Mitochondrial Dysfunction in Diabetic Neuropathy: An Evidence Map of Molecular Mechanisms, Translational Biomarkers, and Emerging Implications for Oral Neuropathy—A Scoping Review

Diabetic peripheral neuropathy (DPN) is a common and disabling complication of diabetes, but treatment still focuses largely on symptom control rather than modification of the underlying nerve injury. Mitochondrial dysfunction is increasingly implicated in the response of peripheral nerves to chronic hyperglycemia, although the literature is spread across different mitochondrial pathways, experimental models, biomarkers, and clinical settings. We therefore conducted a scoping review, following the Joanna Briggs Institute framework, to map this evidence and examine how far it has extended to oral and craniofacial neuropathic manifestations. PubMed, Scopus, and SpringerLink were searched using a predefined Population–Concept–Context strategy, and two reviewers independently screened records in Rayyan. Of 40,863 records identified, 853 studies met the eligibility criteria; 462 (54.2%) were published between 2021 and 2026. Most studies were preclinical. In the hierarchical evidence map, oxidative stress/redox imbalance was the largest evidence-mapping category (n = 591; 69.3%), followed by Schwann-cell degeneration (n = 147; 17.2%) and bioenergetic dysfunction (n = 77; 9.0%), whereas mitophagy (n = 14; 1.6%) and mitochondrial dynamics (n = 14; 1.6%) were much less frequently represented. Craniofacial neuropathy (n = 6; 0.7%) and oral neuropathy (n = 4; 0.5%) represented only a small proportion of the evidence map. Across these domains, recurrent pathways included Nrf2/Keap1 antioxidant defense, NF-κB-associated neuroinflammation, mitochondria-dependent apoptosis, and AMPK-SIRT-PGC-1α signaling. Clinical translation was limited, although mitochondrial DNA copy number, SOD3, and 8-hydroxy-2′-deoxyguanosine were reported as candidate biomarkers. Overall, the expanded evidence base confirms substantial growth in mitochondrial research in diabetic neuropathy but remains predominantly preclinical, with a particularly pronounced translational gap in oral and craniofacial neuropathy.