Peri-implant oral malignancy (PIOM) refers to malignant tumors arising around dental implants and is an increasingly reported complication of implant therapy. PIOM may follow distinct pathophysiological mechanisms, including chronic peri-implant inflammation and implant-related factors that contribute to carcinogenesis. This current review aims to explore the potential role of peri-implantitis (PI) as a risk factor for PIOM, discussing the proposed pathogenic mechanisms, histological findings, and clinical implications. A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science databases. Relevant case reports, clinical studies, and reviews on the keywords “PIOM” and “PI” published from 2019 up to 2025 were included and qualitatively analyzed. Clinicopathologic characteristics are summarized as location and morphology, disease progression, histopathology, and degree of differentiation, and pathophysiological hypotheses involve inflammatory and electrochemical pathways, epithelial barrier dysfunction, molecular alterations, microbiome dysbiosis, and immune dysregulation. Current evidence remains limited and primarily anecdotal. Several studies suggest that chronic inflammation, titanium particle exposure, corrosion byproducts, and sustained tissue damage in peri-implant tissues may contribute to oncogenesis. While a direct causal link between PI and PIOM remains unproven, chronic peri-implant inflammation may contribute to malignancy development in predisposed individuals. Clinicians should consider a biopsy when peri-implant lesions exhibit atypical features, promptly.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Growth differentiation factor 15 (GDF-15), a cytokine within the transforming growth factor-β superfamily, is involved in various malignancies, withimplications in oral squamous cell carcinoma (OSCC). Elevated GDF-15 levels are correlated with unfavorable prognosis, tumor progression, and chemotherapy resistance, and the protein has been identified as a potential diagnostic and prognostic biomarker for OSCC. Personalized treatment strategies based on GDF-15 expression could improve treatment outcomes.

Background/Aims: Direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus. This study investigated whether metabolic dysfunction influences the likelihood of fibrosis regression after DAA treatment in patients with chronic hepatitis C (CHC). Methods: This multicenter, retrospective study included 8,819 patients diagnosed with CHC who were treated with DAAs and achieved a sustained virological response (SVR) between January 2014 and December 2022. Fibrosis regression was defined as a 20% reduction in noninvasive surrogates for liver fibrosis, such as liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) and the fibrosis-4 (FIB-4) score. Hypercholesterolemia (h-TC) was defined as >200 mg/dL. Results: The median age of the study population was 59.6 years, with a predominance of male patients (n=4,713, 57.3%). Genotypes 1, 2, and others were confirmed in 3,872 (46.2%), 3,487 (41.6%), and 1,024 (12.2%) patients, respectively. Diabetes mellitus (DM) was present in 1,442 (17.2%) patients and the median LS was 7.50 kPa (interquartile range, 5.30–12.50). Multivariate analysis revealed that the presence of DM and pre-DAA h-TC were independently associated with a decreased probability of fibrosis regression by VCTE. Additionally, pre-DAA h-TC was independently associated with a decreased probability of fibrosis regression by the FIB-4. Conclusions Metabolic dysfunction has an unfavorable influence on fibrosis regression in patients with CHC who achieve SVR after DAA treatment.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Background/Aims: Direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus. This study investigated whether metabolic dysfunction influences the likelihood of fibrosis regression after DAA treatment in patients with chronic hepatitis C (CHC). Methods: This multicenter, retrospective study included 8,819 patients diagnosed with CHC who were treated with DAAs and achieved a sustained virological response (SVR) between January 2014 and December 2022. Fibrosis regression was defined as a 20% reduction in noninvasive surrogates for liver fibrosis, such as liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) and the fibrosis-4 (FIB-4) score. Hypercholesterolemia (h-TC) was defined as >200 mg/dL. Results: The median age of the study population was 59.6 years, with a predominance of male patients (n=4,713, 57.3%). Genotypes 1, 2, and others were confirmed in 3,872 (46.2%), 3,487 (41.6%), and 1,024 (12.2%) patients, respectively. Diabetes mellitus (DM) was present in 1,442 (17.2%) patients and the median LS was 7.50 kPa (interquartile range, 5.30–12.50). Multivariate analysis revealed that the presence of DM and pre-DAA h-TC were independently associated with a decreased probability of fibrosis regression by VCTE. Additionally, pre-DAA h-TC was independently associated with a decreased probability of fibrosis regression by the FIB-4. Conclusions Metabolic dysfunction has an unfavorable influence on fibrosis regression in patients with CHC who achieve SVR after DAA treatment.

Growth differentiation factor 15 (GDF-15), a cytokine within the transforming growth factor-β superfamily, is involved in various malignancies, withimplications in oral squamous cell carcinoma (OSCC). Elevated GDF-15 levels are correlated with unfavorable prognosis, tumor progression, and chemotherapy resistance, and the protein has been identified as a potential diagnostic and prognostic biomarker for OSCC. Personalized treatment strategies based on GDF-15 expression could improve treatment outcomes.

Growth differentiation factor 15 (GDF-15), a cytokine within the transforming growth factor-β superfamily, is involved in various malignancies, withimplications in oral squamous cell carcinoma (OSCC). Elevated GDF-15 levels are correlated with unfavorable prognosis, tumor progression, and chemotherapy resistance, and the protein has been identified as a potential diagnostic and prognostic biomarker for OSCC. Personalized treatment strategies based on GDF-15 expression could improve treatment outcomes.

Background/Aims: Direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus. This study investigated whether metabolic dysfunction influences the likelihood of fibrosis regression after DAA treatment in patients with chronic hepatitis C (CHC). Methods: This multicenter, retrospective study included 8,819 patients diagnosed with CHC who were treated with DAAs and achieved a sustained virological response (SVR) between January 2014 and December 2022. Fibrosis regression was defined as a 20% reduction in noninvasive surrogates for liver fibrosis, such as liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) and the fibrosis-4 (FIB-4) score. Hypercholesterolemia (h-TC) was defined as >200 mg/dL. Results: The median age of the study population was 59.6 years, with a predominance of male patients (n=4,713, 57.3%). Genotypes 1, 2, and others were confirmed in 3,872 (46.2%), 3,487 (41.6%), and 1,024 (12.2%) patients, respectively. Diabetes mellitus (DM) was present in 1,442 (17.2%) patients and the median LS was 7.50 kPa (interquartile range, 5.30–12.50). Multivariate analysis revealed that the presence of DM and pre-DAA h-TC were independently associated with a decreased probability of fibrosis regression by VCTE. Additionally, pre-DAA h-TC was independently associated with a decreased probability of fibrosis regression by the FIB-4. Conclusions Metabolic dysfunction has an unfavorable influence on fibrosis regression in patients with CHC who achieve SVR after DAA treatment.

A 68-year-old man with no significant medical history was referred for evaluation of incidentally detected hepatic and splenic lesions found during imaging for rib fractures. Cross-sectional imaging with computed tomography, magnetic resonance imaging, and fluorodeoxyglucose F18 positron-emitting tomography revealed multiple variable-sized masses in the liver and spleen. Contrast-enhanced ultrasound (CEUS) using Sonazoid showed mild arterial enhancement, early washout, and a corresponding perfusion defect in the delayed (Kupffer) phase. Ultrasound- guided liver biopsy confirmed Burkitt lymphoma. The patient received systemic chemotherapy, resulting in marked regression of hepatic and splenic lesions on follow-up imaging. This case highlights the diagnostic value of CEUS in characterizing atypical hepatic lesions and its potential to raise early suspicion for lymphoma, facilitating timely biopsy and management.