Subjective tinnitus is common yet poorly understood, and existing models do not fully explain its clinical diversity. This article presents a mechanistic hypothesis, based on existing literature, in which tinnitus may emerge not only from reduced auditory input due to inner ear injury but also from increased activity of the middle ear muscles, which may ultimately increase extracochlear, largely somatosensory, input to the cochlear nucleus. In this framework, auditory deafferentation is necessary but insufficient on its own. We further hypothesise that, in some clinical contexts, somatosensory drive may be amplified by excessive stimulation of putative middle ear mechanoreceptors (MeRs). This stimulation may originate from muscle vibration (tremor) within the tympanic cavity, associated with heightened activity of the stapedius, tensor tympani, and tensor veli palatini muscles. Clinical situations such as loud-noise exposure, temporomandibular disorders, cervical dysfunction, and ear canal irritation may be interpreted within this framework as diverse triggers converging on enhanced middle ear muscle activity and mechanosensory overstimulation. Although hypothetical, the model yields testable predictions. Functional neuroimaging could reveal abnormal activation of somatosensory cortical areas in tinnitus not directly related to acoustic trauma; middle ear muscle activity could be assessed in animal models using electromyography; and refined impedance-based measurements may help detect and characterise middle ear vibratory phenomena. Clinically, inter-individual variability in the stapedius reflex should modulate transient tinnitus and aural fullness after exposure to loud noise. By integrating auditory deafferentation, somatosensory modulation, and middle ear biomechanics, this hypothesis aims to guide future experimental work and therapeutic strategies.