Skeletal pathologies caused by PLS3 inactivation are predominantly associated with impaired cortical bone integrity
Authors' conclusion
Taken together, our data raise the hypothesis that PLS3 inactivation predominantly affects cortical bone parameters in mice and humans and that anti-sclerostin therapy could be effective for the treatment of XLO.
Study context
- Population
- Male X-linked osteoporosis (XLO) patients compared with male OI-I patients; female heterozygous PLS3 carriers; Pls3-deficient mice crossed with Lrp5A213V high bone mass mice
- Exposure
- Male XLO patients vs male OI-I patients
- Outcome
- Skeletal parameters, XLO vs OI-I
Methodological detailscomparative, mouse crossing experiment
- Comparative
- Mouse crossing experiment
Main finding
As reported in the abstract
- No major differences between XLO and OI-I in baseline characteristics, laboratory parameters or BMD by DXA
- Significant difference between groups by high resolution peripheral quantitative computed tomography (HRpQCT)
- XLO had significantly reduced cortical bone parameters vs normal reference ranges and OI-I, especially at the distal radius
Observational data: associations, not effects.
Further findings
Female heterozygous PLS3 carriers
- Carriers with osteoporotic fractures at postmenopausal age, treated with romosozumab, which appeared effective
- 2
- Less affected than male XLO patients
Mouse study: Lrp5A213V allele in wildtype and Pls3-deficient mice
- Lrp5A213V allele led to significantly increased cortical and trabecular bone mass in wildtype and Pls3-deficient mice
Original publication
Skeletal pathologies caused by PLS3 inactivation are predominantly associated with impaired cortical bone integrity. J Bone Miner Res. Published 24 September 2026. doi:10.
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