 1.5 years

        -- and, overall there is a limit by the BMD machines themselves (in general, the issue is that the inherent variability of the BMD determination by the machine is pretty high, such that screening in less than 1.5 years may be not so accurate (differences in results may be less than the variability from the machine)

            -- that being said, there is better accuracy if the patient has their BMD checked using the same machine each time 

        -- it is reasonable to check BMD around 2 years after starting bisphosphonates (and best on the same machine) to assess BMD stability/increase or BMD decrease:

            -- if BMD is stable/increased, recheck BMD 2-3 years later, though if patient has fragility fracture on meds or the T-score that is not better than -2.5, it may be best to use stronger antiresorptive therapy (anti-anabolic)

            -- if BMD is decreased, it is reasonable to check on calcium and vitamin D intake (the 25(OH)vitamin D level), assess medication adherence and appropriateness of med taking (eg, fasting in the morning and not eat/drink for at least 30 minutes, other than the water to take the pill)

                -- also, checking bone turnover markers might also be a useful tool to assess medication adherence and absorption, and if okay, could consider repeat BMD in 1-2 years (1 year only if the BMD machines have less variability than that)

                -- also consider the possibility of secondary osteoporosis (eg CKD, osteomalacia, hyperthyroidism, hyperparathyroidism, meds, celiac disease, alcohol, chronic inflammatory conditions, diabetes, several cancers, etc)

 

Treatment:

-- no comment on the specifics (this document is mostly on screening), just that there are many FDA-approved therapies: bisphosphonates, denosumab, romosozumab, parathyroid hormone, raloxifene, calcitonin and estrogen (with of without progesterone)

-- here are some of the data on effectiveness:

    -- Bisphosphonates:

        -- About 50% decrease in vertebral fractures, absolute rate difference from placebo: 18 fewer fractures per 1000 people treated (the document did not indicate over how many years of treatment or age of starting)

        -- About 30% decrease in hip fractures: absolute rate difference of 3 per 1000 people

            -- [would earlier detection and treatment further decrease the absolute risk over many years??]

            -- time to benefit of bisphosphonate therapy to prevent fractures: 12.4 months (see osteoporosis bisphosph time to benefit jamaintmed2021 in dropbox, ordoi:10.1001/jamainternmed.2021.6745)

        -- [and, perhaps most importantly, If not take on empty stomach, there is about a 60%  decreased absorption!!!, with some studies finding that only a negligible 1% is absorbed if not an empty stomach: https://pmc.ncbi.nlm.nih.gov/articles/PMC3804538/ ] 

            -- [consider IV bisphosphonates in women who cannot take oral ones appropriately]

            -- [there is a delayed-release risedronate that is enteric-coated and does not need the fasting state: https://pmc.ncbi.nlm.nih.gov/articles/PMC380; perhaps that may be useful for some women?]

                -- [in a direct trial comparing alendronate 70mg/week to risedronate 35 mg/week, risedronate did not improve the BMD as much as alendronate nor the bone turnover markers (CTX, NTX and bone-specific alkaline phosphatase), though there was no evident difference in the small number of fractures that occurred, with 26 if on alendronate and 20 if on risedronate; however, these fractures were reported in the total adverse effects, without much granular data on whether these were associated with trauma or if there was radiologic fracture confirmation (https://onlinelibrary.wiley.com/doi/full/10.1359/JBMR.040920)]

 

    --Denosumab:

        -- Very effective: about 60-70% decreased risk of radiographic vertebral fractures and incident clinical vertebral fractures, and 20-30% decrease in nonvertebral and hip fractures. fewer adverse effects than bisphosphonates

    -- [SERMS, or selective estrogen receptor modulators, (tamoxifen and raloxifene), are not included in the USPSTF recommendations], though:

        -- SERMs increase BMD in the spine and decrease vertebral fractures by 40%, but are less strong than alendronate

        -- raloxifene is not associated with endometrial bleeding/cancer/cataracts but does have increased venous thromboembolism and gallbladder disease, as does tamoxifen; similar risk with estrogens. and both SERMs decrease risk of breast cancer

        -- SERMS are mostly used in women not tolerating bisphosphonates]

 

Harms of screening:

-- studies are mixed: pooled analysis of 21 studies found no significant difference in serious adverse events with bisphosphonates vs placebo

-- some studies found increase in GI adverse events

-- a few found increases in atrial fibrillation and MI, not found in many other studies (a study in men found increase in MI in those on zoledronic acid)

-- though rare, the major bisphosphonate adverse events of osteonecrosis of the jaw and atypical femoral fractures:

    -- [osteonecrosis of the jaw: mostly with high doses of bisphosphonates, as used in cancer patients, happening in about .01% to .06% patients: https://academic.oup.com/jcem/article/107/5/1441/6469944 ]

    -- [atypical hip fractures (subtrochanteric or diaphyseal fractures): median bisphosphonate treatment 7 years, absolute risk low at 3.2-50 cases per 100,000 person-years; still many more regular hip fractures avoided with the meds. but the hip surgery is more challenging in the atypical ones, perhaps related to bisphosphonate-associated changes in bone composition and strength]

 

Men (though the USPSTF gave this an "I" grade, they reiterate that this does not mean screening/treatment is not appropriate:

-- men have the same risk factors as females, and these should be incorporated into our clinical decision-making, but these guideline-makers did not think there was enough information on this.

-- though osteoporosis and fragility fracture are less common in women, there is actually higher mortality from these in men

-- [the Am College of Physicians guidelines reviewed 10 studies in men and found that bisphosphonates seem to reduce the risk of radiographic vertebral fractures; no studies on hip fractures: https://www.acpjournals.org/doi/10.7326/M22-1034 ]

  

Other related USPSTF recommendations:

--importance of exercise interventions to prevent falls in those 65yo or older at increased fall risk [I certainly have younger patients with significant balance problems, though physical therapy and exercise helps, but many are still at increased risk of falls and, per the above graphs, may well have osteopenia or osteoporosis and be younger than 65]

--they found insufficient evidence for supplementation of vitamin D with or without calcium. [in reading/blogging on a slew of the vitamin D studies at https://gmodestmedblogs.blogspot.com/search?q=vitamin+d , it is clear to me that almost all of the vitamin D studies are fundamentally poorly designed (not much difference in (25-OH)D levels between the groups, did not check 25(OH)D levels during the study, were too short-term (earlier supplementation of vitamin D might have prevented progressive bone density decreases); and vitamin D receptors are present on essentially all human cells, so people living in the high sun areas of Africa, where humans evolved, did not need supplemental vitamin D as many of us now do to avoid very low vitamin D levels]

  

My Commentary (adding some important issues for us in primary care:

-- bone gain/loss in women over time:

    -- bone accretion in females is particularly profound during puberty

        -- calcium is taken up by bone most efficiently during the growth spurts in early childhood and early adolescence, though it continues throughout life at a slower pace even after peak bone mass has been achieved

            -- which means that this is a public health issue: we in health care should encourage sufficient calcium intake during these periods of time, in order to maximally mineralize bones to thereby minimize the effects of subsequent bone loss and the risk of subsequent osteoporosis     

    -- maximum bone density in women is around age 30

    -- overall bone loss in women begins at that time, around 0.7-1.3% per year (bone loss is more than bone accretion at that time)

    -- at perimenopause, bone loss increases to about 1.6%/year in the spine and about 1.0%/year in the hip

    -- at menopause, up to 20% of bone mass is lost within the first few years

        -- an analysis of bone loss in women, using both BMD as well as a bone strength index, confirmed similar numbers: https://www.nejm.org/doi/full/10.1056/NEJMoa022464

 

-- we do know that BMD is a coarse measurement of bone mineralization, essentially measuring the cross-section of calcium and other minerals in the bone, which brings up several issues:

    -- the cutpoint of osteoporosis is a T-score of -2.5, which was derived from white women and simply extended to other women and men. is this a really true cutpoint per more recent studies? should it really apply to nonwhite women and men?

    -- BMD can be normal in women with fragility fractures, and BMD assessment can be left off the FRAX risk calculator (though including BMD does add to the accuracy of the calculator, and notably it was not included in the standard FRAX calculator in the USPSTF document)

        -- BMD in the spine can be normal or high in those with vertebral fractures

        -- there is pretty clear evidence that bone microstructure is really important (trabecular bone score was mentioned at the end of the USPSTF as a limitation of the FRAX score, but no further comment in the article!!!):

            -- trabecular bone does provide significant bone strength, and is not specifically measured in BMD readings, though vertebral bone is largely trabecular. we in clinical care often value the hip BMD more than the vertebral one, since hip fractures are such an important cause of morbidity/mortality; though, as noted above, 30% of vertebral fracture are associated with chronic back pain, and vertebral bone BMD score, which does include more trabecular bone, does reflect the bone microarchitecture better than the hip score

            -- in fact, not measuring trabecular bone directly is likely the reason that BMD is an insufficient surrogate marker of osteoporotic risk, and why fragility fractures happen in those with normal BMDs

            -- it is notable that bisphosphonates decrease the risk of fracture (especially in the highly trabecular vertebral bones by 50%), though it may be associated with minimal changes in BMD. animal studies and some human ones have found this to be the case: https://pubmed.ncbi.nlm.nih.gov/9294113/

            -- there are noninvasive ways of measuring bone microarchitecture, including high-resolution quantitative CT and high-resolution MRI: https://pmc.ncbi.nlm.nih.gov/articles/PMC4461066/

            -- direct assessment of trabecular bone seems to be an important potential risk for future fractures, and there is a mechanism to measure it in the "trabecular bone score": https://pmc.ncbi.nlm.nih.gov/articles/PMC7539023/

 

        -- bone turnover, as an important marker of increased fracture risk (not mentioned by USPSTF):

            -- exercise seems to decrease bone turnover

            -- the more traditional bone turnover markers measured (serum C-telopeptide crosslinks, and urine N-terminal telopeptide crosslinks) vary dramatically during the day and need to be measured early in the morning (CTX requiring a 12-hour fast). this is not true for bone-specific alkaline phosphatase: https://pmc.ncbi.nlm.nih.gov/articles/PMC5549920/ , and the serum procollagen type 1 N-terminal propeptide (P1NP) also seems to be okay if nonfasting but there still is diurnal variation.

            -- there is concern that measuring bone turnover markers is not sufficiently standardized and there can be assay variability

            -- but, these bone turnover markers do seem to be an important assessment of fracture risk; they decline with antiresorptive therapy, and they have been used in important studies of fracture risk (eg the FIT/FLEX studies and the one on perimenopausal women noted below)

            -- and, it makes intuitive sense that more bone turnover would be associated with more bone weakening

 

-- another issue not addressed by USPSTF (though this current recommendation was more for screening) but quite important (esp since they do get into treatment) is when to stop the alendronate:

    -- it is pretty clear in the Fracture Intervention Trial (FIT), and particularly its extension over time (FLEX study: see osteoporosis FLEX trial jama2006 in dropbox, or Black DM et al. JAMA 2006; 296:2927-2938) that some women can stop the alendronate after five years (though in clinical practice this 5-year mark may being applied too broadly to more women than those qualifying for these studies)

    -- in the FIT trial which compared women on 5 or 10 mg of alendronate per day, women with poor baseline BMD T-scores (worse than -3.5) were excluded

    -- in the included women, those women on placebo after 5 years did have a gradual decline in BMD (-2.4 % at the hip and -3.7% at the vertebrae), though BMD was still higher than initially starting the FIT trial

    -- concomitant with this BMD decline was a gradual increase in bone turnover markers (serum CTX to assess bone resorption and N-propeptide of type 1 collagen for bone formation were measured, as well as serum bone-specific alkaline phosphatase), but these were also lower than starting the FIT trial

        -- specifically, over 5 years, in the placebo group the serum CTX increased 55.6%, the N-propeptide of type 1 collagen increased 59.5%, and the bone-specific alkaline phosphatase increased 28.1%

            -- though the change in the bone-specific alkaline phosphatase was less profound, within a couple of years the difference between placebo and alendronate was statistically significant (though bone-specific alkaline phosphatase overall is less specific/sensitive than the other bone turnover markers)

    -- no difference in nonvertebral fractures at the end of trial, but those continuing alendronate did have a 55% decrease in vertebral fractures vs the placebo group, 2.4% vs 5.3%, RR 0.45 (0.24-0.85)

    -- no cases of osteonecrosis of the jaw, though we do know that the risk of osteonecrosis of the jaw happens more with more extended exposure to bisphosphonates 

    -- comparing those on alendronate 5mg/d vs 10mg/d: there were similar changes in bone markers or in BMD and antifracture efficacy

    -- so, the conclusion of the study was that only women having a low risk of fractures (especially no history of prior fractures) and an achieved T-scores decreasing to better than -2.5 should stop the alendronate, and they should be followed closely with repeated BMD measurements, perhaps every 2 years or so

    -- it seems to me that considering 5mg/d of alendronate (ie 35mg/weekly dose) might be a reasonable approach, but again with checking BMD and/or bone turnover markers regularly (perhaps every 2 years??)

 

-- so, what does this mean???

    -- to me, this process of osteoporosis is very similar to that of coronary artery disease

        -- both are gradual processes that begin in the teenage years (for a recent blog commenting on this, see https://gmodestmedblogs.blogspot.com/2025/04/coronary-artery-calcium-dec-plaque.html)

        -- both manifest themselves clinically decades later

            -- and, using a 10-year risk predictor for these clinical effects is essentially useless in younger people for both of these diseases

        -- both are associated with profound morbidity and mortality after people develop clinical coronary artery disease or osteoporosis

        -- at the time of these adverse clinical effects, corrective measures offer only partial future protection (the bones and heart never achieve their former glory)

        -- several of the risk factors are similar for both (eg, smoking, alcohol, diabetes, increased systemic inflammation, lack of exercise)

        -- which all means that the real public health strategy for both should include:

            -- aggressive interventions early on to decrease the subsequent clinical problems, by focusing on diet, exercise, decreased alcohol and smoking, and a generally healthy lifestyle

            -- more aggressive screening to identify persons at higher risk for bad clinical outcomes at an earlier age, perhaps:

                -- routine BMD screening of women at perimenopause and treatment as indicated; and, many, many patients would qualify as "increased risk" for osteoporosis, when we include diabetes, the extensive list of meds that are associated with osteoporosis, and any condition associated with systemic inflammation (chronic infections, rheumatologic diseases, metabolic dysfunction-associated steatotic liver disease, even air pollution, elevated levels of microplastics.....)

                    -- a 2023 article brought to my attention by talya salant provided a systematic review/meta-analysis finding that short-term bisphosphonates often at ½ dose in women without osteoporosis (osteopenia in about ½ of the studies) led to significant improvement in BMD and decrease in bone turnover markers: see osteop bisph perimenop inc BMD and dec turnover JBonMinRes2023 in dropbox, or doi:10.1002/jbm4.10748

                        -- though there were major differences in these 10 studies, the ones where it was measured found that urinary N-telopeptide decreased by 52.2% and bone-specific alkaline phosphatase decreased by 34.2%

                -- some routine screening of all, perhaps in their early 40's, for coronary artery disease. ?by coronary artery calcium screen ?better by coronary CT angiography, per https://gmodestmedblogs.blogspot.com/2025/04/coronary-artery-calcium-dec-plaque.html

-- we do have a remarkable deficiency of important scientific information on which to base recommendations (which is pretty remarkable given the overall huge public health and individual effects of osteoporosis on morbidity and mortality):

    -- is BMD an accurate a predictor in younger women than the over 65yo crowd? there are minimal data on this (a 10-year British study with 3883 women aged 44-56 found that BMD and quantitative ultrasound were similarly accurate (area under the curve, AUC, of about 0.6), but for the few patients who had a documented fracture, the ultrasound was significantly better than BMD in the 77 who had both done, with ultrasound having an AUC of  0.70 vs BMD of 0.65): https://pubmed.ncbi.nlm.nih.gov/16491289/ 

    -- is bone-specific alkaline phosphatase measurement sufficient in clinical practice? the studies above show a significant but smaller change both by starting and stopping bisphosphonates. and it certainly is easier, not requiring early morning tests or fasting for the serum CTX.

    -- can we use low-dose alendronate (the 35mg/wk dose) after high-risk women have been on alendronate 70mg/wk for 5 years and had a great response with lowering BMD/bone turnover markers? we do know that alendronate hangs around in the bone for a really long time, so perhaps a lower later dose would be sufficient to reinforce bone integrity. and that might prevent the bad long-term adverse effects of bisphosphonates, which seem to be dose-dependent

 

        -- we really need better data for younger women, though the perimenopausal study above using both BMD and bone turnover markers were helpful; of course these are surrogate markersfor osteoporosis risk, and we know the limitations of BMD, as per above

            -- as in the FLEX study, this study found important improvements in the measured bone turnover markers: urinary NTX decreased 52.2% and bone-specific alkaline phosphatase by 34.2%, supporting our using bone-specific alkaline phosphatase as an easy test to do. It is somewhat less sensitive, but these studies did find it to be statistically on a par with the other bone turnover tests. So, it may be really useful for us in primary care to use this test more regularly, perhaps with following elevations with the more sensitive tests???? Would be great to have a study on this

        -- of note, the 2020 American Association of Clinical Endocrinologists guidelines does recommend screening all women aged 50 or older, with a Grade B recommendation: https://www.sciencedirect.com/science/article/pii/S1530891X2042827

-- other questions: for younger women, how long should they be on bisphosphonates? is it okay to start, stop, restart, etc for many cycles as the bone markers or BMD start to get worse? at what level of change? and what dose should be used? will much more prolonged bisphosphonate use lead to more serious adverse effects (esp jaw osteonecrosis, atypical fractures)?

-- we should have more information on men. men do have osteoporosis and do have  hip fractures in older age, about 1/3 the frequency of women, and, as noted above, there is a higher morbidity/mortality than in women

 

--but, the bottom line is that a very large percentage of young postmenopausal women would qualify for earlier BMD testing at the time of menopause per the USPSTF guidelines, if the clinician and patient are interested in doing so

 

geoff

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