October 13, 2025 • 17 mins
A detailed academic overview of the multifaceted concept of dental occlusion and its relationship to the broader masticatory system. The text extensively covers the biological and neurological framework of functional occlusion, examining peripheral sensory mechanisms like periodontal mechanoreceptors and central nervous system components such as neuroplasticity in the sensorimotor cortex, particularly as they relate to adaptation and pain. Significant attention is given to the temporomandibular joint (TMJ), discussing its complex anatomy, movement patterns, and common disorders like disk displacement and osteoarthritis, while challenging the historical assumption of a strong link between occlusal variables and TMJ disorders. Furthermore, the sources discuss clinical management techniques, including the use of articulators, occlusal adjustments, and prosthodontic rehabilitation for both natural teeth and dental implants, emphasizing that mechanical factors and load management are critical for implant success due to the lack of a protective periodontal ligament.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Welcome back to the deep dive. Today, we're tackling a
really crucial text, functional occlusion in restorative dentistry and prostadontics.
It genuinely reshapes how you think about the whole system.
Speaker 2 (00:12):
Yeah. Absolutely. Our aim here is to walk you through
this step by step. And you know, right from the
start the author's stress that how we understand occlusion, Well,
it's changed fundamentally.
Speaker 1 (00:24):
How so what's driven that change?
Speaker 2 (00:27):
Well, things like Asio integration, cadcam technology, and honestly some
really profound insights into neuroplasticity. It means we have to
look beyond just the mechanics of the bite.
Speaker 1 (00:37):
Right, So it's not just about how teeth fit together anymore.
It's more biological adaptive exactly.
Speaker 2 (00:42):
It's a complex adaptive biological system. So our mission today
is to connect those dots for you, you know, from the
brain signals for chewing right down to the clinical steps
that make or break a restoration stability.
Speaker 1 (00:53):
Okay, makes sense. So where do we start peeling back
those layers.
Speaker 2 (00:57):
We really need to start with the basics, the biological
blue print, and that means looking at the brain stem first.
Speaker 1 (01:02):
The brain stem Okay, so things like chewing and swallowing.
They're not just simple reflexes.
Speaker 2 (01:09):
Not at all. They're run by these neural circuits in
the brainstem. You might have heard them called central pattern
generators or CPGs. They set up the basic rhythm.
Speaker 3 (01:18):
The program, like the autopilot for chewing kinda yeah, but
then that basic pattern gets fine tuned by higher brain centers,
particularly the facial sensori motor cortex.
Speaker 1 (01:30):
And that fine tuning relies on feedback, right, sensory information totally.
Speaker 2 (01:34):
It's all about the sensory input, mostly coming through the
trigeminal nerve. And here's a really neat anatomical point the
book highlights.
Speaker 1 (01:41):
Oh yeah, what's up The cell.
Speaker 2 (01:43):
Bodies for the muscle spindles, the sensors that detect muscle stretch,
and the jaw closing muscles, they're actually inside the brainstem,
in the trigeminal miss andcephalic nucleus.
Speaker 1 (01:52):
Huh, that is different. Usually they're outside the central nervous
system right exactly.
Speaker 2 (01:56):
For most other muscles they're in the dorsal root ganglia.
So it's a unique set up for the jaw.
Speaker 1 (02:01):
Okay, fascinating detail. Now you mentioned critical sensory data. What
are the real heavy hitters. When it comes to functional light.
Speaker 2 (02:09):
Ah, that would be the periodontal mechana receptors pmrs. The
text really hammers home how vital these are. They're incredibly
sensitive low threshold receptors.
Speaker 1 (02:20):
Low threshold meaning they pick up really subtle forces precisely.
Speaker 2 (02:24):
They code all the details about the force on a tooth,
where it is, how strong it is, how it changes
over time, whether it's tooth on food or tooth on
tooth contact. Think of them like high definition.
Speaker 1 (02:34):
Sensors providing super precise, real time info to the brain.
Speaker 2 (02:37):
You got it, And that feedback is absolutely crucial for
controlling the jaw muscles precisely. It lets you adjust your
bite force perfectly, for say how hard the food is.
Speaker 1 (02:46):
Okay, that high definition sensing. It leads straight to a
big clinical point, doesn't it Implants versus natural teeth.
Speaker 2 (02:52):
Yes, this is where you see the biology really matter.
People with natural teeth have this amazing force control because
of the pmrs. But when you have plant supported prost theses,
well you lose that specific input.
Speaker 1 (03:04):
So implants don't have pmrs. Do patients feel anything, Oh,
they do feel pressure.
Speaker 2 (03:09):
We call it ossio perception. It probably comes from receptors
in the TMJ, the muscles, maybe the perios DM around
the implant. But it's just not the same. It's like
going from HD two standard definition.
Speaker 1 (03:21):
And the clinical result of that lower resolution.
Speaker 2 (03:23):
Their ability to control static bite force just holding a
clench is way less precise. The book mentions the detection
threshold for that static force can be like ten times
higher for implant patients. Wow, tenfold Okay, Yeah, And that
loss of fine spatial awareness is really why we have
different occlusal rules for implants. We have to protect them mechanically,
because the sensory protection is reduced.
Speaker 1 (03:44):
Right, that makes sense. Okay, Let's shift from the input
signals to how the brain actually processes this. The system adapts, right,
neuroplasticity exactly.
Speaker 2 (03:54):
The nervous system isn't static, it's constantly adapting. And we've
got solid evidence for this, like from fMRI studies.
Speaker 1 (04:00):
What do those studies show.
Speaker 2 (04:01):
Well, if you suddenly change someone's bite, say you increase
their occlusal vertical dimension with an overlay or maybe new dangers,
you see immediate changes in brain activity.
Speaker 1 (04:10):
Right, the brain notices something's different. Where does this activity
show up?
Speaker 2 (04:14):
You see it lighting up in the pre central and
post central gyrus, specifically the areas that mapp to the
lips and mouth on that sensory homunculus map we all
learned about.
Speaker 1 (04:23):
So brain immediately starts recalibrating its map for the new setup.
Speaker 2 (04:28):
Pretty much. Yeah, it kicks off this process of reorganizing
to deal with a new oral environment. It's quite remarkable.
Speaker 1 (04:34):
It sounds like a very robust system. But the text
brings up something called the pain paradox. How does pain
mess with this adaptation?
Speaker 2 (04:44):
Yeah, that's a key point. A cue pain inside the
mouth actually puts the brakes on this sensorymotor neuroplasticity.
Speaker 1 (04:51):
Really, it hinders adaptation significantly.
Speaker 2 (04:53):
If a patient is in pain, their ability to learn
how to function with that altered bite or adapt to
it is really. Pain basically shuts down the brain's willingness
to rewire itself for that new situation.
Speaker 1 (05:05):
That has huge clinical implications, and it kind of leads
into this other challenging condition mentioned a clusal dicesthesia. Can
you break that down?
Speaker 2 (05:13):
Sure? Aclusal diceysthesia is tricky. It's classed is a medically
unexplained symptom or mus Basically a patient complains persistently, like
for over six months, that their bite feels wrong or uncomfortable,
but objectively, there's nothing physically wrong with the occlusion.
Speaker 1 (05:31):
So the feeling doesn't match the physical reality what's going
on there?
Speaker 2 (05:34):
It often involves this destructive cycle. It starts with what
the book calls acclusal hypervigilance. The patient becomes obsessed with
their bite, constantly checking it, focusing all their attention on
how their teeth meet.
Speaker 1 (05:46):
And this intense focus it gets worse if we try
to fix the bite they complain about.
Speaker 2 (05:51):
That's the trap. This hypervigilance, often tied up with psychological distress,
gets amplified every time a well meaning clinician tries to
adjust the collusion based on the patient's sensation.
Speaker 1 (06:02):
Ah So each adjustment reinforces their belief that there is
a physical problem, even if the real issue is central
in how they're processing the sensation or focusing on it precisely.
Speaker 2 (06:12):
It reinforces their conviction that the bite is wrong, making
the underlying issue, which is often more behavioral or psychological,
harder to address. The problem isn't the teeth, it's the
perception and the focus.
Speaker 1 (06:25):
Okay, that's a fundamental shift in thinking. Let's move on
to the actual hardware, the muscles that drive.
Speaker 2 (06:29):
The system, right, the jaw muscles. You've got your main
closers massiter temporalis and medial terygoid and main openers. Yeah,
the gastric and the lateral tariogoid.
Speaker 1 (06:39):
And they have different types of motor units like other muscles.
Speaker 2 (06:41):
Yep, the usual suspects type s slow, fatigue resistant, FR,
fast fatigue resistant, and FF fast fittigable. And they're recruited
in that order. Slow units first for a fine control
and endurance.
Speaker 1 (06:54):
Does bite force vary a lot between people.
Speaker 2 (06:57):
Definitely generally stronger in men, tends to peak young adulthood.
And there's even a correlation with facial shape. People with
stronger muscles often have that more square jawed look.
Speaker 1 (07:07):
Interesting. Okay, Shifting gears to the joint itself. The temperamandibular joint,
the TMJ is pretty unique, right, very unique.
Speaker 2 (07:14):
It's a bilateral joint, meaning you have two working together,
and it combines rotation the condyle rotating against the disc
with translation where the whole condyle disc unit slides forward.
Speaker 1 (07:25):
In the fossa and the joint surfaces themselves are different too.
Speaker 2 (07:28):
Yeah, another key detail. They're covered in fibrocartilage, not the
highline cartilage you find in most other major joints like
the knee or hip. This fibro cartilage gives it different properties,
better suited for the complex loading it handles.
Speaker 1 (07:41):
Now, the text spends some time correcting a common misunderstanding
about one specific muscle, the lateral terygoid.
Speaker 2 (07:48):
Yes, this is important. The old view, the one many
of us learned, was that the superior head attached only
to the articular disc and that the two heads worked
in a simple push pull manner.
Speaker 1 (07:59):
And that's wrong.
Speaker 2 (08:00):
The evidence now shows it's more complex. The inferior head
attaches to the condilar neck, sure, but the superior head
attaches mainly to the coddler neck too, with only some
fibers blending into the discapsule area.
Speaker 1 (08:12):
Okay, so mostly bone assertion for both heads. What about
their function?
Speaker 2 (08:16):
Critically, the idea that they work in simple opposition is
also out. The cns can actually activate parts of both
heads independently depending on the task, so it's much more
nuanced control than we previously thought.
Speaker 1 (08:28):
Good clarification. Thinking clinically about the TMJ, the type of
force applied seems really important, especially when we consider things
like clenching.
Speaker 2 (08:36):
Absolutely, static loading like holding a clench during parafunction, whether
awake or asleep, is much rougher on the joint cartilage
than dynamic loading like chewing.
Speaker 1 (08:46):
Why is static loading worse?
Speaker 2 (08:48):
It seems to squeeze out the proteoglycans, the molecules that
help cartilage resist compression. It can even lead to cell
death and push the tissue towards breaking down rather than
building up. This might increase the risk for osteoarthritis over time.
Speaker 1 (09:02):
Okay, that makes sense. This leads us neatly into probably
the biggest debate in this whole field, the supposed link
between occlusion and pathology, specifically tmd's what's the current scientific
consensus here?
Speaker 2 (09:14):
Look, the evidence when you really pile it up, is
pretty clear. Now there is no strong causal link between
typical variations and how teeth fit together, things like a
slide between centric relation and the main biting position or
specific contact points, and whether someone develops a temporal mandibular disorder.
Speaker 1 (09:32):
That's huge because the idea that a bad bite causes
TMD was clinical dogma for decades. Why did that mechanical
view stick around so long, do you think?
Speaker 2 (09:41):
Well? Probably because mechanical issues are visible, they're measurable, and
fixing them feels like a direct solution. It's a simpler story.
But the book emphasizes that any statistical links found are
generally weak, no causal, not causal, and they might be
explained by other things like trauma history or stress levels.
That's why modern TMD diagnoses this relies on standardized methods
(10:01):
like the DCTMD criteria.
Speaker 1 (10:03):
Right, the diagnostic criteria for TMD that looks at both
physical stuff and psychological.
Speaker 2 (10:07):
Factors exactly axis or covers the physical diagnosis joint issues,
muscle issues, but axis second is crucial. It assesses psychological status,
pain behavior, things like that you need both for a
complete picture.
Speaker 1 (10:19):
And this lack of a causal link it extends to
bruxism too. Right, clenching and grinding aren't caused by bite problems.
Speaker 2 (10:28):
Correct. The evidence strongly indicates that parafunctions, especially sleep bruxism,
are not triggered by local dental factors like an all
clusal interference.
Speaker 1 (10:37):
So what does cause it?
Speaker 2 (10:39):
Sleep bruxism is now understood to be centrally mediated, originating
in the CNS, it's actually classified as a sleep related
movement disorder of parasomnia. Polysomography sleep studies clearly show this.
Speaker 1 (10:51):
So grinding down teeth to eliminate an interference isn't the
way to treat bruxism itself.
Speaker 2 (10:56):
Definitely not to treat the bruxism activity. You might manage
the effects of bruxism on the teeth, but you're not
stopping the behavior by adjusting the bite.
Speaker 1 (11:03):
Got it. Okay, one more link to cover occlusion and
periodontal health. We talk about aclusal trauma, primary and secondary.
What's the key factor there?
Speaker 2 (11:12):
The absolute key is inflammation. The text stresses this excessive
force on a tooth causing mobility that is not on
its own cause loss of periodontal attachment. If the gums
are healthy, no marginal inflammation.
Speaker 1 (11:23):
But if there is inflammation, then.
Speaker 2 (11:25):
Mobility becomes a major problem. It acts like an accelerator,
significantly speeding up attachment loss. So managing that inflammation that
gingovitis or period on titis is always the top priority.
Speaker 1 (11:37):
Right, Control the inflammation first. Okay, let's pivot to applying
all this biology in the clinic therapeutic inclusion. When we're
doing restorative work, we're often making sudden changes we.
Speaker 2 (11:46):
Are, and that challenges the system's ability to adapt instantly.
So when we design restorations, especially larger ones, we need
clear goals.
Speaker 1 (11:54):
What are those main goals?
Speaker 2 (11:56):
First, achieve stable contacts between the arches and the main
biting position icp ideally at least one contact pro opposing tooth. Second,
make sure these contacts happen simultaneously on both sides.
Speaker 1 (12:08):
Okay, stability and synchronicity, anything else, yes, And.
Speaker 2 (12:11):
This is critical. Ensure there are no contacts on the
back teeth when the patient slides their jaw forward. Protrusive
movements should be guided only by the front teeth. That's
anterior guidance.
Speaker 1 (12:22):
It protects the posterior teeth and then that guidance. Does
it matter if it's canine guidance versus say, group function,
where multiple teeth guide is one better?
Speaker 2 (12:30):
You know, scientifically, there's no solid evidence proving canine guidance
is inherently superior for overall health or longevity compared to
group function.
Speaker 1 (12:39):
Really, so why choose one over the other.
Speaker 2 (12:41):
Often it comes down to what the patient already has,
or frankly, what's easier to achieve restoratively. Canine guidance can
be simpler to set up in some cases, but biologically
the jury's out on superiority.
Speaker 1 (12:54):
Interesting, okay. Circling that to implants, we know they lack pmrs.
They don't move much, so specific aclusal rules.
Speaker 2 (13:00):
To protect them, yes, because that difference in movement is huge. Remember,
implants move maybe three to five micrometers elastically, natural teeth
twenty five to one hundred micrometers and its viscoelastic shock absorbing.
Speaker 1 (13:13):
That's a massive difference.
Speaker 2 (13:14):
It is, so the rules are about minimizing damaging forces.
We recommend using shallower cusp angles on implant crowns, making
the chewing services narrower the occlusal platform. Why narrower reduces
the leverage and the amount of force directed onto the implant.
It's all about managing the load carefully.
Speaker 1 (13:31):
And what about cantilevers like extensions off the back implant
in a bridge.
Speaker 2 (13:35):
Keep them short. The standard recommendation is to limit distal
canilevers the part extending backward past the last implant to
no more than one replacement tooth width. Again, it's all
about controlling leverage and stress on the implant and.
Speaker 1 (13:49):
Bone purely mechanical protection because the biological sensors are missing.
Makes sense. Okay. Finally, let's touch on clinical assessment. How
do we actually check these contacts precisely? And what are
provocation tests useful for?
Speaker 2 (14:03):
For contracts, you need good marking tools. The book recommends
using really thin articulating paper or foil, maybe even using
different colors to map out contacts in different positions, like
blue for ICP, red for excursions. That kind of thing.
Speaker 1 (14:17):
Okay, meticulous marking and provocation tests.
Speaker 2 (14:20):
These are incredibly useful diagnostic tools. They help you reproduce
the patient's specific pain or symptoms.
Speaker 1 (14:25):
Can you give examples?
Speaker 2 (14:26):
Sure? The TM joined provocation test have the patient bite
down hard on something firm like a cotton roll on
one side at the back. You're checking if this causes
pain in the opposite joint, which suggests compression or maybe
tension on the same side.
Speaker 1 (14:39):
Okay, testing the joint underload.
Speaker 2 (14:41):
What about for muscles, that's the jaw muscle provocation test.
You have the patient clench hard in their usual biting
position or maybe even directly onto where facets if they
have them for about thirty seconds, and the goal is
to see if you can reproduce the muscle pain they
complain about. If clenching brings on their specific it's powerful
evidence linking their symptoms to a clenching habit, and importantly,
(15:05):
it's a great way to show the patient the connection
to educate them about potentially unconscious habits.
Speaker 1 (15:11):
Very practical, and just a quick word on articulators, those
devices we melt models on.
Speaker 2 (15:16):
Yeah, the book list the types hinge, every value semi adjustable,
fully adjustable. For most day to day restorative and prosedontic work,
a semi adjustable articulator is generally sufficient.
Speaker 1 (15:27):
Do we always need a faceboe record to use one?
Speaker 2 (15:30):
Traditionally yes for fixed work, But interestingly, the text mentioned
systematic reviews showing faceboes aren't strictly necessary for making well
fitting complete dentures or even occlusal splints. Practice varies, but
the evidence suggests they might be optional in some cases.
Speaker 1 (15:45):
Good to know. Okay, So wrapping this all up, what's
the big picture? The core message from this deep dive.
Speaker 2 (15:52):
The real takeaway is that our understanding of occlusion has
shifted profoundly. It's not just mechanics anymore. It's deeply intertwined
with biology. Neuroplasticity, adaptation, and even the patient's psychological state,
especially things like hypervigilance.
Speaker 1 (16:08):
So restoring someone's bite is more than just getting the
teeth to fit much more.
Speaker 2 (16:13):
It's really an application of neuroplasticity. Success or failure often
depends less on tiny mechanical details and more on how
the patient's entire system neural and psychological adapts or fails
to adapt.
Speaker 1 (16:24):
And the text even suggests maintaining occlusion contributes to general health.
Speaker 2 (16:28):
Yeah, there's growing thought around its role and overall well being,
maybe even cognition. So successful treatment really demands a broader view,
recognizing those psychosocial factors alongside the mechanics.
Speaker 1 (16:38):
It's a much more integrated perspective, Okay. To help everyone
consolidate this, here's a review question based on today's material, considering.
Speaker 2 (16:45):
The biological differences in sensory input and how teeth versus
implants move, why do patients with full arch implant pros
theses have much poorer control over their static bite force
compared to someone with natural teeth, and what structures are
thought to provide that residual feeling? The ossio perception that
implant patents still have
Welcome back to the deep dive. Today, we're tackling a
really crucial text, functional occlusion in restorative dentistry and prostadontics.
It genuinely reshapes how you think about the whole system.
Speaker 2 (00:12):
Yeah. Absolutely. Our aim here is to walk you through
this step by step. And you know, right from the
start the author's stress that how we understand occlusion, Well,
it's changed fundamentally.
Speaker 1 (00:24):
How so what's driven that change?
Speaker 2 (00:27):
Well, things like Asio integration, cadcam technology, and honestly some
really profound insights into neuroplasticity. It means we have to
look beyond just the mechanics of the bite.
Speaker 1 (00:37):
Right, So it's not just about how teeth fit together anymore.
It's more biological adaptive exactly.
Speaker 2 (00:42):
It's a complex adaptive biological system. So our mission today
is to connect those dots for you, you know, from the
brain signals for chewing right down to the clinical steps
that make or break a restoration stability.
Speaker 1 (00:53):
Okay, makes sense. So where do we start peeling back
those layers.
Speaker 2 (00:57):
We really need to start with the basics, the biological
blue print, and that means looking at the brain stem first.
Speaker 1 (01:02):
The brain stem Okay, so things like chewing and swallowing.
They're not just simple reflexes.
Speaker 2 (01:09):
Not at all. They're run by these neural circuits in
the brainstem. You might have heard them called central pattern
generators or CPGs. They set up the basic rhythm.
Speaker 3 (01:18):
The program, like the autopilot for chewing kinda yeah, but
then that basic pattern gets fine tuned by higher brain centers,
particularly the facial sensori motor cortex.
Speaker 1 (01:30):
And that fine tuning relies on feedback, right, sensory information totally.
Speaker 2 (01:34):
It's all about the sensory input, mostly coming through the
trigeminal nerve. And here's a really neat anatomical point the
book highlights.
Speaker 1 (01:41):
Oh yeah, what's up The cell.
Speaker 2 (01:43):
Bodies for the muscle spindles, the sensors that detect muscle stretch,
and the jaw closing muscles, they're actually inside the brainstem,
in the trigeminal miss andcephalic nucleus.
Speaker 1 (01:52):
Huh, that is different. Usually they're outside the central nervous
system right exactly.
Speaker 2 (01:56):
For most other muscles they're in the dorsal root ganglia.
So it's a unique set up for the jaw.
Speaker 1 (02:01):
Okay, fascinating detail. Now you mentioned critical sensory data. What
are the real heavy hitters. When it comes to functional light.
Speaker 2 (02:09):
Ah, that would be the periodontal mechana receptors pmrs. The
text really hammers home how vital these are. They're incredibly
sensitive low threshold receptors.
Speaker 1 (02:20):
Low threshold meaning they pick up really subtle forces precisely.
Speaker 2 (02:24):
They code all the details about the force on a tooth,
where it is, how strong it is, how it changes
over time, whether it's tooth on food or tooth on
tooth contact. Think of them like high definition.
Speaker 1 (02:34):
Sensors providing super precise, real time info to the brain.
Speaker 2 (02:37):
You got it, And that feedback is absolutely crucial for
controlling the jaw muscles precisely. It lets you adjust your
bite force perfectly, for say how hard the food is.
Speaker 1 (02:46):
Okay, that high definition sensing. It leads straight to a
big clinical point, doesn't it Implants versus natural teeth.
Speaker 2 (02:52):
Yes, this is where you see the biology really matter.
People with natural teeth have this amazing force control because
of the pmrs. But when you have plant supported prost theses,
well you lose that specific input.
Speaker 1 (03:04):
So implants don't have pmrs. Do patients feel anything, Oh,
they do feel pressure.
Speaker 2 (03:09):
We call it ossio perception. It probably comes from receptors
in the TMJ, the muscles, maybe the perios DM around
the implant. But it's just not the same. It's like
going from HD two standard definition.
Speaker 1 (03:21):
And the clinical result of that lower resolution.
Speaker 2 (03:23):
Their ability to control static bite force just holding a
clench is way less precise. The book mentions the detection
threshold for that static force can be like ten times
higher for implant patients. Wow, tenfold Okay, Yeah, And that
loss of fine spatial awareness is really why we have
different occlusal rules for implants. We have to protect them mechanically,
because the sensory protection is reduced.
Speaker 1 (03:44):
Right, that makes sense. Okay, Let's shift from the input
signals to how the brain actually processes this. The system adapts, right,
neuroplasticity exactly.
Speaker 2 (03:54):
The nervous system isn't static, it's constantly adapting. And we've
got solid evidence for this, like from fMRI studies.
Speaker 1 (04:00):
What do those studies show.
Speaker 2 (04:01):
Well, if you suddenly change someone's bite, say you increase
their occlusal vertical dimension with an overlay or maybe new dangers,
you see immediate changes in brain activity.
Speaker 1 (04:10):
Right, the brain notices something's different. Where does this activity
show up?
Speaker 2 (04:14):
You see it lighting up in the pre central and
post central gyrus, specifically the areas that mapp to the
lips and mouth on that sensory homunculus map we all
learned about.
Speaker 1 (04:23):
So brain immediately starts recalibrating its map for the new setup.
Speaker 2 (04:28):
Pretty much. Yeah, it kicks off this process of reorganizing
to deal with a new oral environment. It's quite remarkable.
Speaker 1 (04:34):
It sounds like a very robust system. But the text
brings up something called the pain paradox. How does pain
mess with this adaptation?
Speaker 2 (04:44):
Yeah, that's a key point. A cue pain inside the
mouth actually puts the brakes on this sensorymotor neuroplasticity.
Speaker 1 (04:51):
Really, it hinders adaptation significantly.
Speaker 2 (04:53):
If a patient is in pain, their ability to learn
how to function with that altered bite or adapt to
it is really. Pain basically shuts down the brain's willingness
to rewire itself for that new situation.
Speaker 1 (05:05):
That has huge clinical implications, and it kind of leads
into this other challenging condition mentioned a clusal dicesthesia. Can
you break that down?
Speaker 2 (05:13):
Sure? Aclusal diceysthesia is tricky. It's classed is a medically
unexplained symptom or mus Basically a patient complains persistently, like
for over six months, that their bite feels wrong or uncomfortable,
but objectively, there's nothing physically wrong with the occlusion.
Speaker 1 (05:31):
So the feeling doesn't match the physical reality what's going
on there?
Speaker 2 (05:34):
It often involves this destructive cycle. It starts with what
the book calls acclusal hypervigilance. The patient becomes obsessed with
their bite, constantly checking it, focusing all their attention on
how their teeth meet.
Speaker 1 (05:46):
And this intense focus it gets worse if we try
to fix the bite they complain about.
Speaker 2 (05:51):
That's the trap. This hypervigilance, often tied up with psychological distress,
gets amplified every time a well meaning clinician tries to
adjust the collusion based on the patient's sensation.
Speaker 1 (06:02):
Ah So each adjustment reinforces their belief that there is
a physical problem, even if the real issue is central
in how they're processing the sensation or focusing on it precisely.
Speaker 2 (06:12):
It reinforces their conviction that the bite is wrong, making
the underlying issue, which is often more behavioral or psychological,
harder to address. The problem isn't the teeth, it's the
perception and the focus.
Speaker 1 (06:25):
Okay, that's a fundamental shift in thinking. Let's move on
to the actual hardware, the muscles that drive.
Speaker 2 (06:29):
The system, right, the jaw muscles. You've got your main
closers massiter temporalis and medial terygoid and main openers. Yeah,
the gastric and the lateral tariogoid.
Speaker 1 (06:39):
And they have different types of motor units like other muscles.
Speaker 2 (06:41):
Yep, the usual suspects type s slow, fatigue resistant, FR,
fast fatigue resistant, and FF fast fittigable. And they're recruited
in that order. Slow units first for a fine control
and endurance.
Speaker 1 (06:54):
Does bite force vary a lot between people.
Speaker 2 (06:57):
Definitely generally stronger in men, tends to peak young adulthood.
And there's even a correlation with facial shape. People with
stronger muscles often have that more square jawed look.
Speaker 1 (07:07):
Interesting. Okay, Shifting gears to the joint itself. The temperamandibular joint,
the TMJ is pretty unique, right, very unique.
Speaker 2 (07:14):
It's a bilateral joint, meaning you have two working together,
and it combines rotation the condyle rotating against the disc
with translation where the whole condyle disc unit slides forward.
Speaker 1 (07:25):
In the fossa and the joint surfaces themselves are different too.
Speaker 2 (07:28):
Yeah, another key detail. They're covered in fibrocartilage, not the
highline cartilage you find in most other major joints like
the knee or hip. This fibro cartilage gives it different properties,
better suited for the complex loading it handles.
Speaker 1 (07:41):
Now, the text spends some time correcting a common misunderstanding
about one specific muscle, the lateral terygoid.
Speaker 2 (07:48):
Yes, this is important. The old view, the one many
of us learned, was that the superior head attached only
to the articular disc and that the two heads worked
in a simple push pull manner.
Speaker 1 (07:59):
And that's wrong.
Speaker 2 (08:00):
The evidence now shows it's more complex. The inferior head
attaches to the condilar neck, sure, but the superior head
attaches mainly to the coddler neck too, with only some
fibers blending into the discapsule area.
Speaker 1 (08:12):
Okay, so mostly bone assertion for both heads. What about
their function?
Speaker 2 (08:16):
Critically, the idea that they work in simple opposition is
also out. The cns can actually activate parts of both
heads independently depending on the task, so it's much more
nuanced control than we previously thought.
Speaker 1 (08:28):
Good clarification. Thinking clinically about the TMJ, the type of
force applied seems really important, especially when we consider things
like clenching.
Speaker 2 (08:36):
Absolutely, static loading like holding a clench during parafunction, whether
awake or asleep, is much rougher on the joint cartilage
than dynamic loading like chewing.
Speaker 1 (08:46):
Why is static loading worse?
Speaker 2 (08:48):
It seems to squeeze out the proteoglycans, the molecules that
help cartilage resist compression. It can even lead to cell
death and push the tissue towards breaking down rather than
building up. This might increase the risk for osteoarthritis over time.
Speaker 1 (09:02):
Okay, that makes sense. This leads us neatly into probably
the biggest debate in this whole field, the supposed link
between occlusion and pathology, specifically tmd's what's the current scientific
consensus here?
Speaker 2 (09:14):
Look, the evidence when you really pile it up, is
pretty clear. Now there is no strong causal link between
typical variations and how teeth fit together, things like a
slide between centric relation and the main biting position or
specific contact points, and whether someone develops a temporal mandibular disorder.
Speaker 1 (09:32):
That's huge because the idea that a bad bite causes
TMD was clinical dogma for decades. Why did that mechanical
view stick around so long, do you think?
Speaker 2 (09:41):
Well? Probably because mechanical issues are visible, they're measurable, and
fixing them feels like a direct solution. It's a simpler story.
But the book emphasizes that any statistical links found are
generally weak, no causal, not causal, and they might be
explained by other things like trauma history or stress levels.
That's why modern TMD diagnoses this relies on standardized methods
(10:01):
like the DCTMD criteria.
Speaker 1 (10:03):
Right, the diagnostic criteria for TMD that looks at both
physical stuff and psychological.
Speaker 2 (10:07):
Factors exactly axis or covers the physical diagnosis joint issues,
muscle issues, but axis second is crucial. It assesses psychological status,
pain behavior, things like that you need both for a
complete picture.
Speaker 1 (10:19):
And this lack of a causal link it extends to
bruxism too. Right, clenching and grinding aren't caused by bite problems.
Speaker 2 (10:28):
Correct. The evidence strongly indicates that parafunctions, especially sleep bruxism,
are not triggered by local dental factors like an all
clusal interference.
Speaker 1 (10:37):
So what does cause it?
Speaker 2 (10:39):
Sleep bruxism is now understood to be centrally mediated, originating
in the CNS, it's actually classified as a sleep related
movement disorder of parasomnia. Polysomography sleep studies clearly show this.
Speaker 1 (10:51):
So grinding down teeth to eliminate an interference isn't the
way to treat bruxism itself.
Speaker 2 (10:56):
Definitely not to treat the bruxism activity. You might manage
the effects of bruxism on the teeth, but you're not
stopping the behavior by adjusting the bite.
Speaker 1 (11:03):
Got it. Okay, one more link to cover occlusion and
periodontal health. We talk about aclusal trauma, primary and secondary.
What's the key factor there?
Speaker 2 (11:12):
The absolute key is inflammation. The text stresses this excessive
force on a tooth causing mobility that is not on
its own cause loss of periodontal attachment. If the gums
are healthy, no marginal inflammation.
Speaker 1 (11:23):
But if there is inflammation, then.
Speaker 2 (11:25):
Mobility becomes a major problem. It acts like an accelerator,
significantly speeding up attachment loss. So managing that inflammation that
gingovitis or period on titis is always the top priority.
Speaker 1 (11:37):
Right, Control the inflammation first. Okay, let's pivot to applying
all this biology in the clinic therapeutic inclusion. When we're
doing restorative work, we're often making sudden changes we.
Speaker 2 (11:46):
Are, and that challenges the system's ability to adapt instantly.
So when we design restorations, especially larger ones, we need
clear goals.
Speaker 1 (11:54):
What are those main goals?
Speaker 2 (11:56):
First, achieve stable contacts between the arches and the main
biting position icp ideally at least one contact pro opposing tooth. Second,
make sure these contacts happen simultaneously on both sides.
Speaker 1 (12:08):
Okay, stability and synchronicity, anything else, yes, And.
Speaker 2 (12:11):
This is critical. Ensure there are no contacts on the
back teeth when the patient slides their jaw forward. Protrusive
movements should be guided only by the front teeth. That's
anterior guidance.
Speaker 1 (12:22):
It protects the posterior teeth and then that guidance. Does
it matter if it's canine guidance versus say, group function,
where multiple teeth guide is one better?
Speaker 2 (12:30):
You know, scientifically, there's no solid evidence proving canine guidance
is inherently superior for overall health or longevity compared to
group function.
Speaker 1 (12:39):
Really, so why choose one over the other.
Speaker 2 (12:41):
Often it comes down to what the patient already has,
or frankly, what's easier to achieve restoratively. Canine guidance can
be simpler to set up in some cases, but biologically
the jury's out on superiority.
Speaker 1 (12:54):
Interesting, okay. Circling that to implants, we know they lack pmrs.
They don't move much, so specific aclusal rules.
Speaker 2 (13:00):
To protect them, yes, because that difference in movement is huge. Remember,
implants move maybe three to five micrometers elastically, natural teeth
twenty five to one hundred micrometers and its viscoelastic shock absorbing.
Speaker 1 (13:13):
That's a massive difference.
Speaker 2 (13:14):
It is, so the rules are about minimizing damaging forces.
We recommend using shallower cusp angles on implant crowns, making
the chewing services narrower the occlusal platform. Why narrower reduces
the leverage and the amount of force directed onto the implant.
It's all about managing the load carefully.
Speaker 1 (13:31):
And what about cantilevers like extensions off the back implant
in a bridge.
Speaker 2 (13:35):
Keep them short. The standard recommendation is to limit distal
canilevers the part extending backward past the last implant to
no more than one replacement tooth width. Again, it's all
about controlling leverage and stress on the implant and.
Speaker 1 (13:49):
Bone purely mechanical protection because the biological sensors are missing.
Makes sense. Okay. Finally, let's touch on clinical assessment. How
do we actually check these contacts precisely? And what are
provocation tests useful for?
Speaker 2 (14:03):
For contracts, you need good marking tools. The book recommends
using really thin articulating paper or foil, maybe even using
different colors to map out contacts in different positions, like
blue for ICP, red for excursions. That kind of thing.
Speaker 1 (14:17):
Okay, meticulous marking and provocation tests.
Speaker 2 (14:20):
These are incredibly useful diagnostic tools. They help you reproduce
the patient's specific pain or symptoms.
Speaker 1 (14:25):
Can you give examples?
Speaker 2 (14:26):
Sure? The TM joined provocation test have the patient bite
down hard on something firm like a cotton roll on
one side at the back. You're checking if this causes
pain in the opposite joint, which suggests compression or maybe
tension on the same side.
Speaker 1 (14:39):
Okay, testing the joint underload.
Speaker 2 (14:41):
What about for muscles, that's the jaw muscle provocation test.
You have the patient clench hard in their usual biting
position or maybe even directly onto where facets if they
have them for about thirty seconds, and the goal is
to see if you can reproduce the muscle pain they
complain about. If clenching brings on their specific it's powerful
evidence linking their symptoms to a clenching habit, and importantly,
(15:05):
it's a great way to show the patient the connection
to educate them about potentially unconscious habits.
Speaker 1 (15:11):
Very practical, and just a quick word on articulators, those
devices we melt models on.
Speaker 2 (15:16):
Yeah, the book list the types hinge, every value semi adjustable,
fully adjustable. For most day to day restorative and prosedontic work,
a semi adjustable articulator is generally sufficient.
Speaker 1 (15:27):
Do we always need a faceboe record to use one?
Speaker 2 (15:30):
Traditionally yes for fixed work, But interestingly, the text mentioned
systematic reviews showing faceboes aren't strictly necessary for making well
fitting complete dentures or even occlusal splints. Practice varies, but
the evidence suggests they might be optional in some cases.
Speaker 1 (15:45):
Good to know. Okay, So wrapping this all up, what's
the big picture? The core message from this deep dive.
Speaker 2 (15:52):
The real takeaway is that our understanding of occlusion has
shifted profoundly. It's not just mechanics anymore. It's deeply intertwined
with biology. Neuroplasticity, adaptation, and even the patient's psychological state,
especially things like hypervigilance.
Speaker 1 (16:08):
So restoring someone's bite is more than just getting the
teeth to fit much more.
Speaker 2 (16:13):
It's really an application of neuroplasticity. Success or failure often
depends less on tiny mechanical details and more on how
the patient's entire system neural and psychological adapts or fails
to adapt.
Speaker 1 (16:24):
And the text even suggests maintaining occlusion contributes to general health.
Speaker 2 (16:28):
Yeah, there's growing thought around its role and overall well being,
maybe even cognition. So successful treatment really demands a broader view,
recognizing those psychosocial factors alongside the mechanics.
Speaker 1 (16:38):
It's a much more integrated perspective, Okay. To help everyone
consolidate this, here's a review question based on today's material, considering.
Speaker 2 (16:45):
The biological differences in sensory input and how teeth versus
implants move, why do patients with full arch implant pros
theses have much poorer control over their static bite force
compared to someone with natural teeth, and what structures are
thought to provide that residual feeling? The ossio perception that
implant patents still have
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