ReviewJBMR plus2026
Mechanisms limiting the long-term anabolic effects of teriparatide (PTH 1-34) on bone.
Review in JBMR plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Teriparatide, (recombinant human PTH 1-34) is an Food and Drug Administration (FDA)-approved anabolic therapy for osteoporosis. In patients with severe bone loss, daily teriparatide injections increase osteoblastic activity and bone turnover, leading to net gain in bone mass, increased BMD, and significantly reduced fracture risk. However, after 6-12 mo of treatment, its anabolic effects, reflected by increased serum bone turnover markers and LS-BMD gain, tend to diminish. Despite various efforts to address this challenge, the underlying mechanisms have remained poorly understood. This review discusses the main mechanisms proposed to limit teriparatide's bone anabolic potential, including osteoprogenitor depletion, changes in bone remodeling dynamics, counter-regulatory molecules (eg, Wnt inhibitors), the influence of mechanical loading, and downstream signaling adaptations. Understanding these mechanisms is important for optimizing osteoporosis therapy and developing strategies to extend teriparatide's "anabolic window."
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.