Defined as discomfort in the lower back, lumbosacral, and sacroiliac areas, lower back pain (LBP) frequently includes radiating pain in the lower limbs (1). It is a prevalent condition affecting approximately 84% of individuals during their lifetime (2). Globally, LBP poses substantial social and economic difficulties and causes extensive workplace absenteeism (3). LBP is estimated to incur annual costs of $34 billion in the United States alone, with additional indirect expenses, such as lost wages, potentially exceeding $100 billion (4). Given its widespread occurrence and substantial economic impact on healthcare systems, the implementation of early screening measures for LBP in populations at high risk using known risk factors, alongside the development of effective treatment protocols, is crucial.

Osteoporosis manifests as diminished bone mass and structural deterioration, leading to reduced skeletal stability and a higher probability of fracture (5). This condition in adults is defined as a bone mineral density (BMD) that is 2.5 standard deviations below their maximum bone density (6). Osteoporotic fractures, the primary complications of this disease, frequently occur in older adults and are associated with a significantly high mortality risk from major fractures (7, 8).

LBP is categorized into non-specific and specific types, depending on its origin. Prior research has pinpointed risk factors for nonspecific LBP, including sex, age, educational level, depression, seated posture, working hours, accidents, and genetic factors (9–11). Additionally, specific types of LBP may result from structural changes in the spine such as spinal stenosis, arthritis, disc degeneration, and kyphoscoliosis (12, 13). Despite numerous studies highlighting the risk factors for LBP, the role of osteoporosis as a contributing factor has often been ignored; however, it may be crucial.

Gaber et al. reported that small sample sizes showed a correlation between LBP and reduced bone density, indicating a potential risk of osteopenia (14). However, individuals with LBP may have higher lumbar BMD than those without, indicating a potential connection between issues such as rotational asymmetry or limited motion and increased bone density in the affected vertebrae (15). However, no consensus has been reached in the academic literature regarding the potential association between osteoporosis and LBP.

This study investigated the association between osteoporosis and LBP, using an extensive cross-sectional study derived from the National Health and Nutrition Examination Survey (NHANES) dataset.

This study revealed that BMD was positively associated with LBP using data from the NHANES from between 1999 and 2004. In our cross-sectional study involving 107,570 participants, we observed a U-shaped relationship between BMD and LBP, with an inflection point at 1.14 g/cm². When BMD was <1.14 g/cm², a negative association was observed between elevated BMD and LBP. However, once the BMD levels surpassed 1.14 g/cm², a positive association was detected between BMD and LBP.

A population-based cross-sectional study revealed that independent of factors such as age, education, and medical history, higher lumbar spine bone density correlated with increased LBP (16). Research involving Taiwanese adults found that LBP frequently accompanies osteoporosis, with elevated risks among women, those with lower educational levels, and individuals in blue-collar occupations (17). Manabe et al. noted a significant link between higher BMD and LBP among middle-aged women (18). Evidence suggests that patients with osteoporosis can experience back pain without fractures; however, treatments such as monthly ibandronate (19) and alendronate sodium (20) can alleviate pain. Nevertheless, the studies mentioned above have certain limitations. The sample sizes used in these investigations were not sufficiently large to ensure robust representativeness. Additionally, the studies did not account for a range of potential confounding variables such as age, sex, ethnicity, educational attainment, PIR, smoking habits, BMI, and BMD. These oversights might have undermined the reliability of the study outcomes.

LBP induced by osteoporosis is a complex, multifactorial issue.

Osteoporosis-induced LBP is associated with biomechanical alterations in the spine. Pan et al. determined that higher bone density in the lumbar facet joints may suggest increased stress on the joints and an uneven distribution of weight, possibly contributing to LBP (21). Andersen et al. found that patients with degenerative spondylolisthesis had lower spinal bone density than those with spinal stenosis, suggesting a possible connection between low BMD and the onset of degenerative spondylolisthesis (22).

An imbalance in bone metabolism is another possible cause of LBP in patients with osteoporosis. In addition to increasing bone resorption, reduced bone formation also increases fragility, making the spine more susceptible to stress and damage (23). Drugs, such as neridronate and alendronate, can alleviate LBP by improving bone density and reducing the bone turnover rate.

Disc herniation frequently emerges as the primary cause of back pain in patients with osteoporosis. This study corroborated previous findings linking higher BMD T-scores with increased spinal sclerosis in individuals experiencing LBP (24). Slowly progressive degenerative changes in the lower back impair the spine structure and functionality. Mechanical stress from spinal motion stimulates disc and facet joints, potentially leading to osteophyte development and endplate sclerosis. Additionally, microfractures contribute to a localized surge in bone turnover, enhancing trabecular density and reducing trabecular spacing (23, 26). These changes lead to increased bone density within the vertebral bodies, often marked by new osteophytes and endplate sclerosis (27). Recent findings indicate that higher bone density in the vertebral bodies correlates with intensified degeneration of the adjacent intervertebral discs. Research using micro-computed tomography has established a positive relationship between vertebral bone density and the severity of disc degeneration, which supports our conclusions (28). Consequently, while stiff vertebrae may subject neighboring discs to greater mechanical stress, osteoporotic vertebrae may offer some degree of protection against such degeneration (18).

During lumbar degeneration, the load distribution on the spinal functional unit is altered, resulting in greater pressure being placed on the intervertebral discs causing microfractures in the endplate. The nucleus pulposus material in the intervertebral disc penetrates these microfractures into the endplate, triggering local inflammatory reactions and ultimately leading to Modic changes (29). Significant differences exist in trabecular bone microstructure and bone remodeling indices among the different types of Modic changes. Modic type 1 changes exhibit higher bone turnover, likely due to inflammatory processes, whereas Modic type 2 changes are associated with reduced bone formation (30). Modic changes are associated with LBP. A cross-sectional study revealed that Modic type 1 changes are significantly associated with chronic LBP, with a higher frequency and severity of pain. In contrast, the relationship between Modic type 2 and 3 changes and the LBP is weaker (31). Other studies indicate that Modic type 1 changes are critical factors in patients with LBP, correlating with pain, functional deterioration, and unsuccessful return to work within 1 year. Among the 325 patients on sick leave owing to LBP, those with Modic type 1 changes reported more severe back pain and no improvement in pain or disability (32). We believe that Modic changes may be a pathway by which bone density influences LBP.

Our findings demonstrate a significant link between BMD and the occurrence of LBP. The data suggest that lower BMD is commonly associated with an increased incidence of LBP, which is consistent with prior studies that connect osteoporosis with such pain. In contrast, a higher BMD appears to increase the risk of developing LBP, likely due to degenerative alterations in the intervertebral discs and articular joints. Clinicians should consider incorporating measures of BMD into routine assessments for patients with or at risk of LBP. Future research should explore the underlying mechanisms linking BMD and LBP in more detail and evaluate the effectiveness of targeted interventions aimed at preventing and managing LBP. This could lead to the development of more effective, personalized treatment strategies that improve patient outcomes and reduce the burden of LBP on individuals and healthcare systems.

Our study had several limitations. First, the cross-sectional design prevented the establishment of causal links between bone BMD and LBP. Second, although numerous covariates were accounted for in the multivariate regression analysis, the possibility of residual confounding factors remained.

The results of this study revealed a non-linear relationship between BMD and the prevalence of LBP among adults in the United States, showing a notable threshold effect. The risk of LBP increases when BMD levels are either too low or too high. However, a deeper understanding of this relationship will significantly aid future research efforts.