October 13, 2025 • 22 mins
Covers the historical, theoretical, and clinical aspects of endodontic procedures, including diagnosis, treatment planning, instruments, and infection control. It provides detailed information on topics such as pulp anatomy, root canal preparation, filling techniques, and the management of complex cases in both permanent and primary teeth, including endodontic surgery and the treatment of traumatized teeth. The excerpts also address important clinical considerations like analgesia, systemic health influences, and the role of modern imaging techniques such as Cone Beam Computed Tomography (CBCT).
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Episode Transcript
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Speaker 1 (00:00):
Welcome to the deep dive. We're here to pull the
absolute core clinical insights from key texts and bring them
straight to you exactly today, we're doing a fast, focused
immersion into modern endodontics using a foundational clinical text as
our guide. So if you're a dental student heading for
the clinic, or maybe a clinician wanting a solid, evidence
(00:21):
based update, this is for you.
Speaker 2 (00:23):
And it's more than just the how to. Our source
really frames modern endoway within high patient expectations for wine
and also quality assurance, clinical governance. You know, but underneath
it all, the mission hasn't changed. Prevent or treat epical
period on titus. That's the core goal.
Speaker 1 (00:41):
Okay, great, so let's lay out the plan. We'll start
with some foundational stuff history, systemic risks, then get into
diagnostics and anatomy sense, and then we'll really dig into
the procedures instrumentation, disinfection, filling, and wrap up with some
of those trickier clinical situations.
Speaker 2 (00:56):
Sound good, perfect, let's dive in.
Speaker 1 (00:58):
So foundational principles. First, where did this all start?
Speaker 2 (01:01):
Well, to really get where we are, it helps to
see how far we've traveled historically. You had theories like
the Chinese and Egyptians blaming toothache on a literal worm
a worm, Wow, yeah, a white worm with a black head,
and clinically believe it or not. Arsenic a tissue destroyer
was actually taught in dental schools as a pulp treatment
(01:21):
right up into the nineteen fifties.
Speaker 1 (01:22):
Yikest So when did the science actually kick in?
Speaker 2 (01:27):
The big aha moment biologically speaking, came late nineteenth century Miller.
He's the one who definitively linked microorganisms to pople and
periopical disease.
Speaker 1 (01:39):
So it's fundamentally about the bugs.
Speaker 2 (01:41):
It really is. Once bacteria breached the dentine, that periopical
lusion you see on an X ray, that's actually the
host fighting back. It's controlled inflammation, controlled chaos, maybe trying
to stop infections spreading into the bone.
Speaker 1 (01:52):
And that involves a whole cascade of things.
Speaker 2 (01:54):
Well, absolutely, a whole soup of inflammatory cells, mediators like
prostaglandin cytokines. It gets a complex fast.
Speaker 1 (02:01):
Okay, So moving from the wide to the what do
we do diagnosis? What a patient walks in hurting? What's
job number one?
Speaker 2 (02:08):
The history? Full stop clinical tests important, Yes, but you
absolutely have to nail down that systematic pain history.
Speaker 1 (02:16):
First, what does that involve specifically?
Speaker 2 (02:18):
It's the classic points duration, how long, character, sharp, dull, throbbing, periodicity, constant, intermittent,
severity scale of one to ten, site, can they pinpoint it?
And radiation does it travel? Getting this right is honestly
your most powerful tool.
Speaker 1 (02:34):
And then we move to the actual tests on the
tooth pulp sensitivity tests. What's the key thing to remember there?
Speaker 2 (02:40):
The crucial distinction is a test neural response, not blood supply,
not vitality in the true vascular sense.
Speaker 1 (02:47):
So which test is most reliable?
Speaker 2 (02:49):
The cold test, it's generally your most accurate, and the
really useful bit is its specificity. If a tooth doesn't
respond to cold, there's an eighty nine percent chance the
pulp is necrotic.
Speaker 1 (02:58):
Okay, And what if it responds, but.
Speaker 2 (03:00):
Ah, that prolonged lingering pain after the cold is removed.
That's your classic sign pointing towards irreversible pulpitis.
Speaker 1 (03:07):
What about the electric pulp tester the EPT, it gives.
Speaker 2 (03:10):
You a relative measure, something to compare against adjacent teeth,
but the reading depends heavily on where you put the
probe and sizle edge versus midtooth, and know how thick
the enamel and denteen are.
Speaker 1 (03:21):
So if you had to rank them, cold test.
Speaker 2 (03:23):
Is generally considered more reliable than the EPT, which is
usually better than the heat test.
Speaker 1 (03:27):
Now, imaging, we've relied on two D X rays forever,
but they have drawbacks.
Speaker 2 (03:33):
Huge strawbacks. You're basically looking at a three D object
flattened into a two D shadower. Stuff gets superimposed, you
miss things.
Speaker 1 (03:40):
So the modern solution.
Speaker 2 (03:41):
CBCT cone being computed tomography. It gives you that undistorted,
accurate three dimensional picture. It's a game changer for diagnosis,
especially finding lesions missed on standard films or planning tricky surgeries.
Speaker 1 (03:56):
Okay, before we even think about touching the tooth, we
have to consider the patient's overall health systemic factors. Let's
start with anti coagulants like warfarind.
Speaker 2 (04:06):
Yeah, the big concern there is obviously bleeding. We monitor
it with the IONR, the international normalized ratio. Now, the
guidelines generally say extractions are okay if the INR is
four or less.
Speaker 1 (04:15):
But there's a catch.
Speaker 2 (04:16):
There is It's not just the number, it's the stability
if a patient's NR is normally, say one point five,
and they come in at three point five even though
it's under four point Oh, that's a significant jump for them.
You need to be cautious, maybe liaise with their doctor.
Speaker 1 (04:30):
What about low dose aspirin? Lots of patients take that.
Speaker 2 (04:33):
Generally, low dose aspirin isn't considered a major problem for
most routine ENDO or even extractions. The bleeding risk is
usually manageable.
Speaker 1 (04:41):
Okay, what about patients on long term steroids?
Speaker 2 (04:44):
That's a big red flag. We're worried about adrenocortical suppression. Basically,
their body might not be able to produce enough cortisol
to handle the stress of the procedure.
Speaker 1 (04:53):
So what's the protocol.
Speaker 2 (04:54):
If they're on more than say seven point five milligrams
of prenice alone daily for over a month, or took
high dose as recently, you need prophylaxis. That typically means
doubling their usual daily dose around the time of treatment,
or sometimes giving a single larger dose like mundred milligram
hydrocordison beforehand. You absolutely need that cover right.
Speaker 1 (05:13):
And one more systemic risk, a really serious one with
long term implications. Bisphosphonates.
Speaker 2 (05:18):
Yes, These drugs are strongly linked to austrienocrosis of the jaw,
especially after dental work like extractions or sometimes even endo.
The mandible, particularly the molar area, seems most vulnerable.
Speaker 1 (05:31):
So knowing if a patient is on these is critical.
Speaker 2 (05:33):
Absolutely critical. It has to be flagged prominently in their history.
It fundamentally changes the risk assessment for any invasive treatment.
Speaker 1 (05:40):
Okay, let's shift focus back to the tooth itself. The
pulp dentine complex it has defenses.
Speaker 2 (05:46):
Right, it does. It's quite remarkable. It can lay down
more dentine. First, there's tubular sclerosis where the tiny tubules
within the dentine kind of will harden or narrow. Then
there's tertiary dentine formation.
Speaker 1 (05:57):
And there are different types of that.
Speaker 2 (05:58):
Yeah, we differentiate based on how bad the insult. Is
a mild irritation the existing cells the odonta blasts lay
down reactionary dentine. But if the insult is severe enough
to kill those cells, new cells are recruited to form
reparative dentine. It's a patch job.
Speaker 1 (06:13):
Basically, what are the main things that irritate the pulp
enough to trigger this carry seems obvious.
Speaker 2 (06:19):
Carrie's is definitely a major one, along with bacterial micro
leakage around fillings, and leakage happens around all restorations pretty much, okay,
but perhaps surprisingly sometimes the operative preceders themselves can be
the most damaging immediate irritant. How so, think about deep
cavity preps, especially when you get really close to the pulp,
like less than zero point three millimeters of dentine left
(06:43):
or full crown preps. Just because you expose so many
dentinal tubules at once, that can trigger a significant inflammatory response.
Speaker 1 (06:51):
And you mentioned something else often overlooked.
Speaker 2 (06:53):
The anesthetic, the vasoconstrictor in it, usually adrenaline. It reduces
blood flow, which is great for keeping the area clear,
but it also reduces blood flow to.
Speaker 1 (07:02):
The pulp ah, potentially causing is schemia exactly.
Speaker 2 (07:06):
Combine that reduced blood flow with the heat from drilling
or the dehydration from air grawing, and you risk pushing
a stressed pulp over the edge into irreversible damage.
Speaker 1 (07:15):
Let's talk about cracked teeth. That's sharp pain on biting.
What's actually happening.
Speaker 2 (07:19):
It's twofold really. First, the crack opens up dentinal tubules
directly to the oral environment instant sensitivity. Second, when they bite,
the pieces flex slightly, creating a wedging.
Speaker 1 (07:31):
Effect, and that pumps fluid.
Speaker 2 (07:33):
Precisely, it pumps fluid within those exposed tubules, stimulating the
nerve endings in the pulp, which is often already inflamed.
That causes that characteristic sharp shooting pain. Treatment then depends
entirely on whether the pulp damage is reversible or not.
Speaker 1 (07:49):
Moving to anatomy inside the tooth. Does the pulp space
stay the same throughout life?
Speaker 2 (07:54):
No, definitely not. It changes quite a bit with age.
Generally the pulp chamber and canals get smaller, decrease in volume.
You see an increase in fibrous tissue and often mineral components,
leading to calcifications.
Speaker 1 (08:06):
Sometimes it looks completely blocked on an X ray.
Speaker 2 (08:08):
Right calcific metamorphosis or bliteration. But here's the thing, even
when it looks totally obliterated radiographically, there's almost always some
tiny pathway left for microbes. You still have to search
meticulously for those canals.
Speaker 1 (08:22):
And what about those side channels. Yeah, lateral and accessory.
Speaker 2 (08:24):
Canals hugely important. There are direct communication lines between the
pulp and the peridontal tissues, especially critical in molars down
in the furcation area, the space between the roots.
Speaker 1 (08:36):
How common are they there?
Speaker 2 (08:37):
Get this? Studies report up to a seventy six percent
incidence of accessory canals and the furcation floor of molars
seventy six percent.
Speaker 1 (08:45):
Wow, So if you only clean the main canals.
Speaker 2 (08:47):
You're potentially leaving a massive microbial reservoir communicating directly with
the supporting bone nearly three quarters of the time. That's
a major reason for treatment failure or persistent inflammation in
that key area.
Speaker 1 (09:00):
Okay, let's get practical core procedures. Isolation first, rubber dam,
is it really always necessary?
Speaker 2 (09:06):
Mandatory, non negotiable. Our source is emphatic and rightly so.
Two main reasons keeping the field clean and dry, free
from saliva and bacteria. That's critical for disinfection.
Speaker 1 (09:18):
And the second reason patient.
Speaker 2 (09:19):
Safety preventing aspiration or swallowing of tiny files or irrogance.
That's a massive medico legal risk you just don't take.
Speaker 1 (09:27):
What if the tooth is really broken down hard to
get a clampon?
Speaker 2 (09:30):
There are ways you might need to place an orthodonic
band first to rebuild the contour, or use techniques like
the split dam for isolated areas, but you must achieve
that seal.
Speaker 1 (09:39):
Okay, isolation sorted. Next finding the right length working lengths determination.
The old way was just X.
Speaker 2 (09:47):
Rays, right, Yeah, estimate with a pre op film, Place
a file, take another film. The rule of thumb was
the file tip should be within about one millimeter of
the radiographic apex.
Speaker 1 (09:56):
Where technology's moved on.
Speaker 2 (09:58):
Massively electronic ape x locators eels, especially the modern multi
frequency ones like the root ZX mentioned in the text.
They are often significantly more reliable than radiographs alone.
Speaker 1 (10:09):
How accurate are they?
Speaker 2 (10:10):
They work based on electrical impedance, and the newer ones
don't even need a completely dry canal. Studies consistently show
accuracy to within zero point five millimeters of the actual
apex in over ninety percent of cases. So you still
use X rays for the overall picture, but the EL
gives you the precision.
Speaker 1 (10:27):
Let's talk about shaping the canal's instrumentation. Yeah, there's been
a philosophical shift, hasn't there.
Speaker 2 (10:32):
Yes, definitely moving away from just mechanically shaping to fit
a filling material towards a more biological approach focused on disinfection.
Speaker 1 (10:42):
And the preferred technique.
Speaker 2 (10:43):
Now the dominant approach is crowned down. You shape the
coronal wider part of the canal first, then work your
way down towards the opex.
Speaker 1 (10:51):
Why is that better?
Speaker 2 (10:52):
Several reasons. Early coronal flaring gets rid of restrictive dentine
up high, reducing stress on the files deeper down. It
also means less de brie gets pushed towards the apex,
and crucially it allows your irrogance your disinfectants to penetrate
much deeper, much earlier in the process.
Speaker 1 (11:09):
Speaking of files, nickel titanium rotary systems are pretty standard.
Now what are their advantages?
Speaker 2 (11:14):
Speed is one, obviously, but the big one is their
super flexibility compared to traditional stainless steel, essential for navigating
curved canals without creating ledges or transporting the canal shape.
Speaker 1 (11:25):
But they have downsides.
Speaker 2 (11:26):
Oh yes, they have a distinct risk profile. Two main
failure modes portional failure where the tip binds but the
motor keeps turning, basically twisting it apart. And cyclic fatigue
that's from the file repeatedly bending and straightening as it
rotates around a curve. Eventually the metal just fatigues and snaps.
Understanding when and why they break is key to preventing it.
Speaker 1 (11:47):
Okay, shaping is done. Now the really critical part disinfection irrigation.
Speaker 2 (11:52):
What's the gold standard sodium hypochlorate NaOCl usually in a
one to five percent solution.
Speaker 1 (11:57):
Why is it so good?
Speaker 2 (11:58):
Because it does two absolutely essential things. One, it's a
potent antibacterial agent kills the bugs. Two, and this is critical,
it has tissue dissolving ability. It breaks down to chrotic
pulp tissue remnants that instruments can't reach.
Speaker 1 (12:12):
What about alternatives like chlorhexidine chx.
Speaker 2 (12:15):
Ctx is a good antibacterial, no doubt. It has substantivity,
meaning it sticks around. But the crucial difference it doesn't
dissolve tissue, so it can't replace NaOCl for that vital function.
They might be used together sometimes, but NaOCl is the workhorse.
Speaker 1 (12:29):
During instrumentation, we create that smear layer on the canal walls.
Do we need to get rid of it?
Speaker 2 (12:34):
Generally yes, The consensus, especially for infected teeth, is that
removing the smear layer is beneficial. It's a mix of
dentine debris, pulp remnants, and bacteria.
Speaker 1 (12:44):
Why remove it?
Speaker 2 (12:44):
Because it can block the dentinal tubules, preventing your earrogance
and sealers from penetrating. Fully removing it typically using seventeen
percent edta, which chilates the inorganic part, alternated with no
cl for the organic part allows for a better dis
infection and ceiling.
Speaker 1 (13:01):
And if you need multiple visits, what goes inside the
canal between appointments.
Speaker 2 (13:05):
Calcium hydroxide KOH two. That's still the standard inter appointment dressing.
It's very high PH's antibacterial, helping to continue the disinfection
process between visits. Plus it has a role in stimulating
hard tissue formation in certain cases like apexification.
Speaker 1 (13:21):
Okay, canals cleaned shaped, disinfected time to fill. The timing
itself is sometimes debated one visit or two.
Speaker 2 (13:29):
Yeah, that's a classic debate. Logically, though, it comes down
to the state of the pulp. If you started with
a vital, non infected pulp and you can do everything efficiently,
a single visit makes sense.
Speaker 1 (13:38):
What for infected cases.
Speaker 2 (13:40):
For teeth that presented with apical period on titus infection
already established, the thinking often leans towards caution, a multiple
visit approach using that calcium hydroxide dressing in between gives
you more certainty that you've maximally reduced the bacterial load
before sealing it all up. Biology should guide the timing.
Speaker 1 (13:59):
The andered filling material is still gut a perchure.
Speaker 2 (14:02):
Right, yes, it remains the core material of choice.
Speaker 1 (14:05):
We hear about cold techniques like lateral condensation versus warm techniques.
Lateral is simple and fast. Why use heat?
Speaker 2 (14:13):
That's a fair question. Lateral condensation is straightforward, especially if
you have a nice apical stop prepared. You basically pack
individual cones of guta percha laterally against the canal wall
with a spreader, but the result isn't a single solid mass,
it's multiple cones kind of held together by the seiler.
Warm tech weeks like warm vertical condensation or continuous wave
(14:34):
soften the guta purchase. You can flow better exactly. It
allows the guta percha to adapt much more intimately to
canal irregularities, fins and importantly, those lateral canals we talked about.
You tend to get a denser, more homogeneous fill, which
theoretically provides a better long term seal, and.
Speaker 1 (14:52):
You always need a sealer with the guta percha.
Speaker 2 (14:54):
Absolutely the seiler is what actually fills the microscopic gaps
between the guta percha and the canal and between the
cones themselves. In lateral condensation. Common types are zinc oxide,
ugenol based, calcium hydroxide based, or resin based.
Speaker 1 (15:10):
Is anything challenging god approachase dominance?
Speaker 2 (15:13):
Well, not as the main core material generally, but mineral
trioxide aggregate MTA is playing an increasingly vital role in
specific situations.
Speaker 1 (15:21):
What makes MTA special It's.
Speaker 2 (15:23):
Got fantastic biocompatibility, seals really well, and crucially, it actively
stimulates hard tissue formation that makes it incredibly useful for
things like perforation repairs, root end fillings, and surgery, and
as we'll see managing immature teeth. Its versatility is definitely
shifting how we handle complex cases.
Speaker 1 (15:41):
Okay, root canal's filled, but we're not done the final restoration.
How important is that paramount?
Speaker 2 (15:47):
Absolutely paramount. You can do the best root canal treatment
in the world, but if the final restoration fails, the
tooth is likely doomed.
Speaker 1 (15:55):
The numbers back that up strongly, right they do.
Speaker 2 (15:58):
Our sources highlight this clearly. Teeth restored with crowns after
endo have a significantly higher survival rate, something like eighty
one percent still functional after ten years compared to compared
to only about sixty three percent for teeth without crowns.
That's a huge difference. More often than not, its restorative
failure leakage fracture that leads to extraction, not the endo
(16:20):
treatment itself failing.
Speaker 1 (16:22):
If there isn't enough tooth left to hold a filling
or crown, we often need a post right to retain
the core build up correct.
Speaker 2 (16:28):
But the success of that post and core hinges entirely
on one critical concept, the ferrule effect. Define that for us,
the ferrule is a band of sound tooth structure at
the gingible margin that the crown encircles. Like the metal
bander and a barrel, you need at least one point
five to two point zero millimeters of vertical solid tooth
structure above the margin all the way around for the
(16:50):
crown to grip onto.
Speaker 1 (16:51):
Why is that ferule so crucial.
Speaker 2 (16:52):
Because it provides bracing It resists the leverage forces that
the post transmits during function. Without an adequate ferrel, the
post acts like a wedge, concentrating stress at the weakest
point and significantly increasing the risk of root fracture. No
feral often means no post or of very guarded prognosis.
Speaker 1 (17:12):
And how long should the post be?
Speaker 2 (17:14):
Ideally longer than the clinical crown height, extending well down
into the root, maybe into the apical third, but this
is critical. You must preserve enough apical root filling to
maintain the seal. At least four to five millimeters of
guttapercha needs to remain untouched at the apex.
Speaker 1 (17:30):
Okay, let's shift gears to some really challenging clinical scenarios,
starting with kids primary teeth.
Speaker 2 (17:37):
Yeah, endo in primary teeth is tricky. Diagnosis is tough
because kids often can't pinpoint pain well and sensitivity tests
are unreliable. The main treatment, when the pulp is involved
but still vital, is usually a popotomy removing the coronal pulp.
Speaker 1 (17:51):
Materials used for that have changed big time.
Speaker 2 (17:54):
Form A chrysal used to be the standard, but there
are significant concerns about its toxicity and potential carcinogenicity.
Speaker 1 (18:00):
Use.
Speaker 2 (18:00):
Now there's been a major shift towards alternatives like ferric sulfate,
mainly for its hemostatic properties and increasingly mta. Mta shows
really high success rates in pulpotomies by inducing a good
denteen bridge that hard tissue barrier.
Speaker 1 (18:14):
What about trauma to young permanent teeth where the root
isn't fully formed yet.
Speaker 2 (18:20):
Maintaining pulp vitality there is the absolute priority, because that's
what drives root maturation, getting longer and thicker walls. If
a young tooth fractures and exposes a.
Speaker 1 (18:30):
Vital pulp, what's the treatment?
Speaker 2 (18:31):
Partial propotomy is often the way to go. You remove
just the inflame surface layer of the pulp and place
a biocompatible material, often MTA again directly on a healthy tissue.
Young culp has amazing healing potential.
Speaker 1 (18:44):
What if the trauma kills the pulp in an immature tooth,
leaving that wide open apex.
Speaker 2 (18:49):
Then we need to induce a hard barrier at the end.
That's apexification. Traditionally this meant packing calcium hydroxide repeatedly over
many months, which was technique sensitive and left the tooth
weak for.
Speaker 1 (18:58):
A long time.
Speaker 2 (18:59):
And the modern approach MTA again. After disinfecting the canal,
you can often place an MTA plug directly at the
open apex. It sets relatively quickly, provides a good seal
and creates that apical barrier much more predictably and efficiently.
It's a huge improvement.
Speaker 1 (19:16):
Let's talk about endoperio lesions where root canal problems and
gum problems meet.
Speaker 2 (19:20):
Right. The communication between the pulp and the periodontium. Classification
is key here for prognosis. A primary endoleusion where the
infection drains out through the periodontal ligament generally has a
good prognosis if you treat the ENDO effectively.
Speaker 1 (19:35):
What about the other way around or both happening at once.
Speaker 2 (19:37):
A primary periollsion rarely affects the pulp unless it reaches
the apex, But a true combined lesion where an ENDO
infection meets an existing periodontal pocket that has a much
more guarded prognosis. Success really depends on how severe the
periodontal disease is and if both issues can be effectively treated.
Speaker 1 (19:55):
Are there anatomical factors that make these worse?
Speaker 2 (19:57):
Definitely? Developmental anomalies like palatal grooves on incisors or deep
grooves on root surfaces act like built in highways for bacteria,
making combined lesions much harder to treat and giving them
a poorer outlook.
Speaker 1 (20:10):
Okay, last scenario, and it's one every clinician dreads. The
emergency hot tooth, acute moltpitius or absess where the local
anesthetic just yeah, doesn't work.
Speaker 2 (20:21):
Ah, yes, the profound anesthesia failure. It's incredibly frustrating for
both the patient and the clinician.
Speaker 1 (20:27):
Why does it happen? Biologically?
Speaker 2 (20:29):
It's a combination of factors in that acutely inflamed tissue
chemical mediators released by the inflammation actually lower the firing
threshold of the nerves, make them hyper excitable. Plus the
increased blood flow the vascularity and DIMA tends to rapidly
buffer and wash away the anesthetic solution before can fully
take effect.
Speaker 1 (20:46):
So your standard block or infiltration fails. What are the options?
Speaker 2 (20:49):
Then you need supplementary techniques. The sources mention things like
intropople anesthesia directly injecting into the pulp chamber itself. It
works partly by pressure forcing the aniste into the nerve tissue.
Speaker 1 (21:01):
What if even that doesn't work.
Speaker 2 (21:02):
Sometimes profound anesthesia is just unattainable at that appointment. In
those cases, the best course might be to achieve drainage.
If they're swelling place a strong sedative dressing like lettermix
which contains a steroid and antibiotic, or even just zinc
oxide eugenol, seal it temporarily and bring the patient back
once things have calmed down Chemically, trying to push through
(21:23):
without adequate anesthesia is often counterproductive. Controlling the infection and
inflammation is key to controlling the pain. So looking back,
we've covered a huge amount, from ancient theories right up
to modern materials like MTA and the precision of ELS.
I think the big takeaway is that endodontics at its heart,
blends biological understanding with technical execution.
Speaker 1 (21:46):
Right. One doesn't work without the other.
Speaker 2 (21:47):
Exactly, you can have the fanciest gadgets, but if you
don't respect the biology, if you don't eliminate the microbes,
the icome won't be favorable long term. It's about diagnosis, disinfection,
and sealing. Biology dictates success, not speed or technique alone.
Speaker 1 (22:01):
That's a fantastic summary, And to help everyone consolidate some
of these critical points, here's a clinical challenge based on
what we've discussed. Exercise for the listener. Okay, picture this.
You have patient in your chair. They've got clear signs
of irreversible pulpitis in a lower molar, that hot tooth scenario.
They also tell you they take warfaring and their I
and R check today came back at three point five. So,
(22:23):
thinking about everything we've covered, what are two absolutely critical
things you need to address in your treatment of plan
concerning first their systemic medication and the associated risks, And second,
how you're going to achieve profound anesthesia for that really
inflamed tooth. Think about stability versus threshold for the I
and R and those supplementary injection techniques we mentioned
Welcome to the deep dive. We're here to pull the
absolute core clinical insights from key texts and bring them
straight to you exactly today, we're doing a fast, focused
immersion into modern endodontics using a foundational clinical text as
our guide. So if you're a dental student heading for
the clinic, or maybe a clinician wanting a solid, evidence
(00:21):
based update, this is for you.
Speaker 2 (00:23):
And it's more than just the how to. Our source
really frames modern endoway within high patient expectations for wine
and also quality assurance, clinical governance. You know, but underneath
it all, the mission hasn't changed. Prevent or treat epical
period on titus. That's the core goal.
Speaker 1 (00:41):
Okay, great, so let's lay out the plan. We'll start
with some foundational stuff history, systemic risks, then get into
diagnostics and anatomy sense, and then we'll really dig into
the procedures instrumentation, disinfection, filling, and wrap up with some
of those trickier clinical situations.
Speaker 2 (00:56):
Sound good, perfect, let's dive in.
Speaker 1 (00:58):
So foundational principles. First, where did this all start?
Speaker 2 (01:01):
Well, to really get where we are, it helps to
see how far we've traveled historically. You had theories like
the Chinese and Egyptians blaming toothache on a literal worm
a worm, Wow, yeah, a white worm with a black head,
and clinically believe it or not. Arsenic a tissue destroyer
was actually taught in dental schools as a pulp treatment
(01:21):
right up into the nineteen fifties.
Speaker 1 (01:22):
Yikest So when did the science actually kick in?
Speaker 2 (01:27):
The big aha moment biologically speaking, came late nineteenth century Miller.
He's the one who definitively linked microorganisms to pople and
periopical disease.
Speaker 1 (01:39):
So it's fundamentally about the bugs.
Speaker 2 (01:41):
It really is. Once bacteria breached the dentine, that periopical
lusion you see on an X ray, that's actually the
host fighting back. It's controlled inflammation, controlled chaos, maybe trying
to stop infections spreading into the bone.
Speaker 1 (01:52):
And that involves a whole cascade of things.
Speaker 2 (01:54):
Well, absolutely, a whole soup of inflammatory cells, mediators like
prostaglandin cytokines. It gets a complex fast.
Speaker 1 (02:01):
Okay, So moving from the wide to the what do
we do diagnosis? What a patient walks in hurting? What's
job number one?
Speaker 2 (02:08):
The history? Full stop clinical tests important, Yes, but you
absolutely have to nail down that systematic pain history.
Speaker 1 (02:16):
First, what does that involve specifically?
Speaker 2 (02:18):
It's the classic points duration, how long, character, sharp, dull, throbbing, periodicity, constant, intermittent,
severity scale of one to ten, site, can they pinpoint it?
And radiation does it travel? Getting this right is honestly
your most powerful tool.
Speaker 1 (02:34):
And then we move to the actual tests on the
tooth pulp sensitivity tests. What's the key thing to remember there?
Speaker 2 (02:40):
The crucial distinction is a test neural response, not blood supply,
not vitality in the true vascular sense.
Speaker 1 (02:47):
So which test is most reliable?
Speaker 2 (02:49):
The cold test, it's generally your most accurate, and the
really useful bit is its specificity. If a tooth doesn't
respond to cold, there's an eighty nine percent chance the
pulp is necrotic.
Speaker 1 (02:58):
Okay, And what if it responds, but.
Speaker 2 (03:00):
Ah, that prolonged lingering pain after the cold is removed.
That's your classic sign pointing towards irreversible pulpitis.
Speaker 1 (03:07):
What about the electric pulp tester the EPT, it gives.
Speaker 2 (03:10):
You a relative measure, something to compare against adjacent teeth,
but the reading depends heavily on where you put the
probe and sizle edge versus midtooth, and know how thick
the enamel and denteen are.
Speaker 1 (03:21):
So if you had to rank them, cold test.
Speaker 2 (03:23):
Is generally considered more reliable than the EPT, which is
usually better than the heat test.
Speaker 1 (03:27):
Now, imaging, we've relied on two D X rays forever,
but they have drawbacks.
Speaker 2 (03:33):
Huge strawbacks. You're basically looking at a three D object
flattened into a two D shadower. Stuff gets superimposed, you
miss things.
Speaker 1 (03:40):
So the modern solution.
Speaker 2 (03:41):
CBCT cone being computed tomography. It gives you that undistorted,
accurate three dimensional picture. It's a game changer for diagnosis,
especially finding lesions missed on standard films or planning tricky surgeries.
Speaker 1 (03:56):
Okay, before we even think about touching the tooth, we
have to consider the patient's overall health systemic factors. Let's
start with anti coagulants like warfarind.
Speaker 2 (04:06):
Yeah, the big concern there is obviously bleeding. We monitor
it with the IONR, the international normalized ratio. Now, the
guidelines generally say extractions are okay if the INR is
four or less.
Speaker 1 (04:15):
But there's a catch.
Speaker 2 (04:16):
There is It's not just the number, it's the stability
if a patient's NR is normally, say one point five,
and they come in at three point five even though
it's under four point Oh, that's a significant jump for them.
You need to be cautious, maybe liaise with their doctor.
Speaker 1 (04:30):
What about low dose aspirin? Lots of patients take that.
Speaker 2 (04:33):
Generally, low dose aspirin isn't considered a major problem for
most routine ENDO or even extractions. The bleeding risk is
usually manageable.
Speaker 1 (04:41):
Okay, what about patients on long term steroids?
Speaker 2 (04:44):
That's a big red flag. We're worried about adrenocortical suppression. Basically,
their body might not be able to produce enough cortisol
to handle the stress of the procedure.
Speaker 1 (04:53):
So what's the protocol.
Speaker 2 (04:54):
If they're on more than say seven point five milligrams
of prenice alone daily for over a month, or took
high dose as recently, you need prophylaxis. That typically means
doubling their usual daily dose around the time of treatment,
or sometimes giving a single larger dose like mundred milligram
hydrocordison beforehand. You absolutely need that cover right.
Speaker 1 (05:13):
And one more systemic risk, a really serious one with
long term implications. Bisphosphonates.
Speaker 2 (05:18):
Yes, These drugs are strongly linked to austrienocrosis of the jaw,
especially after dental work like extractions or sometimes even endo.
The mandible, particularly the molar area, seems most vulnerable.
Speaker 1 (05:31):
So knowing if a patient is on these is critical.
Speaker 2 (05:33):
Absolutely critical. It has to be flagged prominently in their history.
It fundamentally changes the risk assessment for any invasive treatment.
Speaker 1 (05:40):
Okay, let's shift focus back to the tooth itself. The
pulp dentine complex it has defenses.
Speaker 2 (05:46):
Right, it does. It's quite remarkable. It can lay down
more dentine. First, there's tubular sclerosis where the tiny tubules
within the dentine kind of will harden or narrow. Then
there's tertiary dentine formation.
Speaker 1 (05:57):
And there are different types of that.
Speaker 2 (05:58):
Yeah, we differentiate based on how bad the insult. Is
a mild irritation the existing cells the odonta blasts lay
down reactionary dentine. But if the insult is severe enough
to kill those cells, new cells are recruited to form
reparative dentine. It's a patch job.
Speaker 1 (06:13):
Basically, what are the main things that irritate the pulp
enough to trigger this carry seems obvious.
Speaker 2 (06:19):
Carrie's is definitely a major one, along with bacterial micro
leakage around fillings, and leakage happens around all restorations pretty much, okay,
but perhaps surprisingly sometimes the operative preceders themselves can be
the most damaging immediate irritant. How so, think about deep
cavity preps, especially when you get really close to the pulp,
like less than zero point three millimeters of dentine left
(06:43):
or full crown preps. Just because you expose so many
dentinal tubules at once, that can trigger a significant inflammatory response.
Speaker 1 (06:51):
And you mentioned something else often overlooked.
Speaker 2 (06:53):
The anesthetic, the vasoconstrictor in it, usually adrenaline. It reduces
blood flow, which is great for keeping the area clear,
but it also reduces blood flow to.
Speaker 1 (07:02):
The pulp ah, potentially causing is schemia exactly.
Speaker 2 (07:06):
Combine that reduced blood flow with the heat from drilling
or the dehydration from air grawing, and you risk pushing
a stressed pulp over the edge into irreversible damage.
Speaker 1 (07:15):
Let's talk about cracked teeth. That's sharp pain on biting.
What's actually happening.
Speaker 2 (07:19):
It's twofold really. First, the crack opens up dentinal tubules
directly to the oral environment instant sensitivity. Second, when they bite,
the pieces flex slightly, creating a wedging.
Speaker 1 (07:31):
Effect, and that pumps fluid.
Speaker 2 (07:33):
Precisely, it pumps fluid within those exposed tubules, stimulating the
nerve endings in the pulp, which is often already inflamed.
That causes that characteristic sharp shooting pain. Treatment then depends
entirely on whether the pulp damage is reversible or not.
Speaker 1 (07:49):
Moving to anatomy inside the tooth. Does the pulp space
stay the same throughout life?
Speaker 2 (07:54):
No, definitely not. It changes quite a bit with age.
Generally the pulp chamber and canals get smaller, decrease in volume.
You see an increase in fibrous tissue and often mineral components,
leading to calcifications.
Speaker 1 (08:06):
Sometimes it looks completely blocked on an X ray.
Speaker 2 (08:08):
Right calcific metamorphosis or bliteration. But here's the thing, even
when it looks totally obliterated radiographically, there's almost always some
tiny pathway left for microbes. You still have to search
meticulously for those canals.
Speaker 1 (08:22):
And what about those side channels. Yeah, lateral and accessory.
Speaker 2 (08:24):
Canals hugely important. There are direct communication lines between the
pulp and the peridontal tissues, especially critical in molars down
in the furcation area, the space between the roots.
Speaker 1 (08:36):
How common are they there?
Speaker 2 (08:37):
Get this? Studies report up to a seventy six percent
incidence of accessory canals and the furcation floor of molars
seventy six percent.
Speaker 1 (08:45):
Wow, So if you only clean the main canals.
Speaker 2 (08:47):
You're potentially leaving a massive microbial reservoir communicating directly with
the supporting bone nearly three quarters of the time. That's
a major reason for treatment failure or persistent inflammation in
that key area.
Speaker 1 (09:00):
Okay, let's get practical core procedures. Isolation first, rubber dam,
is it really always necessary?
Speaker 2 (09:06):
Mandatory, non negotiable. Our source is emphatic and rightly so.
Two main reasons keeping the field clean and dry, free
from saliva and bacteria. That's critical for disinfection.
Speaker 1 (09:18):
And the second reason patient.
Speaker 2 (09:19):
Safety preventing aspiration or swallowing of tiny files or irrogance.
That's a massive medico legal risk you just don't take.
Speaker 1 (09:27):
What if the tooth is really broken down hard to
get a clampon?
Speaker 2 (09:30):
There are ways you might need to place an orthodonic
band first to rebuild the contour, or use techniques like
the split dam for isolated areas, but you must achieve
that seal.
Speaker 1 (09:39):
Okay, isolation sorted. Next finding the right length working lengths determination.
The old way was just X.
Speaker 2 (09:47):
Rays, right, Yeah, estimate with a pre op film, Place
a file, take another film. The rule of thumb was
the file tip should be within about one millimeter of
the radiographic apex.
Speaker 1 (09:56):
Where technology's moved on.
Speaker 2 (09:58):
Massively electronic ape x locators eels, especially the modern multi
frequency ones like the root ZX mentioned in the text.
They are often significantly more reliable than radiographs alone.
Speaker 1 (10:09):
How accurate are they?
Speaker 2 (10:10):
They work based on electrical impedance, and the newer ones
don't even need a completely dry canal. Studies consistently show
accuracy to within zero point five millimeters of the actual
apex in over ninety percent of cases. So you still
use X rays for the overall picture, but the EL
gives you the precision.
Speaker 1 (10:27):
Let's talk about shaping the canal's instrumentation. Yeah, there's been
a philosophical shift, hasn't there.
Speaker 2 (10:32):
Yes, definitely moving away from just mechanically shaping to fit
a filling material towards a more biological approach focused on disinfection.
Speaker 1 (10:42):
And the preferred technique.
Speaker 2 (10:43):
Now the dominant approach is crowned down. You shape the
coronal wider part of the canal first, then work your
way down towards the opex.
Speaker 1 (10:51):
Why is that better?
Speaker 2 (10:52):
Several reasons. Early coronal flaring gets rid of restrictive dentine
up high, reducing stress on the files deeper down. It
also means less de brie gets pushed towards the apex,
and crucially it allows your irrogance your disinfectants to penetrate
much deeper, much earlier in the process.
Speaker 1 (11:09):
Speaking of files, nickel titanium rotary systems are pretty standard.
Now what are their advantages?
Speaker 2 (11:14):
Speed is one, obviously, but the big one is their
super flexibility compared to traditional stainless steel, essential for navigating
curved canals without creating ledges or transporting the canal shape.
Speaker 1 (11:25):
But they have downsides.
Speaker 2 (11:26):
Oh yes, they have a distinct risk profile. Two main
failure modes portional failure where the tip binds but the
motor keeps turning, basically twisting it apart. And cyclic fatigue
that's from the file repeatedly bending and straightening as it
rotates around a curve. Eventually the metal just fatigues and snaps.
Understanding when and why they break is key to preventing it.
Speaker 1 (11:47):
Okay, shaping is done. Now the really critical part disinfection irrigation.
Speaker 2 (11:52):
What's the gold standard sodium hypochlorate NaOCl usually in a
one to five percent solution.
Speaker 1 (11:57):
Why is it so good?
Speaker 2 (11:58):
Because it does two absolutely essential things. One, it's a
potent antibacterial agent kills the bugs. Two, and this is critical,
it has tissue dissolving ability. It breaks down to chrotic
pulp tissue remnants that instruments can't reach.
Speaker 1 (12:12):
What about alternatives like chlorhexidine chx.
Speaker 2 (12:15):
Ctx is a good antibacterial, no doubt. It has substantivity,
meaning it sticks around. But the crucial difference it doesn't
dissolve tissue, so it can't replace NaOCl for that vital function.
They might be used together sometimes, but NaOCl is the workhorse.
Speaker 1 (12:29):
During instrumentation, we create that smear layer on the canal walls.
Do we need to get rid of it?
Speaker 2 (12:34):
Generally yes, The consensus, especially for infected teeth, is that
removing the smear layer is beneficial. It's a mix of
dentine debris, pulp remnants, and bacteria.
Speaker 1 (12:44):
Why remove it?
Speaker 2 (12:44):
Because it can block the dentinal tubules, preventing your earrogance
and sealers from penetrating. Fully removing it typically using seventeen
percent edta, which chilates the inorganic part, alternated with no
cl for the organic part allows for a better dis
infection and ceiling.
Speaker 1 (13:01):
And if you need multiple visits, what goes inside the
canal between appointments.
Speaker 2 (13:05):
Calcium hydroxide KOH two. That's still the standard inter appointment dressing.
It's very high PH's antibacterial, helping to continue the disinfection
process between visits. Plus it has a role in stimulating
hard tissue formation in certain cases like apexification.
Speaker 1 (13:21):
Okay, canals cleaned shaped, disinfected time to fill. The timing
itself is sometimes debated one visit or two.
Speaker 2 (13:29):
Yeah, that's a classic debate. Logically, though, it comes down
to the state of the pulp. If you started with
a vital, non infected pulp and you can do everything efficiently,
a single visit makes sense.
Speaker 1 (13:38):
What for infected cases.
Speaker 2 (13:40):
For teeth that presented with apical period on titus infection
already established, the thinking often leans towards caution, a multiple
visit approach using that calcium hydroxide dressing in between gives
you more certainty that you've maximally reduced the bacterial load
before sealing it all up. Biology should guide the timing.
Speaker 1 (13:59):
The andered filling material is still gut a perchure.
Speaker 2 (14:02):
Right, yes, it remains the core material of choice.
Speaker 1 (14:05):
We hear about cold techniques like lateral condensation versus warm techniques.
Lateral is simple and fast. Why use heat?
Speaker 2 (14:13):
That's a fair question. Lateral condensation is straightforward, especially if
you have a nice apical stop prepared. You basically pack
individual cones of guta percha laterally against the canal wall
with a spreader, but the result isn't a single solid mass,
it's multiple cones kind of held together by the seiler.
Warm tech weeks like warm vertical condensation or continuous wave
(14:34):
soften the guta purchase. You can flow better exactly. It
allows the guta percha to adapt much more intimately to
canal irregularities, fins and importantly, those lateral canals we talked about.
You tend to get a denser, more homogeneous fill, which
theoretically provides a better long term seal, and.
Speaker 1 (14:52):
You always need a sealer with the guta percha.
Speaker 2 (14:54):
Absolutely the seiler is what actually fills the microscopic gaps
between the guta percha and the canal and between the
cones themselves. In lateral condensation. Common types are zinc oxide,
ugenol based, calcium hydroxide based, or resin based.
Speaker 1 (15:10):
Is anything challenging god approachase dominance?
Speaker 2 (15:13):
Well, not as the main core material generally, but mineral
trioxide aggregate MTA is playing an increasingly vital role in
specific situations.
Speaker 1 (15:21):
What makes MTA special It's.
Speaker 2 (15:23):
Got fantastic biocompatibility, seals really well, and crucially, it actively
stimulates hard tissue formation that makes it incredibly useful for
things like perforation repairs, root end fillings, and surgery, and
as we'll see managing immature teeth. Its versatility is definitely
shifting how we handle complex cases.
Speaker 1 (15:41):
Okay, root canal's filled, but we're not done the final restoration.
How important is that paramount?
Speaker 2 (15:47):
Absolutely paramount. You can do the best root canal treatment
in the world, but if the final restoration fails, the
tooth is likely doomed.
Speaker 1 (15:55):
The numbers back that up strongly, right they do.
Speaker 2 (15:58):
Our sources highlight this clearly. Teeth restored with crowns after
endo have a significantly higher survival rate, something like eighty
one percent still functional after ten years compared to compared
to only about sixty three percent for teeth without crowns.
That's a huge difference. More often than not, its restorative
failure leakage fracture that leads to extraction, not the endo
(16:20):
treatment itself failing.
Speaker 1 (16:22):
If there isn't enough tooth left to hold a filling
or crown, we often need a post right to retain
the core build up correct.
Speaker 2 (16:28):
But the success of that post and core hinges entirely
on one critical concept, the ferrule effect. Define that for us,
the ferrule is a band of sound tooth structure at
the gingible margin that the crown encircles. Like the metal
bander and a barrel, you need at least one point
five to two point zero millimeters of vertical solid tooth
structure above the margin all the way around for the
(16:50):
crown to grip onto.
Speaker 1 (16:51):
Why is that ferule so crucial.
Speaker 2 (16:52):
Because it provides bracing It resists the leverage forces that
the post transmits during function. Without an adequate ferrel, the
post acts like a wedge, concentrating stress at the weakest
point and significantly increasing the risk of root fracture. No
feral often means no post or of very guarded prognosis.
Speaker 1 (17:12):
And how long should the post be?
Speaker 2 (17:14):
Ideally longer than the clinical crown height, extending well down
into the root, maybe into the apical third, but this
is critical. You must preserve enough apical root filling to
maintain the seal. At least four to five millimeters of
guttapercha needs to remain untouched at the apex.
Speaker 1 (17:30):
Okay, let's shift gears to some really challenging clinical scenarios,
starting with kids primary teeth.
Speaker 2 (17:37):
Yeah, endo in primary teeth is tricky. Diagnosis is tough
because kids often can't pinpoint pain well and sensitivity tests
are unreliable. The main treatment, when the pulp is involved
but still vital, is usually a popotomy removing the coronal pulp.
Speaker 1 (17:51):
Materials used for that have changed big time.
Speaker 2 (17:54):
Form A chrysal used to be the standard, but there
are significant concerns about its toxicity and potential carcinogenicity.
Speaker 1 (18:00):
Use.
Speaker 2 (18:00):
Now there's been a major shift towards alternatives like ferric sulfate,
mainly for its hemostatic properties and increasingly mta. Mta shows
really high success rates in pulpotomies by inducing a good
denteen bridge that hard tissue barrier.
Speaker 1 (18:14):
What about trauma to young permanent teeth where the root
isn't fully formed yet.
Speaker 2 (18:20):
Maintaining pulp vitality there is the absolute priority, because that's
what drives root maturation, getting longer and thicker walls. If
a young tooth fractures and exposes a.
Speaker 1 (18:30):
Vital pulp, what's the treatment?
Speaker 2 (18:31):
Partial propotomy is often the way to go. You remove
just the inflame surface layer of the pulp and place
a biocompatible material, often MTA again directly on a healthy tissue.
Young culp has amazing healing potential.
Speaker 1 (18:44):
What if the trauma kills the pulp in an immature tooth,
leaving that wide open apex.
Speaker 2 (18:49):
Then we need to induce a hard barrier at the end.
That's apexification. Traditionally this meant packing calcium hydroxide repeatedly over
many months, which was technique sensitive and left the tooth
weak for.
Speaker 1 (18:58):
A long time.
Speaker 2 (18:59):
And the modern approach MTA again. After disinfecting the canal,
you can often place an MTA plug directly at the
open apex. It sets relatively quickly, provides a good seal
and creates that apical barrier much more predictably and efficiently.
It's a huge improvement.
Speaker 1 (19:16):
Let's talk about endoperio lesions where root canal problems and
gum problems meet.
Speaker 2 (19:20):
Right. The communication between the pulp and the periodontium. Classification
is key here for prognosis. A primary endoleusion where the
infection drains out through the periodontal ligament generally has a
good prognosis if you treat the ENDO effectively.
Speaker 1 (19:35):
What about the other way around or both happening at once.
Speaker 2 (19:37):
A primary periollsion rarely affects the pulp unless it reaches
the apex, But a true combined lesion where an ENDO
infection meets an existing periodontal pocket that has a much
more guarded prognosis. Success really depends on how severe the
periodontal disease is and if both issues can be effectively treated.
Speaker 1 (19:55):
Are there anatomical factors that make these worse?
Speaker 2 (19:57):
Definitely? Developmental anomalies like palatal grooves on incisors or deep
grooves on root surfaces act like built in highways for bacteria,
making combined lesions much harder to treat and giving them
a poorer outlook.
Speaker 1 (20:10):
Okay, last scenario, and it's one every clinician dreads. The
emergency hot tooth, acute moltpitius or absess where the local
anesthetic just yeah, doesn't work.
Speaker 2 (20:21):
Ah, yes, the profound anesthesia failure. It's incredibly frustrating for
both the patient and the clinician.
Speaker 1 (20:27):
Why does it happen? Biologically?
Speaker 2 (20:29):
It's a combination of factors in that acutely inflamed tissue
chemical mediators released by the inflammation actually lower the firing
threshold of the nerves, make them hyper excitable. Plus the
increased blood flow the vascularity and DIMA tends to rapidly
buffer and wash away the anesthetic solution before can fully
take effect.
Speaker 1 (20:46):
So your standard block or infiltration fails. What are the options?
Speaker 2 (20:49):
Then you need supplementary techniques. The sources mention things like
intropople anesthesia directly injecting into the pulp chamber itself. It
works partly by pressure forcing the aniste into the nerve tissue.
Speaker 1 (21:01):
What if even that doesn't work.
Speaker 2 (21:02):
Sometimes profound anesthesia is just unattainable at that appointment. In
those cases, the best course might be to achieve drainage.
If they're swelling place a strong sedative dressing like lettermix
which contains a steroid and antibiotic, or even just zinc
oxide eugenol, seal it temporarily and bring the patient back
once things have calmed down Chemically, trying to push through
(21:23):
without adequate anesthesia is often counterproductive. Controlling the infection and
inflammation is key to controlling the pain. So looking back,
we've covered a huge amount, from ancient theories right up
to modern materials like MTA and the precision of ELS.
I think the big takeaway is that endodontics at its heart,
blends biological understanding with technical execution.
Speaker 1 (21:46):
Right. One doesn't work without the other.
Speaker 2 (21:47):
Exactly, you can have the fanciest gadgets, but if you
don't respect the biology, if you don't eliminate the microbes,
the icome won't be favorable long term. It's about diagnosis, disinfection,
and sealing. Biology dictates success, not speed or technique alone.
Speaker 1 (22:01):
That's a fantastic summary, And to help everyone consolidate some
of these critical points, here's a clinical challenge based on
what we've discussed. Exercise for the listener. Okay, picture this.
You have patient in your chair. They've got clear signs
of irreversible pulpitis in a lower molar, that hot tooth scenario.
They also tell you they take warfaring and their I
and R check today came back at three point five. So,
(22:23):
thinking about everything we've covered, what are two absolutely critical
things you need to address in your treatment of plan
concerning first their systemic medication and the associated risks, And second,
how you're going to achieve profound anesthesia for that really
inflamed tooth. Think about stability versus threshold for the I
and R and those supplementary injection techniques we mentioned
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