title: Relationship between bone turnover and density with teriparatide, denosumab or both in women in the DATA study.
abstract: While changes in biochemical markers of bone turnover (BTM) have been reported to predict changes in bone mineral density (BMD), the relationship between changes in BMD and BTMs with combined antiresorptive/anabolic therapy is unknown.
  
  
  
  In the DATA study, 94 postmenopausal osteoporotic women (ages 51-91) received either teriparatide 20-mcg SC daily, denosumab 60-mg SC every 6months, or both for 2years. Pearson's correlation coefficients (R) were calculated to determine the relationship between baseline and early changes in BTMs (as well as serum sclerostin) and 2-year changes in BMD.
  
  
  
  In women receiving teriparatide, baseline BTMs did not correlate with 2-year BMD changes though 12-month increases in osteocalcin and P1NP were associated with 2-year increases in spine BMD. In women receiving denosumab, spine and hip BMD gains correlated with both baseline and changes in P1NP and C-telopeptide. In women receiving combined teriparatide/denosumab, while both baseline and decreases in P1NP were associated with spine BMD gains, distal radius increases were associated with less CTX suppression. Neither baseline nor changes in serum sclerostin correlated with BMD in any treatment group.
  
  
  
  In women treated with teriparatide or denosumab, early BTM changes (increases and decreases, respectively) predict 2-year BMD gains, especially at the spine. In women treated with combined teriparatide/denosumab therapy, BMD increases at the distal radius were associated with less suppression of bone turnover. These results suggest that efficacy of combination therapy at cortical sites such as the radius may depend on residual bone remodeling despite RANKL inhibition.
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, Boston, MA, United States. Electronic address: jntsai@mgh.harvard.edu.
authors.forename: J N
authors.initials: JN
authors.lastname: Tsai
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, Boston, MA, United States.
authors.forename: S M
authors.initials: SM
authors.lastname: Burnett-Bowie
authors.affiliation: Biostatistics Center, Massachusetts General Hospital, Boston, MA, United States.
authors.forename: H
authors.initials: H
authors.lastname: Lee
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, Boston, MA, United States.
authors.forename: B Z
authors.initials: BZ
authors.lastname: Leder
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects; D019485:Bone Morphogenetic Proteins / Q000097:blood; D016723:Bone Remodeling / Q000187:drug effects; D024042:Collagen Type I / Q000097:blood; D000069448:Denosumab / Q000494:pharmacology*; D004359:Drug Therapy, Combination; D005260:Female; D005819:Genetic Markers; D006801:Humans; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000378:metabolism; D013131:Spine / Q000503:physiopathology; D019379:Teriparatide / Q000494:pharmacology*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D015415:Biomarkers; D019485:Bone Morphogenetic Proteins; D024042:Collagen Type I; D005819:Genetic Markers; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C422903:SOST protein, human; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide; D019379:Teriparatide; D000069448:Denosumab
keywords: Bone formation; Bone resorption; Bone turnover markers; Denosumab; Osteoporosis; Teriparatide