# Bone turnover markers in patients with inflammatory bowel disease in remission: a cross-sectional comparison of anti-TNFα therapy with conventional maintenance therapy

**Authors:** S. Jarmakiewicz-Czaja, P. R. Kiela, D. Piątek, A. Sokal-Dembowska, W. Guz, R. Radzki, J. Sztembis, R. Filip

PMC · DOI: 10.3389/fmed.2026.1729584 · Frontiers in Medicine · 2026-02-10

## TL;DR

This study compares bone health in inflammatory bowel disease patients using anti-TNFα therapy or conventional treatment, finding no significant bone benefits from anti-TNFα drugs.

## Contribution

The study is the first to compare bone turnover markers in IBD remission patients using anti-TNFα therapy versus conventional treatment.

## Key findings

- IBD patients had higher osteopontin (OPN) levels and lower total T-scores compared to healthy controls.
- Anti-TNFα therapy did not improve bone turnover markers more than conventional treatment.
- IBD patients remain at risk for reduced bone density despite remission.

## Abstract

Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are associated with increased risk of bone loss due to chronic inflammation, nutritional deficiencies, and pharmacological treatment.

The purpose of this study was to evaluate bone mineral density (BMD) and selected bone turnover markers in IBD patients in clinical and endoscopic remission, treated with conventional therapy or anti-TNF-α agents.

This single-center study included 100 participants: 35 with CD, 37 with UC, and 28 age-matched healthy controls. Patients IBD participated in the study received conventional treatment or anti- TNF-α therapy with ADA (adalimumab) or IFX (infliximab). IBD patients were in confirmed remission, without steroid use or comorbidities affecting bone metabolism. BMD was measured using dual-energy X-ray absorptiometry (DXA) at the lumbar spine (L2–L4), the left femoral neck, and whole body. Serum levels of osteocalcin (OC), parathyroid hormone (PTH), sclerostin (SOST), fibroblast growth factor 23 (FGF23), Dickkopf-1 (DKK1), osteoprotegerin (OPG), and osteopontin (OPN) were assessed.

The IBD group demonstrated a statistically significant higher OPN value (p < 0.001) compared to the control group. Additionally, the total T-score revealed a significant difference between the groups (p = 0.005), with the control group exhibiting the highest values. No significant differences were found in the levels of other bone density markers studied between the biologically treated group and the conventionally treated group.

Our study indicates that patients with IBD are at risk of developing reduced bone mineral density and osteoporosis. While some bone turnover markers appear to normalize during remission, anti-TNF-α treatment does not offer added benefits for bone metabolism compared to conventional therapy.

## Linked entities

- **Proteins:** bglap2 (bone gamma-carboxyglutamate (gla) protein (osteocalcin) 2), dkk1.S (dickkopf WNT signaling pathway inhibitor 1 S homeolog)
- **Diseases:** inflammatory bowel disease (MONDO:0005265), Crohn's disease (MONDO:0005011), ulcerative colitis (MONDO:0005101), osteoporosis (MONDO:0005298)

## Full-text entities

- **Genes:** CX3CL1 (C-X3-C motif chemokine ligand 1) [NCBI Gene 6376] {aka ABCD-3, C3Xkine, CXC3, CXC3C, NTN, NTT}, TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}, SPP1 (secreted phosphoprotein 1) [NCBI Gene 6696] {aka BNSP, BSPI, ETA-1, OPN}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, SOST (sclerostin) [NCBI Gene 50964] {aka CDD, DAND6, SOST1, VBCH}, DKK1 (dickkopf Wnt signaling pathway inhibitor 1) [NCBI Gene 22943] {aka DKK-1, SK}, BGLAP (bone gamma-carboxyglutamate protein) [NCBI Gene 632] {aka BGP, OC, OCN}, TNFRSF11B (TNF receptor superfamily member 11b) [NCBI Gene 4982] {aka OCIF, OPG, PDB5, TR1}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, FGF23 (fibroblast growth factor 23) [NCBI Gene 8074] {aka ADHR, FGFN, HFTC2, HPDR2, HYPF, PHPTC}
- **Diseases:** immune (MESH:D007154), CD (MESH:D003424), osteoporosis (MESH:D010024), bone loss (MESH:D001847), PK (MESH:C564858), complications (MESH:D008107), Chronic inflammation (MESH:D007249), nutritional deficiencies (MESH:D044342), bone fractures (MESH:D050723), bone fragility (MESH:C536063), chronic (MESH:D002908), UC (MESH:D003093), IBD (MESH:D015212), bone metabolism abnormalities (MESH:D001851), CTX (MESH:D019294), reduced bone resorption (MESH:D001862)
- **Chemicals:** Azathioprine (MESH:D001379), Sulfasalazine (MESH:D012460), 5-ASA (-), phosphate (MESH:D010710), calcium (MESH:D002118), IFX (MESH:D000069285), bisphosphonates (MESH:D004164), steroid (MESH:D013256), ADA (MESH:D000068879)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

60 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929429/full.md

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Source: https://tomesphere.com/paper/PMC12929429