Inflammation-driven carcinogenesis in oral cancer - A systematic review of cellular mechanisms and clinical perspectives

Sep 22, 2026

Inflammation-driven carcinogenesis in oral cancer is addressed through a systematic synthesis of mechanistic and clinical evidence on oral squamous cell carcinoma (OSCC). Using PRISMA 2020-guided searches across major biomedical databases, studies from 2020–2025 are evaluated for inflammatory biomarkers, activated signalling pathways, and prognostic or therapeutic implications. Findings link chronic inflammation to cytokines, chemokines, NF-κB/STAT3 activation, oxidative DNA damage, and immune evasion, with elevated inflammatory markers associated with poor outcomes. The review supports integrating biomarker profiles and anti-inflammatory strategies to improve detection and survival.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages9

Reading Time23 min

AccessFree to download

Background and objectives

Methods

Results

Interpretation and conclusions

Eligibility criteria

Information sources and search strategy

Indian J Med Res 163, May 2026, pp 640-648 DOI: 10.25259/IJMR_2452_2025 Systematic Review Inflammation-driven carcinogenesis in oral cancer: A systematic review of cellular mechanisms and clinical perspectives Munish Rastogi,1 Alka Katiyar1 and Dheeraj Kumar1 1School of Health Sciences, Chhatrapati Shahu Ji Maharaj University, Kanpur, Uttar Pradesh, India Received September 7, 2025; Accepted December 21, 2025; Published May 16, 2026 Background and objectives: Oral squamous cell carcinoma (OSCC) represents the predominant form of oral cancer and remains a major cause of morbidity and mortality worldwide. Beyond traditional risk factors such as tobacco, alcohol, and betel quid consumption, mounting evidence implicates chronic inflammation as a driving force in oral carcinogenesis. This review synthesises current literature exploring how inflammatory mediators contribute to tumour initiation, progression, and clinical outcomes in OSCC. Methods: A systematic search of PubMed, Scopus, Web of Science, Embase, and Cochrane Library databases was conducted according to PRISMA 2020 guidelines. Studies from 2020–2025 examining molecular and clinical interactions between inflammation and OSCC were analysed. Extracted data included inflammatory biomarkers, activated signalling pathways, and prognostic or therapeutic implications. The risk of bias was assessed using the Newcastle–Ottawa Scale and Cochrane RoB-2 tool. The review protocol was registered with PROSPERO (CRD420251141942) . Results: Forty-three eligible studies revealed that inflammatory cytokines such as TNF-α, IL-6, and IL-1β, together with chemokines like CXCL8, trigger oncogenic cascades involving NF-κB and STAT3, leading to enhanced proliferation, angiogenesis, and epithelial– mesenchymal transition. Oxidative DNA damage and immune suppression mediated by M2 macrophages and PD-1/PD-L1 signalling further facilitate tumour aggressiveness. Elevated COX-2, STAT3, and systemic inflammatory ratios were strongly associated with poor prognosis. Interpretation and conclusions: Persistent inflammation acts as a critical determinant in OSCC pathogenesis. Integrating inflammationrelated biomarkers and anti-inflammatory therapeutic strategies may improve early detection, prognostication, and patient survival outcomes. Keywords Carcinogenesis; Chronic inflammation; Cytokines; Oral cancer; Oral squamous cell carcinoma (OSCC); Therapeutic targets Oral cancer remains a major global health concern, with oral squamous cell carcinoma (OSCC) constituting over 90% of malignancies arising in the oral cavity.1 Despite improvements in diagnostic and treatment strategies, global mortality rates remain high, primarily due to late-stage detection and limited therapeutic success in advanced disease.2 The burden of OSCC varies geographically and is closely tied to established risk factors such as tobacco use, alcohol consumption, and high-risk human papillomavirus (HPV) infection. In regions of South and Southeast Asia, betel quid chewing further elevates disease incidence.3 Beyond direct carcinogenic injury, these risk factors exert profound effects through chronic inflammation, an established contributor to nearly 15% of human cancers and often described as the‘seventh hallmark of cancer. Persistent inflammatory conditions including oral lichen planus and chronic periodontitis create a microenvironment favourable for malignant transformation.4 This state is characterised by sustained immune cell activity and continuous release of cytokines, chemokines, growth factors, and reactive oxygen species (ROS), which promote DNA damage, angiogenesis, tumour invasion, and immune evasion.5 Given these interconnected mechanisms, this systematic review synthesises current evidence to clarify how inflammation drives OSCC development How to cite this article: Rastogi M, Katiyar A, Kumar D. Inflammation-driven carcinogenesis in oral cancer: A systematic review of cellular mechanismsand cl

FAQs

What is the main focus of this systematic review on OSCC?

It synthesises evidence on how chronic inflammation contributes to OSCC tumour initiation, progression, and clinical outcomes, including mechanistic pathways and clinical implications.

Which databases and guideline framework were used for the literature search?

The review searched PubMed, Scopus, Web of Science, Embase, and Cochrane Library and followed PRISMA 2020 guidelines.

What key inflammatory mediators and signalling pathways are highlighted in the results?

The review reports roles for cytokines such as TNF-α, IL-6, and IL-1β, chemokines like CXCL8, and oncogenic cascades involving NF-κB and STAT3.

Sep 22, 2026

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