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.

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: 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: 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: 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: 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.

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: 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.

In recent years, many advances have been made in surgical fields of oral and maxillofacial reconstruction, and the variety and complexity of available surgical approaches consider different functionalities of the jaw and the aesthetics of the face. There is no validated or scientifically proven basis for deciding which flap to use for reconstruction, so decisions are often made based on the direct and indirect experiential knowledge of the reconstructive surgeon. Considering the modified ladder, elevator, and pie reconstructive options, their risk and donor morbidity, and their long-term outcomes, the simplest option that will achieve the best long-term outcome in terms of form and function and with the lowest donor morbidity should be chosen for the patient’s health and social welfare. This manuscript summarizes current options for jaw and facial reconstruction and their limitations by offering updated guidelines for various defect conditions.