Water-soluble vitamins are essential micronutrients that sustain systemic and oral health through their roles in energy metabolism, DNA synthesis, redox regulation, collagen formation, and neurological function. Unlike fat-soluble vitamins, they are not significantly stored in the body and therefore require consistent daily intake. Deficiency rapidly affects high-turnover tissues, particularly the oral mucosa, making the oral cavity an early indicator of systemic imbalance. This thesis examines the biochemical functions of the vitamin B-complex (B1, B2, B3, B5, B6, B7, B9, B12) and vitamin C, and analyzes the mechanisms linking deficiency states to specific oral manifestations. The work is based on a structured literature review of scientific publications (2000–2025) retrieved from PubMed, NCBI, and Google Scholar, supported by authoritative textbooks. Priority was given to human clinical studies evaluating vitamin status, deficiency, supplementation, and oral findings. Functional biomarkers such as methylmalonic acid, homocysteine, transketolase activity, pyridoxal-5′-phosphate, and plasma ascorbate were considered to integrate biochemical and clinical perspectives. The evidence demonstrates that water-soluble vitamin deficiencies frequently present with characteristic oral signs. Riboflavin and niacin deficiencies are associated with glossitis and angular cheilitis. Pyridoxine deficiency contributes to mucosal inflammation and increased infection susceptibility. Folate and cobalamin deficiencies impair DNA synthesis, resulting in megaloblastic anemia, atrophic glossitis, mucosal pallor, and delayed wound healing. Thiamine deficiency may be linked to neuropathic oral burning sensations. Vitamin C deficiency disrupts collagen cross-linking, leading to gingival bleeding, periodontal instability, and impaired tissue repair. Because dietary and absorptive factors overlap, multiple deficiencies often coexist, necessitating comprehensive diagnostic evaluation. Accurate diagnosis requires integration of clinical examination with targeted laboratory testing to detect both overt and subclinical deficiencies. Management involves correcting the underlying cause through dietary modification and appropriate supplementation, whether oral or parenteral, depending on severity. Early intervention enables reversal of hematologic, mucocutaneous, and neurological manifestations. Prevention strategies—including nutritional education, food fortification, and targeted screening of high-risk populations—remain critical for reducing morbidity. Recognition of oral manifestations in dental practice supports early detection, interdisciplinary collaboration, and improved patient outcomes. Incorporating micronutrient awareness into routine clinical care strengthens both oral and general health promotion.