Evidence map›Paper›PMID 41693190›Full record

ReviewPediatric endocrinology, diabetes, and metabolism2025

Chemotherapy-induced osteoporosis in pediatric oncology: pathophysiology and treatment.

Jakub Pobideł, Julia Piekarz, Natalia Picheta, Katarzyna Szklener

Abstract readReview
In one paragraph

Review in Pediatric endocrinology, diabetes, and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jakub PobidełStudent Academic Group, Department of Clinical Oncology and Chemotherapy, Medical University, Lublin, Poland.
Julia PiekarzStudent Academic Group, Department of Clinical Oncology and Chemotherapy, Medical University, Lublin, Poland. piekarzjulia1@gmail.com.
Natalia PichetaStudent Academic Group, Department of Clinical Oncology and Chemotherapy, Medical University, Lublin, Poland.
Katarzyna SzklenerDepartment of Clinical Oncology and Chemotherapy, Medical University, Lublin, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Juvenile osteoporosis is an increasingly recognized long-term complication in pediatric oncology. While advances in cancer therapy have improved survival, aggressive treatment protocols - chemotherapy, glucocorticoids, radiotherapy, surgery - often disrupt skeletal development during key phases of bone accrual. This review outlines the multifactorial pathophysiology of therapy-induced bone loss in children with cancer. The imbalance between bone formation and resorption is driven by inflammation, oxidative stress, hormonal deficits and direct drug toxicity. Agents such as methotrexate and glucocorticoids impair osteoblast function and enhance osteoclastogenesis. Endocrinopathies - particularly hypogonadism and growth hormone deficiency - further compromise peak bone mass acquisition. Compounding these effects are post-treatment nutritional deficits, physical inactivity, and psychological fatigue. Many survivors consume high-fat, low-nutrient diets and avoid exercise, worsening musculoskeletal health. These behaviors often stem from insufficient rehabilitation support and emotional exhaustion, perpetuating deconditioning and elevating fracture risk. Genetic factors are also implicated. Mutations in low-density lipoprotein receptor-related protein 5 (LRP5) and estrogen receptor 1 (ESR1) are associated with reduced bone mineral density in pediatric patients. Diagnosis is complicated by evolving pediatric criteria for bone density and growth-related variability in biomarkers. Nonetheless, early identification and continuous monitoring are essential. Interventions such as individualized physical activity programs, nutritional repletion, endocrine evaluation, and bisphosphonate therapy may counteract skeletal decline. In conclusion, secondary osteoporosis in pediatric cancer survivors reflects a convergence of oncologic, metabolic, behavioral, and genetic factors. Effective management requires early, multidisciplinary strategies targeting modifiable risks and predictive markers to preserve bone integrity and improve long-term quality of life.

Indexed as

Antineoplastic AgentsNeoplasmsOsteoporosisBone DensityChildHumansAntineoplastic Agentsbone mineral densitycancer in pediatric populationchemotherapyjuvenile osteoporosisosteoporosis

Identifiers

PMID41693190
PMCPMC12928147

What OpenQuestion holds

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Registered trials

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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.