yes

What do you mean by osteopenia? Do you refer to  the so called WHO definition with T-scores -1 to -2,5. According to the literature there is an increase in RR of 1.5 per change in T-score. If this is true there is an association between osteopenia and vertebral deformities. However, with T-scores >-2 the effect of a variation in aBMD  seems to be very small. But, With aBMD < -2 there seems to be an exponential increase in the incidence of (incident) vertebral deformities. 

But, please, do not use the term osteopenia, in this connection it is noncensical, as pointen out in the paper New Yourk Times. I will se if I can find the reference, it is a very good article!

The Reference concerning the nonsensical osteopenia grading is: New York Times, Sept.  2009: "The Confusing diagnosis of osteopenia". Some very able experts have given their views on this subject. Not least is it important to notice the comment by Cummings that by using the osteopeia grading a substantial overtreatment of patients may follow. 

Thank you so much Ame for your answer . And sending reference for this article.

Variance in bone density is a continous process as well as the increasing risk for fracture by change of bone mineral density from lowest baseline risk (in the region of +/- 1 SD of young healthy persons). Even if the bone density increases, the risk for fracture also increases! So You see a U-shaped curve for the relation of bone density (or bone mass) and fractures. There is no cut-off point for fractures! And You can obviously see typical osteoporotic fractures despite normal bone density (thus,the risk is never sero)!

In other words: bone mineral density is just one of many risk factors for fractures...

THREE POINTS:

Why talk about bone density. In a natural scientific community density is weight/volume. Density is not a structural parameter, it does not describe strength, it is a means of describing material properties. Of course, material properties are also important, but stregnth is the combination of the material properties and size and shape. aBMD is NOT density, it is the mathematical product of density (weight of calcium/volume) and the average thickness of the bone. This is much more like a mass parameter, it is certainly not densty. Why not use natural scientific terms correctly and avoid confusion.

aBMD must be considered a surrogate for bone strength. As a bone does not have just on setrength, but innumerable, aBMD, or any other parameter, is bound to be only an approxiamtion to "strength". This is "imprecision of the definition". It has profound consequences on the analyses we performe. Typically we do regression analyses and find r2 less than 1, meaning that, for examle aBMD does not expalin 100 percent of fracture risk. Typically we find r2 to be 0.7 and we conclude that other factors (than aBMD) accounts for 30 percent of the fracture risk. However, it may be incorrect to conclude that there are other factors than aBMD that we must look for. In regression analyses we use residuals which is a measure for what is not explained by the independent factor used in the analysis; however due to the imprecision of the independent parameter (aBMD in this connection) we get "confounding residuals". Unfortunately, this parameter is typically not taken into account in the studies that Burkhard's final remark is based on.This  conclusion may be wrong and  may have led to a in vain search for the  missing fracture risk factors. (This does not mean that we should not look for better strength surrgates  than aBMD.) Of course, it is unlikely that even the most perfect strength paramater will give us r2=1, the way wi fall is certainly also a factor to take into account, but, for example, I do not hink that a previuos fracture is causing an increased risk for further fractures, it probably just improves our strenght estimation.

I fail to see how the bi-phasic risk pattern is supported.

"Osteopenia" means just "lack of bone tissue within a bone organ", with no reference at all to bone strength. "Osteoporosis" means just "a higher tan usual porosity within bone tissue" (obviously leading to an osteopenia). "Bone fragility" means just a reduction in bone resistance to fracture, regardless of the presence of osteopenia, osteoporosis, or whatever other posible cause of that problem. A problem arose when bone mineral content could be measured absorptiometrically ("densitometrically"), as the amount of mineral present within the mass of bone tissue placed between a radiation source and a set of suitable detectors. 

Then, the lack of mineral within specific regions of either "osteopenic" or "osteoporotic" (or whatever other kind of) bones could be quantified as their crude "bone mineral content", BMC, in mass units, or the (areal) "bone mineral density" as calculated by expressing the BMC per unit of projected bone area of the specific region studied, in mass/area units.

Immediately after that development, highly significant, obviously negative relationships were statistically demonstrated between the BMC or BMD of a given bone region and the incidence of fractures in that region. Then, a reference scale of "normal" BMD T-scores was developed from an extensive analysis of bones from young, healthy individuals, and the diagnosis of "osteopenia" and "osteoporosis" were  just ascribed to individuals showing T-scores between -1.0 and -2.5 and lower tan -2.5, respectively, regardless of bone tissue "porosity". In addition, it was also established that such a curious distinction between "osteopenias" and "osteoporoses" should be also regarded as a mechanical distinction between healthy and fragile bone, respectively, and well performed T-score tables that were suitable for such "diagnosis" were adopted by the WHO and broadcasted worldwide.   

From the mechanical point of view, bone strength is a combination of bone stiffness (ability of bone structure to resist deformation by a load) and toughness (ability of bone structure to resist cracks -determined by deformation- and separation into fragments). There are only two biological determinants of bone strength, namely, the mechanical quality (stiffness + toughness) of the mineralized tissue and the spatial distribution of that tissue as related to the direction of the deforming force (bone geometry, or bone design). Tissue mechanical quality depends on the microstructure of the mineralized matrix (which shows a high degree of anisotropy) and on the degree of tissue (micro) porosity. The architectural (directional) efficiency of bone design (cortical shells and trabecular networks, which also show a high degree of anisotropy) depends on modeling "drifts" that are oriented by bone mechanostat as a function of the (highly oriented) mechanical usage of the bone in question.

Importantly, bone tissue quality and distribution are excluding determinants of bone strength in fixed geometrical conditions of testing (including thjose occurring in normal life). This means that bone "density" (BMC, BMD) or whatever else bone property (weight, hardness, water content, etc etc) dont play ANY SPECIFIC ROLE in determining bone strength.

When any biological variable is just something measurable within the system one is analyzing to evaluate some specific property (as bone strength here) but it plays no independent role in the biological determination of that property, the variable is regarded as a "surrogate" of the really significant, determinant variables. Here, "surrogate" means "negligible as a determinant" (just that), regardless of the significance of the correlations one may calculate between any "surrogate" variable and the analyzed property.

Statistics is a mathematical, not biological science. If one finds an R2=0.7 correlation between, say, bone "density", or bone weight, or bone water content, etc (x) and bone strength (y), one can only say that about 70% of the variance of the "Y variable" is "mathematically associated" with the variance of the "X variable". The causal relationship must be investigated and analyzed otherwise.

Example wanted? When I invented the Bone Strength Index (BSI - Ferretti et al, Bone, 1996), I found an R2=0.91 association between the real bone strength and the product between an indicator a bone material quality (volumetric -not "areal"- BMD of cortical tissue) and an indicator of the distribution of that tissue (cross-sectional moment of inertia). This meant that no less tan 91% of the variance of bone strength (as assayed, i.e. 3-point bending test of rat femurs) depended on the product of the tissue quality (as assayed, i.e. cortical vBMD) and distribution (as assayed, i.e. bending moment of inertia), and the remaining 7% of the strength variance was left to the real influence of bone material quality and design that was not catched by the experimental assessment of these properties. The millon dollar question here is, where is the "areal" BMD of the assayed bones? The paper shows that.  The answer is, "NOWHERE".

Now, what about that damned R2=0.7 association between bone strength and "areal" (DEXA) BMD? This is a SPURIOUS (false) relationship, which denotes no causal ("functional") association at all. To show a "true" (causal) association between "areal" BMD (either within or outside the "osteopenic" WHO range) and bone strength you has to show that by increasing the areal BMD you increase bone strength proportionally, and vice.-versa, and this is far from a real possibility.

And now, to your question, is there any (real, functional, causal) association between vertebral fracture and osteopenia? My answer is, NOT AT ALL.

Thank you for this comprehensive answer 

 prof Ferretti that k you for your comprehensive answer . But I read it several times . I will be thankful if you sumarise it in easy way so I can understand what you .mean .exactly. 

Dear Dr Al hadidi,

Just four points:

1. The resistance of a bone to fracture does not depend directly on the mass of its mineralized tissue but on the stiffness and toughness (mechanical quality) and the spatial distribution of that tissue (architectural quality, bone design) concerning the resistance to be bent (and fractured) by the usual loads..

2. "Osteopenia" is merely a reduction of the mineralized tissue mass, with no specific involvement of the stiffness, toughness and distribution of that tissue.

3. Hence, "osteopenia" does not imply "bone fragility".

4. Therefore, the mere presence of "osteopenia" of the vertebral bodies (despite being an undesirable condition concerning bone health) is not necessarily associated with a higher rate of incidence of vertebral fractures.

This is the easiest way to understand it, I hope it helps.

With my best rest regards,

Dr JL Ferretti

It helps alot.thank so much indeed for fast and clear answer . I appreciate your time and efforts.

Prof Ferretti if you don't mind , is this also applicable for osteoporosis also , if the answer is yes .why there is strong relation between osteoporosis and fractured?

The answer is "NO" for all osteopenias, osteporoses, and any kind of bone-weakening diseases.

Example 1. You have two 65-yr "osteopenic" or "osteoporotic" women (WHO criteria) with similar skeletons and similar DEXA DMO values in the spine, in which there are comparable lots of loose vertebral trabeculae to be reabsorbed by the mechanostat system because these do not play any mechanical role (i.e. they do not deform with use). You give effective doses of a bisphosphonate to one of the women (women 1) and nothing to the other (women 2) during 1 year. After that you measure DEXA BMD in both and find that in woman 1 the DMO values were maintained while in women 2 the same were reduced. You conclude that the bisphosphonate was "effective" in protecting the (functional) skeleton in woman 1 as compared with woman 2. Right or wrong?. WRONG, because the "protected" bone tissue was mechanically ineffective in women 1.

Example 2. You have again two 65-yr "osteopenic" or "osteoporotic" women (WHO criteria) with similar skeletons but with just one difference. Woman 1 has the same BMC on the femoral neck than woman 2 but her neck is a bit wider and thinner-walled than that of woman 2, such that the real cross-sectional moment of inertia calculated for upper-to-lower bending is significantrly higher in woman 1 than it is in woman 2. Obviously, if you measure both femoral necks by DEXA you will find that BMD in women 1 will be lower than that of women 2 because the same BMC would be divided by a larger projecting area, OK?. Then, you conclude that the femortal neck of woman 1 is weaker than that of woman 2. Rigfht or wrong? WRONG, because it is not BMC nor BMD what defines bone strength but other, mechanically-related variables (in this case, an indicatoir of the architectural efficiency of the bone concerning one of the ways it is deformed by usage).

Example 3. You have only one woman this time (an easier way to live) in which the vertebral trabecular bone shows a normal value of DEXA BMC and BMD but the corresponding trabecular network is significantly disconnected as compared with that of a normal woman. From just the DEXA values you could conclude that your woman has a normal spine and would not have any reason of concern about vertebral fractures. Right or wrong? WRONG, because it is not BMC or BMD what accounts for bone strength, but other mechanically relevant indicators, as, in this case, would be the inter-trabecular connectivity which is an indicator of the architectural efficiency of the trabecular network concerning the whole-bone strength.

Example 4. You have now a new woman (you should change woman from time to time, it looks to be a healthy habit) with a similar skeleton to that of the woman in Example 3, but in this case her DEXA BMC and BMD are "osteopenic" or "osteoporotic" according to the WHO criteria. You give an anabolic treatment to the woman (PTH) and find that, after one year, her BMC and BMD reach the normal (WHO) values. You conclude that you have "improved" the strength of her vertebral bodies until reaching the normal standards. Right or wrong? WRONG, because you have added new bone on disconnected trabeculae that does not have any supporting role within the vertebral bodies.

Example 5. You have lots of "osteopenic" and "osteoporotic" women (including cases like those quite common ones I have referred to above as Examples) in which DEXA measurements have been made and you can assess their Fx rate during a sufficiently long time. If you correlate their BMD values with the incidence of Fx, you will surely find a nice (0.7) correlation, because the relevant factors to bone strength (volumetric BMD of the "solid" bone, cross-sectional moments of inertia, etc) are also correlated somehow (less tan 0.7) with the bone mass as a SURROGATE, i.e. through SPURIOUS (not "true") correlations. Now you conclude that BMD is a relevant indicator of bone strength in "osteopenic" or "osteoporotic" (WHO criteria) women. Right or... wrong?

Thank you for this comprehensive. Answer I benefit alot from this information

Are any body familial with paper about the incidence of asymptomatic vertebral fracture in osteopenic patients 

Please be precise. What do you mean by "osteopenic ..  ". Are you the Word according to the "WHO-definition" or just as a general term for low bone mass or ... ?

Yes, osteopenia according to WHO ?

This is extreemely difficult. Appreciate that by increasing age almost 70 to 90 percent of all (men and women) will be either osteopenic or osteoporotic, 50 persent of women will be osteoporitc by age 67. Furthermore, by inceasing age the BMD-value measured in vertebral bodies will increase, due to degenerative changes. So, the WHO definition is, to be polite, confusing. If you search for articles in the New York Times and you will find good reasons for just deleting the nonsensical grade called osteopenia.  

I would rephrase your question: Is there an association between BMD-value and vertebral compression fractures. Again, it is difficult to find a reliable answer. I fail to find a study showing such an association, however studies combining BMD and age, as the "independent factor", there is a strong association. However, is that mainly due to age or BMD. Are there as yet unknown mechanical bone factors that we need to look for?

I consider BMD to be a close to useless parameter for assessing vertebral fracture risk and I would certainly not consider osteopenic patiens as being in a risk group for vertebral compressions.

JR Ferretti: Your mainly theoretical considerations need verification by experimental or clinical research. I feel that things are not that easy.

Thank you for this answer .

Dear all, my aim was not 'making the things easier', but making your brains think about a purely mechanical fact (a bone fracture) and the (poor) resources we have at hand to properly evaluate the risk a given individual has to suffer such event. Certainly BMD is good for nothing (just a bit better than merely weighing the bone). What one really needs to assess to properly evaluate the bone mechanical integrity as related to a given method of fracture is the mechanical quality (stifness and toughness) of the mineralized tissue (i.e. at tissue level of complexity) and the architectural efficiency of the spatial distribution of that material (i.e. at organ level of complexity) as related to the direction in which the force eventually fracturing the bone would act. To make it really "simple", what you need is just three things: mechanical indicators at the tissue level, geometric indicators at the organ level, and... directionality (please). Everything else is just accessory ('anecdotic', you could also say). This does not need any 'clinical verification', this is just the pure "physical background" from which anyone wishing to solve the diagnosis of this really complex problem must start with.

The practical problem is to find those at high risk of having a fracture, and who may thus benefit from pharmacological fracture intervention. There are several mehanical factores such as  stiffness, toughness and bone shape and theer are different ways of falling. Typically, a fall on the side is used for femoral neck fracture models. We can have theories and use different experimental designs. These considerations and eperimental designs do, hoewer, not take into account biological and other variations. Therefore, in the end we need clinical verification.   Arne Høiseth