Bones: How to Read a DXA Measurement
Updated: Dec 27, 2023
When I was younger, I thought the human skeleton resembled those in the Halloween aisle at Super Store (similar to America’s Walmart)—a static set of bones that never changed over time.
But bones are ever-evolving like other tissues throughout the body. Bones can also be used to screen for bone fracture risk and osteoporosis.
Before discussing how to interpret bone data on a Dual X-Ray Absorptiometry (DXA) body composition report, it’s useful to understand bones and how to discuss them and their importance to the athlete. In this post, you’ll learn:
What bones are made of and the concepts of bone remodeling and peak bone mass.
The differences between T- and Z-scores and what they mean for athletes.
The impact that chronic LEA has on bone health.
What are Bones Made From?
Bones are a mixture of water (5-10%), lipids (less than 3%), protein and ground substance* (20-40%), and minerals (50-70%), mainly calcium and phosphorus, but also sodium, potassium, fluoride, and strontium. The minerals are what provide the bone its strength and rigidity, whereas the protein provides shape and structure. Ninety-nine percent of the body’s calcium is found in the bones and teeth with 85% of phosphorus in the bones (paragraph source).
Collagen isn’t typically discussed, yet 85-90% of the protein found in bone is type 1 collagen.
Often I hear people talk about the importance of vitamin D for bone health. Vitamin D is important for increasing calcium absorption from the intestines and into the blood, ultimately setting the stage for calcium to be deposited into the bone. Vitamin D is not deposited into bone. When blood vitamin D levels (measured as 25-OH D) are normalized at ~30-40 ng/mL, calcium absorption at the intestinal level is maximized at a value of ~30%. Yet in the presence of a vitamin D deficiency, calcium absorption can drop to 10-15%.
Here's what that means: If 100 milligrams of calcium were orally consumed AND vitamin D blood levels were normalized in the range of 30-40 ng/mL, 30 milligrams (30%) of calcium would be absorbed into circulation. However, this would drop to 10-15 milligrams (10-15%) in the presence of a vitamin D deficiency.
*Ground substance: "A gelatinous material… [that] fills the spaces between fibres and cells.”
Bone Architecture and Remodeling
There are two main types of bone tissue:
The outer dense layer of cortical tissue represents 75-80% of bone mass.
The inner, spongier layer of trabecular tissue represents the remaining 20-25%. This type of bone is more prone to calcium depletion, osteoporosis, and fractures, especially of the wrist, hip, and spine that contain higher levels of trabecular tissue. This area of bone also includes the marrow, which is where immune and red blood cells are produced.
Given bones are an active tissue, they are simultaneously being built and broken down. This process occurs throughout the lifespan and is called bone remodeling.
Within bones, there are four types of cells that are involved in the remodeling process:
Osteoclast cells = Bone breakers. Osteoclasts contain hydrochloric acid (pH ~4), responsible for dissolving the bone matrix, and acid phosphatase, responsible for breaking down bone protein.
Osteoblast cells = Bone builders that reside on the surface of the newly-formed bone.
Osteocytes = Mature osteoblasts. These live within the bone and represent 90% of cells found in this space. Inside, they monitor the bending and stresses imposed on the bone (e.g., weight lifting, sprinting), communicate this to the osteoblasts on the surface of bones, and thus can respond by strengthening those stressed areas.
Osteogenic stem cells: These can become osteoblasts and are present during childhood and adolescence for normal bone growth, and in adulthood in response to bone injury and stress from resistance exercise.
Overall, bone health is measured as bone mineral density (BMD), sometimes referred to as bone mass. BMD is a measure of "how much calcium and other types of minerals are in an area of your bone.”
Peak Bone Mass and the Aging Bone
If you are able to deposit the maximum $1,000 limit into a bank account that is going to decline by $100 every year—and the goal is to stretch your dollars as far into the future as possible—it’s in your best interest to deposit the maximum of $1,000. For instance:
Scenario A: Year one you deposit $1,000. By year two you have $900, year three $800, etc. By year 11, you have $0 remaining.
Scenario B: You only deposit $700. By year two you have $600, year three $500, etc. Now, you reach $0 by year eight. That’s three years lost to Scenario A’s $1,000 deposit.
This is similar to reaching your bones' full potential during the first few decades of life.
Bonjour et al. (1994) wrote that peak bone mass is “defined as the amount of bony tissue present at the end of skeletal maturation.” Peak bone mass tends to be higher in males and African Americans and lower in non-Hispanic whites and women. The latter is due to women having thinner bones than men.
The age at which peak bone mass is acquired is debatable in the research. On the earlier side, Lu et al. (2016) described (1) women hitting their peak earlier than men and (2) both men and women hitting their peak some time in their early-to-late twenties. More specifically, men hit their peak bone mass at 23.34* to 26.86** years and females 21.96* to 22.31** years. Mountjoy et al. (2014) offered a lower proposal, writing that women reach their peak by 19 years and men by 20.5 years. However, others extend this to 25 to 30 years of age.
Regardless of the specific peak time, the period thereafter up until approximately age 40 is when brittle bone tissue is replaced with new tissue. Thereafter, less of the bone tissue is replaced and total bone loss declines at a faster rate.
The hormone estrogen is a protector of bone mass. When estrogen levels are lower, bone breakdown occurs more rapidly than new bone formation, resulting in reduced bone mass. These reductions occur in post-menopausal women, men with estrogen deficiencies, and those of any age suffering from chronic LEA. For the post-menopausal woman, the estrogen reduction can result in bone loss upwards of 20% in the first 5-7 years.
Although genetics plays a role in what one’s peak bone mass can be, a healthful diet that provides adequate calories and certain types of exercise are instrumental in improving bone strength, whereas an unhealthful diet, smoking, calorie restriction, a low body weight and body mass index score, eating disorder or disordered eating, and alcohol intake worsen BMD. Females menstruating by the age of 15 years and doing so regularly thereafter are also beneficial to bone mass.
*Total bone mineral content peak. **Total BMD peak.
T-Score versus Z-Score
On the DXA printout, the Z- and T-scores provided depend on the type of scan used:
Lumbar, total hip (and femoral neck), and forearm scans (i.e., when a bone mineral density diagnostic is desired): These are separate scans of each area, which provides multiple data points for a physician to use in a diagnosis. In my practice, physicians prefer the lumbar and bilateral hip scans.
Full body scan (i.e., when body composition and segmental values are desired): This presents a total body T- and Z-score, which is inappropriate to use for diagnostic measures of bone mineral density. In my practice, I don't review these values with athletes, as I don't want to communicate normal bone values, if in case they truly aren't (see above for the site-specific scans of the lumbar, hip, and forearm).
But what are T- and Z-scores?
The T-score compares an individual’s bone mass to that of a healthy 25- to 35-year old of the same sex and ethnicity (i.e., the apparent average peak adult BMD). T-score values tend to be single digits hovering around zero, either positive or negative. For instance, a zero T-score represents a bone mass of the average, a +1 is roughly 10-12% above the average, and a -3 roughly 30-36% below the average. Thus, one standard deviation from the mean of zero represents a 10-12% change in BMD. Each standard deviation decrease from the average equates to doubling the risk of a stress fracture. However, low BMD on its own does not promise a fracture.
The World Health Organization (WHO) uses the T-score to map osteoporosis risk. Using this chart, an adult with a T-score of -0.5 would be considered normal, -1.5 low bone mass, and -2.8 osteoporotic.
In 2008, the International Society for Clinical Densitometry (ISCD) recommended that children and pre-menopausal women should not be diagnosed under the WHO guidelines. Rather, Z-scores would be used to better compare BMD to age-matched peers.
The Z-score compares bone density to age-, ethnicity-, and sex-matched peers. For instance, if Person A was an 18-year old Caucasian female, their Z-score would be compared to that of the average 18-year old female of the same ethnicity, whereas the T-score would only compare them to the average 25- to 35-year old of the same sex and ethnicity.
There are two pitfalls to the DXA and using either the T- or Z-score:
Both values are based off of data lacking representation of every ethnicity as to make fair comparisons. If an athlete states they are a mixed race or of Aboriginal decent, DXA software does not contain those data sets.
DXA can only report total bone—not trabecular and cortical bone. As mentioned above, trabecular bone loss means a higher risk of calcium loss and fracture. To measure changes in the two bone tissues, a quantitative CT scan would be needed.
Do Athletes Have the Same Predicted Z-Scores as the General Population?
Research has shown that “athletes in weight-bearing sports usually have 5-15% higher BMD than non-athletes," meaning an athlete with bone health concerns would be screened as normal under the WHO guidelines. For this reason, both the American College of Sports Medicine (ACSM) and the International Olympic Committee (IOC) adopted the recommendations originally defined by the ISCD: Normal BMD in athletes is represented by a Z-score greater than or equal to -1.0.
Further, Mathisen et al. (2022) proposed sport-type recommendations, which for some athletes with a low BMD would be flagged at less than zero (e.g., gymnasts, distance runners and weight lifters). For both the normal population and low-impact athletes (e.g., coxswains, jockies, cyclists, swimmers), above -1.0 is in the clear, identical to the ISCD guidelines.
What Does a Provider do with a Concerning BMD?
As of right now, utilizing the ISCD guidelines for the BMD Z-score is only a starting point. If an athlete flags at under -1, a medical and nutritional follow-up is warranted. However, in my clinical experience, athletes with eating disorders, both in the low and normal body weight and fat ranges, have had normal BMD levels. BMD on its own cannot be the only screening method for health and nutritional concerns.
Following the guidance of Nattiv et al. (2007), which adopted the ISCD guidelines, a Z-score of -1.0 warrants further analysis of the athlete, whether or not they have suffered from a stress fracture. The updated REDs Clinical Assessment Tool 2 (REDs CAT2) describes a primary indicator as a BMD Z-score less than -1.0 at the lumbar spine, hip, or femoral neck for an athlete 15 years of age or older.
Ultimately, can a Low BMD and Z-Score be Improved?
Managing an athlete’s expectations is key in the trust-building and care management process. For some athletes, BMD loss may never be fully restored, yet the answer to this section is that it depends.
In the presence of prolonged LEA, BMD suffers. Both estrogen and testosterone have positive effects on bone health, yet deficiencies in both hormones have been linked to low BMD. De Souza et al. (2014) wrote that “amenorrhoeic women will lose approximately 2-3% of bone mass per year if the condition remains untreated.” Every missed menstrual cycle is additive regarding BMD decline.
Achamrah et al. (2017) monitored patients with anorexia nervosa with low BMD over a three-year period. Even in the presence of weight gain as part of the patients’ medical care plan, BMD did not improve. This pattern was observed in those with the lowest body mass index measurements and longest duration of anorexia nervosa. However, other researchers found that weight with menstrual restoration may be predictors of BMD recovery.
De Souza et al. (2014) reported that as the Female Athlete Triad* is treated to normalize energy intake and restore estrogen levels, the recovery of BMD is expected to take years, but is possible.
Taken all together:
The longer the athlete is underweight and lacking a menstrual cycle, the more BMD is lost, which will impact the length of time needed to restore BMD, if fully possible and if the medical and nutritional care plan is followed (i.e., the athlete remains in remission).
Weight restoration alone for an underweight female athlete experiencing a BMD decline may not be adequate to restore BMD. Menstrual restoration is also required for BMD gains, so long as the female has hit menarche.
Not discussed above, but medical interventions involving hormone therapy can also have a positive effect on bone.
Alternatively, consider peak bone mass and the age of nutrition intervention for a low BMD. For example, a dietitian is counseling a 12-year old with low BMD related to an eating disorder. In a healthy child of this age, bone-building should be outpacing breakdown. So long as the dietitian can help the child improve their nutritional intake and restore weight, this athlete still has another decade (or more) on their side to maximize BMD.
Lastly, in the adult athlete with low BMD, a follow-up DXA scan is warranted at 12 months. For children, this is set at six months.
*The Female Athlete Triad is a condition triggered and sustained by chronic LEA. Mountjoy et al. (2014) expanded the Triad to RED-S by including males and other affected physiological systems.
Further Reading
Reviews LEA, contributing causes, and how to calculate it (plus the difficulties of doing so).
Jonvik, K.L., Torstveit, M.K., Sundgot-Borgen, J., & Mathisen, T.F. (2022). J Appl Physiol,132(5):1320-1322.
Stellingwerff, T., et. al. (2023). Br J Sports Med,57(17): 1068-1072.
Mountjoy, M., Ackerman, K.E., Bailey, D.M., Burke, L.M., Constantini, N., ... & Erdener, U. (2023). Br J Sports Med,57(17):1073-1097.
Farr, J.N., & Khosla, S. (2015). Nat Rev Endocrinol,11(9): 513-521
De Souza, M.J., Nattiv, A., Joy, E., Misra, M., Williams, N.I., ... & Matheson, G. (2014). Br J Sports Med,48:289.
Native, A., Loucks, A.B., Manore, M.M., Sanborn, C.F., Sundgot-Borgen, J., & Warren, M.P. (2007). Med Sci Sports Exerc,39(10):1867-1882.
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