Oral mucosal diseases arise at a highly exposed barrier interface where microbial communities, mucosal immunity, and epithelial repair programs must remain dynamically balanced. Increasing evidence suggests that oral microbial dysbiosis is not merely a compositional shift, but a context-dependent functional state involving altered microbial localization, virulence programs, metabolic activity, and host sensing thresholds. In this Review, we examine oral candidiasis (OC), oral lichen planus (OLP), recurrent aphthous ulcer (RAU), oral leukoplakia (OLK), and oral squamous cell carcinoma (OSCC) as representative disease contexts along the continuum from oral homeostasis to barrier failure. We integrate microbial signals, immune remodeling, epithelial barrier states, and disease-stage transitions into an evidence-graded framework. We propose that dysbiosis may function as an initiating trigger, inflammatory amplifier, chronic maintenance factor, risk-associated ecological signal, or secondary colonization event, depending on disease context, stage, localization, and evidence certainty. OC currently has the strongest mechanistic and interventional support, whereas evidence in OLP, RAU, OLK, and OSCC remains more heterogeneous. This framework may guide future microbiota-informed risk stratification, prevention, adjunctive therapy, and supportive care.