Ok fair enough, I'll buy the Hough Ear Institute story for now...
Also, may I ask, what does curing inflammation do?
Tinnitus is ridiculously complex and multi factorial. I feel like you and everyone on the forum knows this and it is almost akin to a stoner saying "woaaahhh, the universe is deep, man" but anyway bear with me because this is going to be kinda long...
It seems to me that T = x + y + z.
x is structural damage or hearing impedance. Structural damage would be things like hair cell loss, synapse damage, etc and what I am calling "impedance" without permanent structural damage would be things like hydrops or TMJ.
y is inflammation
z is intrinsic factors like having a more "predictive brain" or neurotransmitter effects.
All of these contribute to tinnitus.
Complicating it further, everyone's equation is probably different (for instance, if your tinnitus was caused by benzos you would have an equation with a higher "z" value. For most people though, the most important of these factors is probably "x", so the equation might look like T = x + xy + y + z.
You get the idea.
Chronic cochlear inflammation has a long list of differentials including: viral or rickettsial / Lyme infection, TMJ, auto immune, toxic exposure (usually medications) etc but *acutely* anything that causes the death of hair cells or synapses does so through primarily through inflammation and oxidative damage. This is why many times, if you treat hearing loss very early, you can prevent some or all of the damage from becoming permanent. That's the theory behind steroids (which have such a variable penetrance into the cochlea that they don't work for everyone, unfortunately but for some it's very significant), the "Bomb Blast Pill", antioxidants given acutely etc.
There is also a subtype of inflammation which seems to be a big component of this also which is more of a "neuroinflammation" from a glutamate surge. This often especially happens with noise induced injury (and is the theory behind OTO-313 blocking the glutamate NMDA receptor acutely to prevent tinnitus).
My take is that most people will have a pretty big "y" component acutely but inflammation is self limiting unless you have a continued stimulus.
Since "y" is so variable, this is why some people have better responses to things like anti oxidants and an anti inflammatory diet ("y" was a bigger part of their tinnitus). There things help by lowering the mediators of inflammation in the whole body.
For others, structural damage probably can potential neuro inflammation on its own (one mechanism is that IHCs control the flow of glutamate across the synapse).
A bit of a tangent too but this is important. Just because you have noise induced hearing loss, do not assume you don't have cofactors that can make your tinnitus much worse. Some of you probably have TMJ making your tinnitus louder (for instance) and don't realize this because it started with a noise injury.
Tl;dr: Addressing inflammation addresses the "y" component of a really complex issue.