The tibialis posterior tendon (TPT) maintains the medial longitudinal arch and is the primary dynamic stabilizer of hindfoot control, ankle inversion, and load transmission. TPT pathology ranges from early inflammatory stages (tendinitis, tenosynovitis, tendinosis, rupture) to posterior tibial tendon dysfunction (PTTD) and adult-acquired flatfoot deformity. This review presents current knowledge regarding the etiology, clinical presentation, diagnosis, and management of tibialis posterior tendon pathologies. Primary pathologies are discussed with emphasis on etiologic factors and pathophysiologic mechanisms. TPT posterior tendon disorders have multiple causes including overuse, pes planus, accessory navicular, metabolic factors such as diabetes and hyperlipidemia, and age-related degeneration. Histopathologic studies show that chronic TPT pathology is primarily degenerative, characterized by collagen disorganization, mucoid degeneration, and neovascularization. Evidence shows TPT dysfunction rarely occurs alone; spring ligament attenuation, deltoid ligament insufficiency, and peritalar instability frequently accompany tendon degeneration. These findings led to Progressive collapsing foot deformity (PCFD). PCFD is classified based on pathophysiology and 3D biometric analysis, examining dynamic stabilizers, static ligamentous structures, peritalar subluxation, and clinico-anatomic relationships. PCFD diagnosis uses weightbearing computed tomography, magnetic resonance imaging, and axial radiographs to evaluate sinus tarsi impingement, subtalar joint subluxation, and subfibular impingement. Treatment includes conservative and surgical approaches, with selection based on disease stage, deformity flexibility, and progression risk factors. Early recognition and stage-specific treatment are essential to preventing progression of TPT disorders and achieving optimal outcomes. Contemporary surgical techniques incorporate joint-preserving approaches, TPT preservation, spring and deltoid ligament reconstruction, and selective lateral column lengthening.