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Dr. Foad Shahabian
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Dense Bone: A Sign of Old Bruxism?

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A discussion on full-arch implants.

∆ Where this started

A prosthodontist made the following point to a group of surgeons: when you are in surgery and you see that the bone is dense and voluminous and you think to yourself what excellent bone this is, also consider that this bone volume may come from the patient's old bruxism. That force is still there, and later on this patient's prosthesis becomes a problem.

The question is simple: can you tell from the bone that the patient was a bruxer?

∆ The short answer

No, you cannot.

But as a reminder the statement has value. Its real message is that good bone means an easy surgery, not an easy case. As a reminder it is good; as a diagnostic sign it is not.

∆ This statement contains three separate claims

We will look at all three separately, because a chain is only as strong as its weakest link.

∆ Claim one: tori come from bruxism

There is a real association here, but not the one that is usually quoted.

The only systematic review that addressed this question directly had just one positive finding: abnormal tooth wear is associated with tori, mainly torus mandibularis. For the association of tori with the other signs of bruxism, the evidence was insufficient to confirm or refute. Self-reported tooth grinding gave contradictory results, and the overall quality of the evidence was rated low.

The fourfold figure quoted in lectures comes from a Brazilian study: bruxer patients were roughly four times more likely to have a mandibular torus.

And the finding that is almost never quoted: in that same study, the presence of a wear facet raised the odds of a torus about twentyfold. In other words, wear was tied to tori far more strongly than the diagnosis of bruxism itself was. Keep this point in mind, because the discussion later converges on exactly this.

One important limitation: all of this literature is about specific localized lesions — torus palatinus, torus mandibularis and buccal exostoses. No source has said anything about a "voluminous ridge" in general.

∆ Claim two: the muscle still works after edentulism

No study has measured bruxism in an edentulous patient before and after treatment. This is a genuine gap.

What we do know is this: in patients treated with a fixed implant-supported prosthesis, the thickness of the masseter and the anterior temporalis increases and within roughly six months reaches that of dentate individuals. EMG studies likewise show muscle activity returning to the pattern of dentate individuals.

The clinical translation: muscle capacity comes back. If the bruxism habit is still present in the patient, the means of carrying it out has been restored. But those studies themselves did not say that the habit returns. That bridge is our own reasoning, not their finding.

∆ Claim three: bruxism damages implants

This is the most solid part, and it is not in dispute.

In a large retrospective study, implant failure was 13 percent in bruxers versus 4.6 percent in the rest. Meta-analyses put the risk of failure at roughly two to four times higher.

But the nature of the problem matters more than the risk figure itself. What is seen more often in bruxers is mechanical complications: porcelain chipping and fracture, framework fracture, screw loosening and screw fracture.

By contrast, the evidence on marginal bone loss is considerably weaker. The meta-analysis could not examine it at all, because the studies had not separated the data between bruxers and non-bruxers. In other words, the sentence "bruxism causes bone loss around implants" does not have the same backing as the sentence about failure.

This distinction matters for follow-up. In a high-force patient, what you should expect and plan for is mechanical rather than biological in nature.

∆ Wear: the sign that connects both ends of the story

There is a point here worth raising separately, and it has nothing to do with that instructor's remark about bone volume.

Tooth wear is the very sign on which the implant literature bases its identification of the high-risk patient. According to the international consensus, a diagnosis of probable bruxism means self-report plus clinical examination, and tooth wear is one of those clinical signs. In practice, nearly every study that has shown a higher implant risk in bruxers defined being a bruxer through a combination of patient self-report and observed wear.

So when we say "bruxers carry a higher risk," we are in practice talking about patients one of whose identifying signs was precisely this wear. From this angle, the claim that seeing wear should worry you does have backing.

But that same consensus adds an important caveat that is usually overlooked: wear may be a sign of bruxism, but it does not rule out past bruxism without current activity. In other words, wear too is a record, just a more precise and more accessible one.

And the evidence confirms this caveat. In a case-control study with sleep EMG recording, individuals with attrition-type wear did not show greater muscle activity during sleep than matched controls. The authors' conclusion was that the clinician cannot take the presence of wear as a direct sign of active bruxism.

Wear also has a multifactorial etiology, with erosion, abrasion and diet all contributing. For this reason implant reviews likewise emphasize that attrition on its own is not a diagnosis of bruxism.

The summary of this section: wear is the best clinical sign available to you and is considerably more valuable than bone shape. But wear has exactly the same timing problem described next. See the wear and take it seriously, but combine it with evidence of current activity rather than making it the sole basis of a decision.

∆ So where is the problem with that statement?

The direction of the inference has been reversed. The studies say: bruxers more often have tori. The statement wants to say: people with tori are bruxers.

These two are not the same. A simple example makes it clear. The numbers below are hypothetical and come from no paper.

Imagine a thousand patients:

Why are there so many tori in the non-bruxer group as well? Because tori are common in the general population too, and genetics and ethnicity play a prominent role in them.

Now the patient with a torus is in your chair. He is one of 260 people with tori, of whom only one hundred are bruxers. That means his probability of being a bruxer is about 38 percent, whereas without seeing the torus it was 20 percent.

Seeing a torus doubles your suspicion, but it is still more likely than not that the patient is not a bruxer. For prompting you to ask more questions it is excellent. For making a treatment decision it is not enough.

∆ The second objection, and perhaps the most important: the question of time

A torus is a cumulative record of years of loading. You are judging the patient's muscular status today from an old imprint. As we saw in the previous section, this objection applies to wear as well.

And this is not merely a theoretical point. In many people bruxism decreases with advancing age. The systematic review of the epidemiology of bruxism in adults states explicitly that the prevalence of bruxism decreases with age and is lower in the elderly, while there is no difference between men and women. This finding has been repeated in later reviews as well. The available data, however, are largely based on questionnaires and self-report.

This point is vital for the full-arch case. The edentulous patient who is a candidate for a full arch is usually an older patient. The torus you see in his mouth may be the product of the third and fourth decades of his life, while that same parafunctional pattern today may be considerably reduced or absent altogether. Bone preserves the imprint of the past. The muscle does not necessarily preserve the same behavior.

So even if we fully accept the association of tori with bruxism, there is still a real distance between "this patient was once a bruxer" and "this patient is high-force now," and what matters for your prosthesis is the latter.

∆ Two further objections

A voluminous ridge is not the same as a torus. Ridge volume in an edentulous patient depends more on how many years have passed since the teeth were extracted, why they were extracted, and what the patient's own pattern of bone resorption has been.

The other side of the coin is more dangerous. If we say dense bone means bruxer, we have inadvertently said thin bone means non-bruxer. The high-force patient with poor bone is exactly the one who needs the greatest caution, and this rule makes us walk right past him.

∆ So what do we do chairside?

The logic is simple: place every sign in one of two columns.

Column one, records of the past. These say the patient was once high-force:

Column two, evidence of current activity. This is what matters for your prosthesis:

Base the treatment decision on column two, not column one. Column one should only prompt you to ask the questions in column two.

And if column two is positive, that is when parafunction should change the number and dimensions of the implants, the prosthesis design and the material selection — not simply when you hand the patient a night guard.

∆ Summary

The third link of the chain is solid: bruxism really does raise implant risk, mainly in the form of mechanical complications. The second link has no direct study. The first link has limited backing, and only for tori and exostoses, and its path of association runs through tooth wear rather than through bruxism.

And between these links there is a time gap that usually goes unnoticed: bone and wear both preserve the imprint of the past, but bruxism itself decreases with advancing age. That is, even when the sign is correct, it may be speaking about a disease that no longer exists.

The complete chain — using bone shape as a predictor of risk in a full-arch candidate — has no dedicated study in the literature. It is a logical inference, not a scientific finding.

If the audience for that sentence is a surgeon who forgets the case on the day the prosthesis is delivered, it is a useful statement and it does its job. If it is quoted as a diagnostic sign and someone makes a decision on the basis of it, it has gone beyond what the evidence permits.

∆ References

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