For osteoporosis a wide range of sophisticated biomarkers are known.
There are bone turnover marker, theses can not be used for osteoporosis diagnosis but for individual risk assessment.
Very good markers are bone formation markers including alkaline phosphatase, procollagen type 1
Especially alkaline phosphatase consists several dimeric isoforms, that are associated with tissues, from liver, bone, intestine, spleen, kidney, and placenta. the extraction of serum alkaline phosphatase can be easily performed from any mentioned tissue.
In contrast to that osteocalcin yield to heterogenous predicitive values.
Procollagen typ1 can be derived from radioimmunoassay, it's very sensitive for bone formation rate in osteoporosis.
Then there various biomarkers for predicting future bone loss.
In large health survey s bone mineral density (BMD) calculator are used. As an example please folloe Miazgowski et al. (2012) Secondary osteoporosis: endocrine and metabolic causes of bone mass deterioration.J Osteoporos. 2012;2012:907214.
BMD can be also assessed with dual-energy x-ray absorptionmetry (DEXA)
In my opion I recommand to use BMD because very are specific individual cutpoints for pre- and postmenopausal women available.
Bone turnover markers (BTM) are supposed to depict accurate bone quality as bone is a physiologically active tissue and imaging modality like DEXA and other only provide quantitative data. N terminal markers in urine for catabolic activity and osteocalcin and other markers for anabolic status are widely used among others.
Using the term "osteoporosis" requires å precise definition. Usually it is not a disease, and particylarly not a generalized condition. The Word osteoporosis is usually used to indicate high fracture risk due to frail (thin) bones. This is part of normal physiological / biological variation, associated to (normal/physiological) body weight. In normals (free of disease) there er no markes that can be used to for assessing what we normally call "ostreoporosis".
Only in some unphysiological situations may these markers be of any use.
I strongly endorse the reply from Arne Horseth to this question. The study of bone fragility was set back dramatically by the misdirected WHO decision to endorse a surrogate marker for bone fragility. This directly lead to answers such as that from Dr Westerman above. Why have we, as a specialty, not learned sufficiently from the publications of Stone in 2003 and Siris in 2004 that the DXA-determined bone mineral density is an inadequate surrogate for fragility risk? The very word "osteoporosis" became defined by something it is not: a T-score less than or equal to -2.5. Osteoporosis (and by this we mean senile osteoporosis - there are other etiologies for other forms - the "unphysiological" exceptions) is in fact the variably penetrating bone fragility resulting from decreasing 17-beta estradiol levels. There are no markers for osteoporosis. The absolutely hysterical embracing of bone turnover markers entirely misses the point.