Background: Tuberculosis remains a persistent infectious disease whose control is complicated by latent infection, delayed treatment, incomplete recovery, reinfection, and continuing transmission from infectious individuals. Although treatment is central to tuberculosis management, it is frequently represented only as a transition parameter in mathematical models rather than as a separate epidemiological state. In this study, treatment was therefore incorporated explicitly as an independent compartment so that its influence on transmission, recovery, disease-induced mortality, and long-term disease persistence could be evaluated. Methods: A deterministic nonlinear compartmental model was formulated by dividing the total population into susceptible, exposed, actively infected, treated, and recovered classes. Reinfection of recovered individuals, progression from latent infection to active disease, movement of infectious individuals into treatment, treatment-associated recovery, natural mortality, and disease-induced mortality were included. Positivity and boundedness of the solutions were examined to establish biological validity. The basic reproduction number, R0, was derived through the next-generation matrix approach. Disease-free and endemic equilibria were determined, and their local and conditional global stability properties were investigated using Jacobian analysis, the Routh-Hurwitz criterion, center manifold theory, Lyapunov functions, and LaSalles invariance principle. Normalized sensitivity indices, Latin hypercube sampling, partial rank correlation coefficients, and numerical simulations were also applied. Results: The disease-free equilibrium was shown to be locally asymptotically stable when ,R01. Under the stated reduced-model assumptions, stability of the endemic equilibrium was established. Transmission-related parameters were identified as the strongest positive contributors to disease persistence. In contrast, treatment and recovery parameters were found to reduce the reproduction number and infectious burden. Numerical simulations indicated that stronger treatment implementation and reduced transmission opportunities produced substantial reductions in active tuberculosis cases. Conclusion: Treatment was shown to function as both a clinical pathway and an epidemiological control mechanism. The proposed framework may support the design of treatment-centered strategies for reducing tuberculosis prevalence and preventing long-term endemic persistence.