Evidence map›Paper›PMID 33668588›Full record

ReviewInternational journal of environmental research and public health2021

Mechanisms of Bone Impairment in Sickle Bone Disease.

Paola Giordano, Flavia Urbano, Giuseppe Lassandro, Maria Felicia Faienza

Open access · goldAbstract readReview
In one paragraph

Review in International journal of environmental research and public health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Bone Turnover Markers Levels in a Cohort of Egyptian Children with Sickle Cell Disease.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Sickle cell bone disease and response to intravenous bisphosphonates in children.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022
    Article
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Paola GiordanoPaediatric Unit, Department of Biomedical Sciences and Human Oncology, University of Bari "A. Moro", 70124 Bari, Italy.
Flavia UrbanoPaediatric Unit, Department of Biomedical Sciences and Human Oncology, University of Bari "A. Moro", 70124 Bari, Italy.
Giuseppe LassandroPaediatric Unit, Department of Biomedical Sciences and Human Oncology, University of Bari "A. Moro", 70124 Bari, Italy.
Maria Felicia FaienzaPaediatric Unit, Department of Biomedical Sciences and Human Oncology, University of Bari "A. Moro", 70124 Bari, Italy.ORCID 0000-0002-1899-8337
University of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sickle bone disease (SBD) is a chronic and invalidating complication of Sickle cell disease (SCD), a multisystem autosomal recessive genetic disorder affecting millions of people worldwide. Mechanisms involved in SBD are not completely known, especially in pediatric age. Among the hypothesized pathogenetic mechanisms underlying SBD are bone marrow compensatory hyperplasia and bone ischemic damage, both secondary to vaso-occlusive crisis (VOC), which leads to cell sickling, thus worsening local hypoxia with a negative impact on osteoblast recruitment. Furthermore, the hypoxia is a strong activator of erythropoietin, which in turn stimulates osteoclast precursors and induces bone loss. Hemolysis and iron overload due to a chronic transfusion regimen could also contribute to the onset of bone complications. Vitamin D deficiency, which is frequently seen in SCD subjects, may worsen SBD by increasing the resorptive state that is responsible for low bone mineral density, acute/chronic bone pain, and high fracture risk. An imbalance between osteoblasts and osteoclasts, with a relative decrease of osteoblast recruitment and activity, is a further possible mechanism responsible for the impairment of bone health in SCD. Moreover, delayed pubertal growth spurt and low peak bone mass may explain the high incidence of fracture in SCD adolescents. The aim of this review was to focus on the pathogenesis of SBD, updating the studies on biochemical, instrumental, and biological markers of bone metabolism. We also evaluated the growth development and endocrine complications in subjects affected with SCD.

Indexed as

Anemia, Sickle CellBone DiseasesVitamin D DeficiencyAdolescentBlood TransfusionChildHumansOsteoclastsboneendocrine complicationsgrowthmetabolismsickle cell disease

Identifiers

PMID33668588
PMCPMC7918363
OpenAlexW3132738567

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.