Plasticity allows for habituation, and possibly a lower (or higher) perception of the tinnitus, as it involves the nucleus accumbens and the auditory cortex, but it has nothing to do with the actual cause of tinnitus, in fact what is defined as plasticity is nothing more than a deregulation of multiple receptors (most likely dopamine related receptors) within the nucleus accumbens which processes repetitive sounds (which eventually leads to habituation), which is a natural process that occurs in most (but not all, for unknown reason) brains and takes at the very least 6 months of residual chronic exposure to a specific noise.
Actually, it's a bit more complicated than that. Plasticity, in abstract, it simply the ability for the brain to "reconfigure itself", ie neuronal topology. It happens all the time as we live through life. That's how learning happens.
The problem is that if you have hearing loss, the brain reorganizes itself "the wrong way". That's why it's called maladaptive plasticity. It thinks it's doing the right thing by allocating more "neuronal paths" to try and "crank up the volume" where you can't hear, but the outcome from that is worse than its cause, as you end up only amplifying noise rather than a useful signal. That is the genesis of Tinnitus in this particular case (there are other mechanisms for other root causes, such as otosclerosis).
Many studies have established that, and that is why many treatments try to reverse this (they try to trigger plasticity in the other direction). Sound therapies such as notch/windowed white noise/ACRN work under this assumption. Bi-modal stimulation too, but uses a somatic pathway to try to accomplish the reversal.