A hip condition you were born with might be silently influencing your fracture risk decades later.
Imagine a slight imperfection in your hip joint at birth, one so subtle it may have gone unnoticed for years. Now, fast forward several decades—could that same minor structural difference determine whether a simple fall results in a devastating broken hip? This is the compelling question scientists have been exploring as they connect the dots between developmental dysplasia of the hip (DDH), a common congenital condition, and future bone mineral density.
For the millions affected by osteoporosis worldwide, where bones become fragile and prone to fracture, identifying new risk factors is crucial for early intervention and prevention. Emerging research suggests that the story of bone health may begin much earlier in life than we once thought—perhaps even at birth.
Developmental dysplasia of the hip (DDH) represents a spectrum of conditions where a baby's hip joint doesn't develop properly. The socket (acetabulum) may be too shallow, or the ball (femoral head) may not be stable within the socket. This affects approximately 2-3% of all newborns, with girls being more commonly affected than boys .
While DDH is often detected and treated in infancy, its implications may extend far beyond childhood. The condition is recognized as a pre-osteoarthritic condition and accounts for 30% of all total hip arthroplasties in adults under 40 years of age . The connection to bone mineral density, however, presents a more recently discovered dimension to its long-term impact.
of newborns affected
of hip replacements in adults under 40
heritability from genetic factors
DDH is not just a childhood condition—it may have lifelong implications for joint health and bone density.
The relationship between DDH and bone mineral density (BMD) has proven to be surprisingly complex, with studies revealing seemingly contradictory findings.
A groundbreaking study published in 2000 provided the first compelling evidence linking DDH to reduced bone density. Researchers assessed 240 premenopausal women, 31 of whom had a history of conservatively treated DDH.
Their findings revealed that BMD in DDH patients was significantly lower at the hip (by approximately one standard deviation) compared to controls, while spinal BMD remained comparable 4 .
Most strikingly, their logistic regression model indicated that conservatively treated DDH was associated with a 6.3-fold increased risk for low BMD at the hip. The researchers concluded that "about 1 out of 10 women" with a history of DDH might be affected by this reduced bone density 4 .
Adding complexity to the narrative, a 2011 study comparing 40 women scheduled for pelvic osteotomy for DDH against 31 healthy controls found precisely the opposite pattern.
Their measurements showed that BMDs of the lumbar spine, ultradistal radius, and calcaneus were significantly higher in the DDH patients than in the controls 7 .
This contradiction highlights the complexity of bone metabolism and suggests that multiple factors—including age, treatment history, and measurement sites—may influence the relationship between DDH and bone density.
| Study Aspect | Obermayer-Pietsch et al. (2000) | Okano et al. (2011) |
|---|---|---|
| Participant Profile | 240 premenopausal women (31 with DDH) | 40 women with DDH vs. 31 controls |
| Average Age | 33 ± 7 years | 45.3 years (DDH group) |
| Hip BMD | Significantly lower | Not specifically reported |
| Spine BMD | No significant difference | Significantly higher in DDH |
| Other Sites | - | Radius and calcaneus higher in DDH |
| Conclusion | 6.3-fold increased risk for low hip BMD | Higher BMD at multiple sites in DDH |
The 2000 study by Obermayer-Pietsch et al. remains particularly influential as it first proposed DDH as a potential risk factor for osteoporotic fractures. Let's examine this crucial experiment more closely.
The researchers conducted a prospective evaluation of 240 premenopausal women with an average age of 33 years. Through detailed medical history, they identified 31 participants (12.9%) with a history of conservatively treated congenital hip dysplasia, plus an additional four (1.2%) who had undergone surgical treatment.
All participants underwent:
The research team ensured both groups were comparable in terms of anthropometric data, lifestyle factors, and hip axis length, strengthening the validity of their comparisons.
The findings revealed a distinctive pattern: women with a history of DDH showed significantly lower bone mineral density specifically at the hip, while their spinal bone density remained normal. This site-specific reduction is particularly noteworthy because it suggests localized rather than systemic bone metabolism alterations.
Additionally, the researchers found that osteocalcin (OC) levels were significantly higher in the DDH group, indicating potentially increased bone turnover. The combination of these findings led to their conclusion that childhood hip dysplasia might represent a previously unrecognized risk factor for low hip bone density in adulthood.
| Measurement | DDH Group | Control Group | Significance |
|---|---|---|---|
| Hip BMD | Significantly lower | Normal | p < 0.05 |
| Spine BMD | Normal | Normal | Not significant |
| Osteocalcin Level | Significantly higher | Normal | p < 0.05 |
| Relative Risk for Low Hip BMD | 6.3-fold increase | Reference | Statistically significant |
The potential mechanisms linking DDH to altered bone mineral density involve both mechanical and biological factors:
The hip joint bears the body's weight during walking and other activities. In a dysplastic hip with improper joint alignment, the distribution of mechanical forces across the joint becomes abnormal. Since bone adapts to mechanical stress (Wolf's Law), these altered loading patterns may lead to localized changes in bone remodeling, potentially explaining why density differences are often most notable at the hip itself 2 .
DDH has a substantial genetic component, with twin studies estimating that approximately 74% of the phenotypic variance is due to genetic factors . Certain genes implicated in DDH, such as GDF5 (involved in bone and joint development), may also influence bone quality and metabolism independently of the structural hip abnormality .
Even successfully treated DDH may lead to subtle alterations in gait and weight-bearing patterns over a lifetime. These adaptations could potentially influence bone remodeling at specific sites, particularly if they result in reduced mechanical loading on the affected structures.
While the potential connection between DDH and bone density is compelling, it's important to view this factor within the broader context of osteoporosis and fracture risk.
Osteoporosis affects over 200 million people worldwide, with approximately one in three women and one in five men over age 50 experiencing osteoporotic fractures 9 . The condition is characterized by low bone mineral density and altered bone microstructure, leading to increased fracture risk, particularly of the hip, spine, and wrist.
Well-established risk factors include:
The potential addition of DDH to this list emphasizes that fracture risk may be influenced by factors operating across the entire lifespan, from birth to advanced age.
Our understanding of the DDH-bone density connection relies on sophisticated research tools:
Measures bone stiffness through ultrasound waves, often used in larger epidemiological studies 1 .
Identifies specific gene variants (like GDF5) that may predispose individuals to both DDH and altered bone metabolism .
Blood tests measuring bone turnover indicators like osteocalcin, which revealed increased bone remodeling in DDH patients 4 .
So what does this mean for you or someone with a history of hip dysplasia?
First, awareness is crucial. If you know you had DDH as a child, consider mentioning this to your healthcare provider when discussing bone health. Second, remember that DDH is just one potential factor among many. The most effective approach to bone health involves addressing modifiable risk factors:
For children currently being treated for DDH, ensuring optimal bone development through nutrition and appropriate physical activity may have long-term benefits that extend far beyond correcting the structural hip problem.
The question of whether congenital hip dysplasia represents a new risk factor for osteoporotic fracture continues to intrigue researchers. While evidence from the 2000 study suggested a strong connection, subsequent research has revealed a more complex relationship that may depend on age, measurement sites, and other factors.
What remains clear is that our bone health story begins early in life, and childhood conditions like DDH may write important chapters in that story. As research continues to evolve, this connection highlights the importance of lifelong attention to bone health—from our earliest days to our later years.
For now, the emerging link between DDH and bone density serves as a powerful reminder that sometimes, to understand where we're going, we need to examine where we began—even if that beginning was at our very first hip joint.