Evidence map›Paper›PMID 38239327›Full record

ReviewFrontiers in pain research (Lausanne, Switzerland)2023

A bone to pick-cellular and molecular mechanisms of bone pain in sickle cell disease.

Jahnavi Gollamudi, Kristine A Karkoska, Oluwabukola T Gbotosho, Wei Zou, Hyacinth I Hyacinth, Steven L Teitelbaum

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pain research (Lausanne, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 14% of its field
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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Alendronate preserves bone mineral density in adults with sickle cell disease and osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Article
  5. Review
  6. Should we use bisphosphonates to treat bone complications in sickle cell disease?Hematology. American Society of Hematology. Education Program · 2024
    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

6 authors at 2 institutions in 1 country.

Jahnavi GollamudiDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Kristine A KarkoskaDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Oluwabukola T GbotoshoDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Wei ZouDepartment of Medicine, Division of Bone and Mineral Diseases, and Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, St. Louis, MO, United States.
Hyacinth I HyacinthDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
Steven L TeitelbaumDepartment of Medicine, Division of Bone and Mineral Diseases, and Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, St. Louis, MO, United States.
University of Cincinnati Medical Center · USWashington University in St. Louis · US

Funding

Sickle cell disease and the functional circuit of adult-born neurons in the dentate gyrusR01HL156024 · NHLBI · UNIVERSITY OF CINCINNATI · PI HYACINTH, HYACINTH IDU · 2021 to 2025
$4.0M
FAT TALKS TO BONER01DK111389 · NIDDK · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2017 to 2021
$1.9M
NHLBI NIH HHS R01 HL156024NIDDK NIH HHS R01 DK111389
6 · The paper itself

Abstract

The bone is one of the most commonly affected organs in sickle cell disease (SCD). Repeated ischemia, oxidative stress and inflammation within the bone is largely responsible for promoting bone pain. As more individuals with SCD survive into adulthood, they are likely to experience a synergistic impact of both aging and SCD on their bone health. As bone health deteriorates, bone pain will likely exacerbate. Recent mechanistic and observational studies emphasize an intricate relationship between bone remodeling and the peripheral nervous system. Under pathological conditions, abnormal bone remodeling plays a key role in the propagation of bone pain. In this review, we first summarize mechanisms and burden of select bone complications in SCD. We then discuss processes that contribute to pathological bone pain that have been described in both SCD as well as non-sickle cell animal models. We emphasize the role of bone-nervous system interactions and pitfalls when designing new therapies especially for the sickle cell population. Lastly, we also discuss future basic and translational research in addressing questions about the complex role of stress erythropoiesis and inflammation in the development of SCD bone complications, which may lead to promising therapies and reduce morbidity in this vulnerable population.

Indexed as

bone remodelinghemolytic anemiainflammationnervous systempainsickle cell disease

Identifiers

PMID38239327
PMCPMC10794347
OpenAlexW4390583898

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.