Vitamin D, a steroid hormone essential for calcium and phosphorus homeostasis, regulates bone mineralization and overall skeletal metabolism. Its deficiency, common and often underdiagnosed worldwide, causes rickets in children and osteomalacia in adults [88, 89]. Correction of deficiency is essential before initiating OP therapy; therefore, serum 25OHD measurement is recommended for all patients, as it represents the most reliable indicator of vitamin D status due to its abundance as a circulating metabolite, and longer half-life compared with calcitriol [1,25-(OH)₂D₃] [71, 88, 90, 91]. Optimal bone health requires maintaining serum 25OHD levels ≥ 30 ng/mL (75 nmol/L), while levels of 10–16 ng/mL (25–40 nmol/L) are associated with secondary hyperparathyroidism and OP, and < 8–10 ng/mL (20–25 nmol/L) with osteomalacia [71, 88, 89, 92, 93]. The American Association of Clinical Endocrinologists’ definitions of vitamin D deficiency and insufficiency are summarized in Table 5 [88, 89, 94].

Most recommendations for correcting vitamin D deficiency or insufficiency are provided by international societies. In a general manner, patients at risk of vitamin D deficiency are recommended to receive doses of 800 IU to 1,000 IU daily along with calcium [88]. For rapid repletion, a loading dose of 25,000–50,000 IU/week for 4–6 weeks is suggested, adjusted to baseline 25OHD levels (< 20 ng/mL for 8 weeks; 20–30 ng/mL for 4 weeks), and indicated in severe deficiency (< 10 ng/mL), severe obesity, malabsorption, post-bariatric surgery, or when treatment with potent antiresorptive agents such as denosumab or intravenous bisphosphonates needs to be initiated [88, 95–97]. After this initial regimen, a maintenance dose varying from 800–2,000 IU daily or 50,000 IU per month can be prescribed in order to maintain the target blood level [88, 95, 96, 98–103]. High-dose vitamin D supplementation should be avoided, as excessive intake may elevate FGF-23, leading to inhibition of 1α-hydroxylase (CYP27B1) activity, reduced circulating vitamin D metabolites, and activation of 24-hydroxylase pathways that catabolize calcitriol and calcidiol into less active compounds such as calcitroic acid. This process ultimately limits vitamin D receptor (VDR) activation and prevents excessive downstream signaling [88, 104–108]. The choice of initial and maintenance dosing should be individualized at the clinician’s discretion, tailoring therapy to each patient’s clinical profile and biochemical response.

Vitamin D is fat-soluble molecule with pleiotropic effects in bone, participating in calcium and phosphorus metabolism by acting on three main organs: intestine, bone and kidney. The main source of vitamin D in humans is the cutaneous synthesis after sun exposure, although it can also be obtained from vitamin D-rich foods, but in minor amounts. The two forms of vitamin D are cholecalciferol (vitamin D3) of animal origin, and ergocalciferol (vitamin D2) of vegetable origin; both share a common metabolic pathway that leads to the synthesis of calcitriol in the kidney, which constitutes the active form of vitamin D [1, 109]. The main causes of vitamin D deficiency are the lack of sun exposure, as in institutionalized patients or the use of sunscreen, especially for skin cancer prevention, or in patients with systemic lupus erythematosus (SLE) who must avoid solar exposure. The age-associated decline in cutaneous vitamin D synthesis, with older skin producing approximately 40% less vitamin D, contributes to diminished intestinal calcium absorption and subsequent reductions in bone mass and mineralization [1, 110, 111]. As calcium bioavailability varies by source, being highest in dairy products [112–114], adequate intake, together with vitamin D, is essential for skeletal integrity, with combined supplementation shown to reduce fracture risk [115]. Adequate intake is fundamental for OP prevention and should be carefully considered at the start of treatment to ensure optimal levels are maintained for the patient’s age. Recommended daily intakes of calcium and vitamin D by age are presented in Table 6.

Vitamin D and calcium supplementation remain cornerstone strategies for fracture prevention. In a two-year cluster randomized controlled trial of 7,195 institutionalized older adults (mean age 86 years) with adequate vitamin D levels but low calcium intake, Iuliano et al. [116] reported that achieving a calcium intake of 1,300 mg/day and < 1 g/kg protein/day through increased dairy consumption reduced the risk of all fractures by 33%, hip fractures by 46%, and falls by 11% (p = 0.04), with benefits evident as early as three to five months.

A review of 26 randomized clinical trials by Voulgaridou et al. [117] showed that combined calcium and vitamin D supplementation, but not vitamin D alone, significantly increased BMD. Similarly, Yao et al. [118] found that each 10 ng/mL (25 nmol/L) increase in serum 25OHD was associated with a 7% reduction in overall fracture risk and a 20% reduction in hip fracture risk. Vitamin D alone did not significantly reduce fracture incidence (RR = 1.06; 95% CI: 0.98–1.14), whereas combined supplementation reduced the risk of any fracture by 6% and hip fractures by 16% [118]. Consistent results were reported by Manoj et al. [119] in a meta-analysis of seven randomized controlled trials including 12,620 participants. Daily supplementation with vitamin D3 (800 IU) plus calcium significantly reduced hip fracture risk by 25% (p = 0.0003) and non-vertebral fracture risk by 20% (OR = 0.80; 95% CI: 0.72–0.89; p < 0.0001). The most effective regimen was 800 IU of vitamin D3 with 1,200 mg of calcium, which reduced hip fracture risk by 31% (OR = 0.69; 95% CI: 0.58–0.82; p < 0.0001) [119].

Vegetarian and particularly vegan diets are associated with lower BMD compared with omnivorous diets, likely due to reduced intake of calcium, vitamin D, protein, and lower body weight [120–122]. Lacto-ovo-vegetarians consume dairy and eggs, which provide higher calcium, vitamin D, and animal protein, favoring bone health. However, both vegetarian and vegan diets often fail to meet all nutrient requirements, making them more susceptible to low BMD and fractures [120, 123, 124]. In a Bayesian meta-analysis including 2,749 participants, vegetarians had about 4% lower BMD at the femoral neck and lumbar spine than omnivores, with a greater reduction in vegans [ratio of means (RoM) = 0.94; 95% CI: 0.91–0.98] than in lacto-ovo vegetarians (RoM = 0.98; 95% CI: 0.96–0.99) [122]. Vitamin B12 is crucial for bone metabolism through its role in taurine and IGF-1 synthesis, supporting bone mass and structure [124, 125]. Deficiency is observed in 11% of omnivores, 77% of lacto-ovo vegetarians, and up to 92% of vegans, leading to increased methylmalonic acid and homocysteine levels [126]. Low vitamin B12 is linked to reduced BMD, BMC, and impaired bone cell function [124]. In elderly Dutch women, vitamin B12 deficiency was associated with higher OP prevalence (37%) compared to those with normal levels (6%), with B12 contributing 1.3–3.1% to BMC and BMD variance [127]. Therefore, individuals following vegan or vegetarian diets should be advised to ensure adequate intake or supplementation of calcium, vitamins D and B12, and protein, with regular monitoring of bone health.

CKD is a well-established contributor to impaired bone health, OP, and an increased risk of fractures [153–156]. CKD-mineral and bone disorder (MBD) is a systemic condition characterized by disturbances in calcium, phosphate, PTH, and vitamin D metabolism, leading to abnormalities in bone turnover, mineralization, structure, and growth, as well as vascular and soft-tissue calcification [153, 154, 156]. According to the National Kidney Foundation/Kidney Disease Outcomes Quality Initiative (NKF/KDOQI), CKD is classified into five stages based on estimated glomerular filtration rate (eGFR), with advanced CKD (stages G4–G5, eGFR < 30 mL/min/1.73 m²) affecting 0.5–1% of the population [153]. Renal impairment is particularly prevalent in older adults, with only 26% of those aged ≥ 70 years maintaining normal kidney function [156]. In assessing OP, kidney function must be considered alongside traditional risk factors. A dynamic bone disease, characterized by low bone turnover, is frequent among dialysis patients [153, 154]. Phosphate retention, impaired vitamin D synthesis, and secondary hyperparathyroidism further exacerbate bone loss, even at early stages of CKD [153, 154, 156]. Epidemiological data demonstrate a twofold increase in hip fracture risk among patients with moderate to severe CKD [156]. NHANES III reported that participants with an eGFR < 60 mL/min/1.73 m² had higher odds of hip fracture (OR = 2.12; 95% CI: 1.18–3.80), and CKD prevalence was nearly three times greater among those with prior fractures aged 50–74 years (19.0% vs. 6.2%; p = 0.04) [157].

Patients on hemodialysis (HD) show markedly increased fracture risk, with Alem et al. [158] reporting a fourfold increase compared to the general population and up to a 10–100-fold increase among those < 65 years [156]. Meta-analyses confirm a graded relationship between declining eGFR and fracture risk, especially for hip fractures [155, 159]. Falls affect approximately 25% of patients with advanced CKD annually [160, 161], with risk factors including frailty, hypotension, malnutrition, anemia, and antidepressant use. In HD cohorts, fractures, most frequently ribs, affect roughly 25% of patients, with age, low hemoglobin, and high phosphorus as independent predictors [162]. A comprehensive assessment of renal function and bone health is essential to reduce fracture risk in this vulnerable population.

Bone metastases are a frequent and serious complication of advanced malignancies, particularly those originating in the breast, prostate, lung, thyroid, and kidney. Disseminated tumor cells disrupt the normal balance between bone formation and resorption, leading to skeletal-related events (SREs) such as bone pain, pathological fractures, hypercalcemia, and spinal cord or nerve root compression [163–168]. The metastatic process is driven by complex interactions between cancer cells, the bone microenvironment, immune mediators, and signaling pathways that promote tumor growth at distant sites. Depending on the tumor type, lesions may be osteolytic, osteoblastic, or mixed [163, 164, 167, 168]. Prostate and breast cancers show the highest propensity for bone involvement, affecting up to 65–75% of patients with advanced disease [168].

Lung cancer has been identified as the most frequent primary source of de novo bone metastases. In an analysis by Ryan et al. [169], lung cancer exhibited the highest incidence (8.7 per 100,000 in 2015), followed by prostate and breast cancer (3.19 and 2.38 per 100,000, respectively). Among younger patients (< 20 years), endocrine malignancies and soft-tissue sarcomas predominated, with a notable increase in bone metastasis incidence from prostate and gastric cancers [169]. Similarly, a retrospective series of advanced non-small-cell lung cancer reported bone metastases in 39% of patients [170]. The lumbar and thoracic vertebrae are the most common metastatic sites, followed by the cervical spine and sacrum [171].

Disruption of the balance between bone resorption and formation leads to three main patterns of metastases: osteolytic, osteoblastic, and mixed [168]. In multiple myeloma, 80–90% of patients develop osteolytic lesions driven by malignant plasma cells that stimulate osteoclast activation and suppress osteoblast function through mediators such as RANKL, interleukin 6 (IL-6), macrophage inflammatory protein-1α (MIP-1α), and stromal-derived factor-1α (SDF-1α) [172, 173]. Similarly, osteolytic metastases in breast cancer are associated with tumor secretion of parathyroid hormone-related peptide (PTHrP), IL-1, IL-6, GM-CSF, and TNF-α, which enhance osteoclastogenesis while inhibiting osteoblast activity [164, 166, 168]. Tumor-derived inhibitors such as dickkopf-1 (DKK1) and sclerostin (SOST) further suppress osteoblast differentiation by blocking Wnt/β-catenin signaling, exacerbating bone destruction [166, 167]. Conversely, osteoblastic or sclerotic metastases, characteristic of prostate cancer, result from increased osteoblast activity driven by endothelin-1, bone morphogenetic proteins (BMPs), TGF-β, Wnt proteins, and IGFs [167, 174]. Elevated osteoprotegerin (OPG) levels inhibit osteoclast differentiation, favoring bone formation [166, 175]. Prostate-specific antigen (PSA) may further contribute by cleaving PTHrP, thereby reducing osteoclastic activity [166–168]. In certain breast and prostate cancers, mixed lesions arise through interactions mediated by platelet-derived growth factor (PDGF) and endothelin-1 via PDGFRα/β and ETAR, along with β-catenin-dependent signaling that determines lesion phenotype [168, 174–177].

Assessing bone involvement at diagnosis is therefore crucial to prevent skeletal complications [164]. Bone pain is the most prevalent SRE, affecting 60–84% of patients with advanced cancer [164, 165, 168, 178]. It results from periosteal irritation, structural damage, inflammatory processes, and remodeling of sensory and sympathetic nerve fibers that sensitize nociceptors [165, 168]. Hypercalcemia, a common paraneoplastic syndrome, occurring in 5–10% of patients with advanced breast, lung, renal, or hematologic malignancies [164, 168]. It arises from focal or generalized osteolysis, humoral factors (notably PTHrP in ~80% of cases), increased tubular calcium reabsorption, and decreased glomerular filtration [168, 178, 179]. Clinical manifestations range from gastrointestinal and neurocognitive symptoms to cardiac arrhythmias due to QT shortening [168, 178]. Pathological fractures represent a late and debilitating complication, reported in 9–30% of patients with skeletal involvement [164, 168, 178]. They typically affect weight-bearing bones, particularly the vertebral column, often leading to spinal instability and neurologic compromise. Other common sites include the proximal femur, pelvis, humerus, and ribs, resulting in pain, reduced mobility, and frequent need for surgery [164, 168, 178, 180]. Spinal cord compression, most common in breast, prostate, and lung cancer, arises from vertebral collapse or direct tumor invasion. It presents as progressive, nocturnal pain often preceding neurological deficits and associated with microfractures [168, 178, 181, 182]. In suspected cases, bone scintigraphy is recommended to evaluate disease extent and exclude or confirm spinal cord involvement [168, 181, 182].

In chronic arthritic and autoimmune conditions such as rheumatoid arthritis (RA), the inflammatory pannus releases cytokines that disrupt bone homeostasis by stimulating osteoclast differentiation and inhibiting osteoblast maturation, leading to accelerated bone resorption and bone loss. Persistent inflammation exposes patients to multiple risk factors for low BMD and OP, including elevated cytokines, reduced physical activity, long-term glucocorticoid therapy, vitamin D deficiency, and postmenopausal status [183, 184]. In RA, chronic inflammation driven by IL-1, IL-6, IL-17, IL-23, and TNF-α enhances osteoclastogenesis through RANKL and macrophage colony-stimulating factor (M-CSF), contributing to bone erosion and systemic bone loss [183, 185]. Dysregulation of DKK1, a Wnt signaling inhibitor, also plays a key role: its overexpression in RA and multiple myeloma promotes bone resorption, while its downregulation in ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis (DISH) leads to aberrant bone formation. TNF-α-mediated DKK1 upregulation provides a mechanistic link between chronic inflammation and bone loss [183, 186–190]. Vitamin D further influences bone and immune regulation by binding to VDR on T and B lymphocytes and dendritic cells, modulating cytokine production and immune activation. Deficiency is common in autoimmune and rheumatic diseases and correlates with increased inflammatory activity and disease severity. In RA and SLE, low vitamin D levels are associated with greater disease activity and flare risk, highlighting its potential as an adjunctive immunomodulatory factor in chronic inflammatory conditions [109].

OP, falls, and fractures are well-documented complications in individuals with cognitive impairment and dementia [191–201]. These patients have a markedly higher risk of falls, morbidity, and mortality, while those with fragility fractures face increased institutionalization and refracture rates, highlighting the need for early detection [191, 198]. Risk factors include cognitive and motor dysfunction, postural instability, autonomic impairment, sarcopenia, polypharmacy, environmental hazards, depression, sensory deficits, vitamin D deficiency, and frailty, a clinical state of diminished physiological reserve [192, 202, 203]. In a prospective study of 179 older adults with dementia, fall incidence was nearly eightfold higher than in controls, with prior falls and Lewy body dementia predicting recurrence; modifiable factors included orthostatic hypotension and depressive symptoms [191]. OP is also more prevalent in cognitive decline. A meta-analysis of 9,872 patients showed a higher risk of OP (RR = 1.56; 95% CI: 1.30–1.87) and an even greater risk in Alzheimer’s disease (RR = 1.70; 95% CI: 1.23–2.37) [194]. Jeon et al. [195] found dementia independently increased hip fracture risk (10.66% vs. 5.53% in controls), and Matsumoto et al. [196] reported elevated fracture risks even in early-onset dementia, with hip (OR = 8.79), vertebral (OR = 1.73), and major osteoporotic fractures (OR = 2.05). Interestingly, the use of cholinesterase inhibitors was associated with a reduced risk of hip fractures (OR = 0.28) [196]. Patients with OP may face further hip fracture risk, underscoring early cognitive assessment and preventive care [197]. Similarly, individuals with Parkinson’s disease (PD) show an increased risk of OP and fractures, particularly hip fractures [193, 199]. Bone loss in PD is multifactorial, related to immobility, low body weight, reduced muscle strength, vitamin D deficiency, malnutrition, and levodopa-induced hyperhomocysteinaemia [199, 204–206]. Reduced BMD at the spine and femoral neck has been consistently reported [205, 206], and a meta-analysis confirmed lower BMD across skeletal sites [206]. Large cohort studies also demonstrate nearly doubled fracture risk in PD (adjusted HR = 1.89; 95% CI: 1.67–2.14) [200, 201]. Early identification of modifiable risk factors and integrated interventions—cognitive screening, fall prevention, and bone health optimization are essential to improve outcomes in these vulnerable populations.

Polypharmacy, defined as the concurrent use of five or more medications, is strongly associated with an increased risk of fragility fractures in older adults [207–209]. Cumulative drug exposure may heighten fracture susceptibility, underscoring the importance of regular medication review in aging populations [210, 211]. Although several medications independently increase fall and fracture risk, it remains unclear whether these risks are directly compounded by the concurrent use of multiple agents [208]. Beyond skeletal effects, polypharmacy has been linked to adverse outcomes such as cognitive and physical decline, hospitalizations, functional dependence, and higher mortality [212]. In a large cohort of osteoporotic women in South Korea, Park et al. [209] reported a dose-dependent relationship between medication number and hip fracture risk, which remained significant after adjustment for confounding factors. Similarly, a prospective cohort study of 2,023 patients followed for 5.6 years found that polypharmacy (≥ 5 medications) and hyperpolypharmacy (≥ 10 medications) were more prevalent among individuals with CKD, particularly those on dialysis. Fracture risk rose with medication count (HR = 1.32 for polypharmacy; HR = 1.99 for hyperpolypharmacy), accounting for 9.9% of all fractures and 42.1% among dialysis patients [211]. Comparable trends were observed in type 2 diabetes. In the Fukuoka Diabetes Registry, fracture incidence increased from 21.2 to 44.0 per 1,000 person-years across medication categories, with adjusted HRs of 1.34, 1.76, and 1.71 for 3–5, 6–8, and ≥ 9 drugs, respectively; each additional drug raised fracture risk by 5% (p < 0.001) [210]. In a population-based study of 2,328 elderly patients, Lai et al. [213] found that hip fracture risk rose sharply with medication count, patients taking ≥ 10 drugs had an OR = 8.42 (95% CI: 4.73–15.0) compared to those using 0–1. Among those aged ≥ 85 years, the risk increased 23-fold (OR = 23.0; 95% CI: 3.77–140) [213]. Post-fracture outcomes are also influenced by medication burden. Among 272 patients after hip replacement, 31.6% were readmitted and 13.2% died within six months. The number of discharged medications correlated with rehospitalization risk (OR = 1.08; 95% CI: 1.01–1.17; p = 0.030), particularly with the use of antiosteoporotic agents, SSRIs, vitamin K antagonists, thiazides, and tramadol [214]. Overall, polypharmacy represents a significant, potentially modifiable risk factor for fractures and adverse outcomes in older adults and individuals with chronic diseases.

Socioeconomic constraints and the lack of adequate caregiving infrastructure exert a substantial negative impact on the management and prognosis of OP. Financial hardship frequently delays diagnosis and restricts access to essential diagnostic modalities, such as bone densitometry, as well as pharmacologic therapy and nutritional supplementation, ultimately increasing the risk of preventable fractures and impeding recovery [1–4, 9]. The absence of structured caregiving systems, including nursing homes, rehabilitation centers, and home-based support, further exacerbates clinical outcomes by elevating fall risk and hindering functional recovery following fractures. Individuals lacking adequate caregiver support often experience reduced mobility, poor adherence to prescribed treatments, and limited engagement in rehabilitation programs, all of which contribute to accelerated bone loss and functional decline. These challenges are reflected in population-based studies demonstrating that social and economic disparities are strongly associated with increased fracture incidence, prolonged hospitalization, and higher mortality among individuals with OP [5, 9–12]. Addressing these inequities through improved access to healthcare services, nutritional support, and post-fracture rehabilitation is essential to enhance outcomes and quality of life in this vulnerable population.

Incorrect patient positioning is a major source of DXA error, particularly in hip and lumbar spine scans. For accurate lumbar imaging, the patient should lie supine with hips and knees flexed at 90° to minimize lumbar lordosis and enhance vertebral visualization. Proper trunk and limb alignment reduces soft tissue variability, and consistent positioning across serial scans ensures measurement reproducibility. Positioning aids, such as foam blocks or head supports, facilitate alignment and image quality [4]. The lumbar spine region of interest (ROI) should include vertebrae L1 to L4 in PA view, analyzing only structurally intact segments free of artifacts. Vertebrae with abnormalities may be excluded if at least two remain for analysis; if only one is evaluable, another skeletal site should be used. Exclusion is also warranted when a vertebra’s T-score differs by > 1.0 from adjacent levels. The final T-score is calculated using the remaining valid vertebrae. The lateral spine is not recommended for diagnosis but may be used for follow-up [3, 4]. Vertebral Fracture Assessment (VFA), a densitometric lateral spine image, is indicated when the T-score is < –1.0 and at least one of the following criteria is met: women ≥ 70 years or men ≥ 80 years, historical height loss > 4 cm, prior unconfirmed vertebral fracture, or glucocorticoid therapy ≥ 5 mg prednisone (or equivalent) daily for ≥ 3 months [4, 45]. For hip DXA, bilateral measurement is recommended, as BMD is usually symmetrical but may differ due to immobilization or asymmetric loading. The total hip ROI should include the femoral neck, proximal femur, and trochanteric regions, excluding the greater trochanter. The patient’s legs should be straight and parallel, with 15–20° internal rotation to align the femoral neck with the scanning plane; minimal visibility of the lesser trochanter confirms proper positioning. Foot positioners and straps maintain alignment. Soft tissue misidentification and ischial overlap must be corrected. Both the total hip and femoral neck should be analyzed, using the same (typically non-dominant) hip for follow-up [4, 45]. Forearm DXA of the non-dominant arm is indicated when spine or hip sites are unsuitable due to artifacts (fractures, implants, severe degeneration) or when proper positioning is not possible. The diagnostic site is the one-third (33%) radius, mandatory in primary hyperparathyroidism, and useful when spine-hip discordance exceeds 1 T-score. The radius and ulna should be parallel to the table’s short axis, free of fractures or hardware. Manufacturer protocols differ: Hologic systems do not require a positioner, whereas GE systems do. For Hologic devices, forearm length from the styloid to the elbow must be entered manually. Correct positioner use is essential to prevent artifacts. Although scans are usually performed seated, a supine position may minimize motion artifacts in select cases [4, 45].

Errors in DXA interpretation arise from incorrect data analysis or clinical judgment, leading to misclassification of bone density status, inappropriate application of T- or Z-score criteria, or failure to recognize artifacts and anatomical abnormalities that distort measurements. Such inaccuracies can result in misdiagnosis, suboptimal treatment decisions, or failure to identify patients at high fracture risk. To ensure diagnostic reliability, clinicians should adhere to ISCD recommendations emphasizing appropriate staff training, routine equipment calibration, standardized scan acquisition, and interpretation within the broader clinical context. Reporting errors, in turn, involve inaccuracies or omissions in the communication of DXA findings, such as incorrect diagnostic categorization, misapplied T-score thresholds, or neglect of relevant clinical risk factors. These errors can lead to inappropriate management decisions and underscore the importance of standardized reporting practices [3, 219–223]. As noted, reporting inaccuracies are common in clinical practice, with studies showing that up to 90% of BMD reports contain at least one error [217]. Krueger et al. [216] assessed DXA-related errors in a U.S. clinical population referred for OP evaluation and analyzed their potential clinical impact. Major errors, defined as inaccuracies that could alter patient management, were observed in 42% of cases, while technical errors occurred in 90% and influenced interpretation in 13% of patients. The most frequent major errors involved incorrect reporting of BMD change (70%) and misdiagnosis (22%). Implementation of a standardized reporting template in the study’s second phase reduced major errors by 66%, highlighting the value of structured reporting systems [216]. Similar findings were reported in an analysis of densitometry procedures across imaging centers in Ecuador, where patient positioning errors, including improper centering or misalignment, occurred in 21.4% of cases. In 38.5% of scans, the assessed vertebral region did not correspond to L1–L4, while artifacts such as metallic implants were identified in 3.5%. The ROI was incorrectly defined in 24.1% of lumbar and 19.9% of femoral assessments [3]. Lewiecki et al. [223] evaluated perceptions of DXA quality among 3,488 clinicians and 2,362 technologists from the ISCD. Over half of technologists (55%) reported incorrect entry of patient demographic data at least monthly, and 71% of clinicians identified inaccurate interpretations with the same frequency; 27% noted errors more than once per week. Nearly all clinicians (98%) believed low-quality DXA reports negatively affected patient care, with 59% rating the impact as moderate or severe [223].