If what is true? Are you having doubts about hearing restoration in general or something in specific? You doubt that hearing restoration can reduce tinnitus?
how well would these new hair cells actual have to "work" to get a reduction in T.
A little? Less efficient hair cells giving less reduction, more efficient hair cells giving more reduction? No one really knows for sure. We don't even have an objective way to measure tinnitus. It's all based on your perception, and so is the standard hearing test.
Lets say they were only mildly effective in sensing sound (summing them together say a response level of 25dBA at X frequency) and relaying that to the brain.
This statement doesn't make a lot of sense. We are talking about hearing level. A hearing level of 25 dB on average is a subjective perception of sound that takes place in the brain. Decibels are not objects that need to be stored or relayed by the ears to the brain. If anything, it's something that your brain relays somatically (you press a button) or verbally (you say a word) to the audiologist administering the test. It's about using physics to measure hearing sensitivity. But ears and brains don't understand what Decibel is. They operate on the basis of chemistry.
This brings us to people who appear to have perfect hearing when you look at their audiograms. You would think that a person that has a hearing level of 10 dB on average across all frequencies has perfect hearing. Yet they complain about not hearing conversation well in noisy environment, and some of them even have tinnitus. That's because they likely have hidden hearing loss. The damage inside their ears cannot be measured with a standard hearing test. Synaptic loss is largely attributed to this condition. Once you have that kind of hearing loss, measuring Decibels won't help you to assess the damage. Likewise, once you have had a hearing restoration therapy, using an audiometer to measure the improvement in hearing is not ideal. Which points to the lack of diagnostic tools in this medical practice.
I should not have to tell you that people who have noise induced hearing loss also have tinnitus. When you look at their audiograms right after the damage has been done, they will display maybe mild to moderate drops in hearing level. When they take the same test a few months later, they may display an improvement in hearing level. But they may also develop tinnitus. You would think that these people don't need hearing aids or hearing restoration therapy because their hearing levels measured by an audiologist are within the "normal" 0 - 20 dB range. But if you can find a way to do it, look inside their cochleas and you will discover they have sensory and synaptic damage. How much of that post-damage boost in hearing level is to thank recovered hair cells for and how much is to blame on central gain increase in the brain, no one really knows.
Would the brain then stop sending signal back to the ear or would it simply send less signal back to the ear (aka milder T)?
Assuming that tinnitus is a side effect of or maladaptation to sensory cell loss or synaptic loss, then restoring these cells and synapses may reverse this process and either significantly lower the tinnitus or completely eliminate it. No one knows for sure until we have thoroughly tested this in people. Hopefully this will happen in not too far off future.
I don't think it's the signal from the brain to the cochlea that's causing tinnitus. I think it begins with the lack of input from the cochlea to the brain. It's a two way street. Sound input to the brain comes mainly from inner hair cells, but outer hair cells help in sound perception by amplifying the sound and they receive input from the brain to do so. That's my very simplistic version of how it works. The outer hair cells actually vibrate on their own without any external sound stimulation, and this is what's causing the so called otoacoustic emissions. I think it's safe to say that the discovery of these emissions is one of the biggest discoveries in otology in the last 100 years. The inner hair cells also receive some input from the brain, but I don't understand yet what the function of that is.
To get back to your question, you should not expect the brain to stop sending signals to the cochlea. That's just not normal function. You won't be able to hear! Remember what I said about outer hair cells and how they amplify sounds. You don't want to lose that function. But this signaling to amplify the sound may be reduced if the normal function of inner hair cells is restored.
Basically what you want to do is reduce signaling in both directions, to the brain and back to cochlea. The best way to do that is to have any damaged inner and outer hair cells repaired or missing ones regenerated. Likewise, you want to have those connective nerves restored.
No one really knows at what stage of hearing process tinnitus occurs. The hypothesis presented by Liberman is that it's the loss of afferent nerve fibre density of inner hair cells that stages tinnitus. But no one has been really able pinpoint exact location along the auditory pathway where tinnitus is generated. Given it's subjective nature, it's difficult to link it to physiology.
But it's hard to ignore the fact that tinnitus is evident in so many people with hearing damage, measurable or not (hidden hearing loss). With that in mind, perhaps the best way to go forward is by experimentally proving this in human subjects, by providing a first-ever therapeutic treatment for hearing restoration. That's what everyone is busy working on now, and what patients with tinnitus as well as people with hearing loss are waiting for. Hearing restoration research is so much in focus now that tinnitus research has taken the back seat, awaiting results from these hearing restoration attempts. Restoring hearing therapeutically should put some of these old and new tinnitus hypotheses to rest once and for all.