Evidence map›Paper›PMID 42078326›Full record

ArticleJournal of orthopaedic translation2026

Elevated calcitonin gene-related peptide expression through prostaglandin E2-EP4 receptor pathway in promoting proliferative periosteum formation in primary hypertrophic osteoarthropathy.

Qianqian Pang, Ruotong Zhou, Ye Li, Le Huang, Jiankun Xu, Yue Chi, Xuan Qi, Mei Li, Yan Jiang, Ou Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Qianqian PangDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Ruotong ZhouDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Ye LiDepartment of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong.
Le HuangMusculoskeletal Research Laboratory and Bone Quality and Health Assessment Centre, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong.
Jiankun XuMusculoskeletal Research Laboratory and Bone Quality and Health Assessment Centre, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong.
Yue ChiDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Xuan QiDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Mei LiDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Yan JiangDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Ou WangDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Xiaoping XingDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.
Ling QinMusculoskeletal Research Laboratory and Bone Quality and Health Assessment Centre, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong.
Weibo XiaDepartment of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan No.1, Wangfujing Street, Beijing, 100730, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Periosteosis is an imaging hallmark of primary hypertrophic osteoarthropathy (PHO). Increased level of prostaglandin E2 (PGE2) is the pathogenesis of PHO. PGE2 has been shown to bind its EP4 receptor in sensory nerves to stimulate bone formation. Sensory neuropeptide calcitonin gene-related peptide (CGRP), richer in the periosteum, has been revealed to promote osteogenic differentiation of periosteum-derived stem cells (PDSCs) and contributed to periosteum proliferation at peripheral cortical sites. The study hypothesized that CGRP might have a role in regulating proliferative periosteum formation in PHO through the PGE2/EP4 receptor pathway. Methods: We explored the regulatory mechanisms of CGRP in proliferative periosteosis of PGE2 Results: PGE2 administration induced significant bone gain phenotype with higher cortical areas and cortical and trabecular bone volumes at the microarchitectural level. Histological and molecular analysis of the periosteum isolated from the PGE2-treated rats revealed that high CGRP expression in the PGE2/EP4 pathway promoted osteogenesis and mineralization in the peripheral cortex of the femur. Furthermore, Conclusion: Both Translational potential of this study: This study identifies CGRP as a key mediator in PGE2/EP4-induced periosteal bone formation, revealing its critical role in the pathogenesis of periosteosis in primary hypertrophic osteoarthropathy (PHO). Targeting the CGRP signaling pathway offers a promising therapeutic strategy to modulate aberrant periosteal proliferation and bone remodeling in PHO patients. These findings pave the way for developing novel treatments aimed at inhibiting CGRP activity to alleviate periosteal hyperplasia and improve clinical outcomes in PHO.

Indexed as

CGRPEP4OsteogenesisPDSCsPeriosteosisPGE2

Identifiers

PMID42078326
PMCPMC13133950

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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 OpenQuestion graph.