Speaker 1: Imagine a patient walks into your clinic complaining that their
Speaker 1: favorite hat just doesn't fit anymore, and on top of that,
Speaker 1: their dentures are suddenly falling out. A regular mechanic might
Speaker 1: look at that and see two completely different parts, you know,
Speaker 1: like a head issue and a mouth issue.
Speaker 2: Right, But a great diagnostician they know that patient's skull
Speaker 2: is actively growing. It's the ultimate clinical puzzle.
Speaker 1: Really exactly. You aren't just looking at isolated mechanical failures.
Speaker 2: No, not at all. The mouth is essentially the check
Speaker 2: engine light for the entire human body.
Speaker 1: And that is the exact kind of medical detective work
Speaker 1: we are getting into today. Welcome to this deep dive.
Speaker 1: We're looking at a massive stack of clinical data today,
Speaker 1: specifically the DENTIN NBD Part two board review material.
Speaker 2: It's a huge amount of information, it really is.
Speaker 1: So whether you are a dental student staring down your
Speaker 1: exams or you know a practitioner looking to sharpen your
Speaker 1: diagnostic edge, we are going to look way past the
Speaker 1: rote memorization. We are going to figure out out how
Speaker 1: to read the subtle, often hidden clues the body leaves
Speaker 1: right there in the oral cavity. So to solve that
Speaker 1: hat puzzle right out of the gate, What is actually
Speaker 1: happening to that patient.
Speaker 2: Well, you're likely looking at Paget's disease, yeah, or Ossiidi's deformans.
Speaker 2: The normal process of bone breaking down and rebuilding goes
Speaker 2: completely haywire.
Speaker 1: It just loses its structure exactly.
Speaker 2: It becomes incredibly unorganized. Like if you run a blood test,
Speaker 2: you'll see a massive spike in serum alkaline phosphatase. And
Speaker 2: if you take a cranial radiograph, the skull looks bizarrely.
Speaker 1: Fluffy, like the classic cotton wool appearance right exactly cotton wool.
Speaker 2: The bone is literally expanding, which is exactly why the
Speaker 2: hat doesn't fit, and the dentures just lose their seat entirely.
Speaker 1: Man, that perfectly illustrates how a systemic issue crashes right
Speaker 1: into clinical dentistry.
Speaker 2: Let's look deeper into that systemic oral connection, because I mean,
Speaker 2: before we even pick up a mirror to look at
Speaker 2: a tooth, we really have to respect the endocrine system.
Speaker 2: Hormones are basically the master switches for the entire body.
Speaker 1: They absolutely are, and the thyroid gland is a prime
Speaker 1: example of how extreme those switches can be. Take hyperthyroidism,
Speaker 1: where you have this huge excess of the hormone thyroxin.
Speaker 2: The patient's metabolism is just redlining at that point.
Speaker 1: Oh completely, They're sweating, they're losing weight, their heart rate
Speaker 1: is up. You'll often see Graves disease, which presents with
Speaker 1: a visibly bulging neck, a goiter, and bulging eyes.
Speaker 2: Right, But then there's Plumber's disease, which is similar but different.
Speaker 1: Yeah, Plumber's disease features toxic nodules on the thyroid, though
Speaker 1: usually you know, without the bulging eyes you see in Graves.
Speaker 2: Okay, but flip that switch the other way to hypothyroidism,
Speaker 2: and everything just grinds to a halt. The engine is flooded.
Speaker 2: You get weight gain, chronic fatigue. Right, And if it's
Speaker 2: severe in adults, it's called mixed adema where the skin
Speaker 2: gets really puffy and dry, or you know, it could
Speaker 2: be hashimotos which is an autoimmune attack on the thyroid itself.
Speaker 1: But what I find crucial is how this actually manifests
Speaker 1: in a developing child.
Speaker 2: Yeah, that's a massive topic. In children, severe hypothyroidism is
Speaker 2: called cretanism, and because the thyroid drives metabolic development, a
Speaker 2: lack of it just severely stunts physical growth.
Speaker 1: So clinically, what are you seeing in the chair?
Speaker 2: You're going to see a delayed eruption of the teeth,
Speaker 2: a very underdeveloped jaw, and a macroglossic or abnormally large tone.
Speaker 1: Wow, so the mouth is directly reflecting a metabolic traffic jam.
Speaker 1: We see similar calcium traffic jams with the parathyroid gland.
Speaker 2: Definitely, a hyperactive parathyroid gives you kidney stones and these
Speaker 2: crazy giant cell granulomas.
Speaker 1: In the jaws, and underactive is linked to conditions like
Speaker 1: to Georgia syndrome. But I'm stuck on the pituitary gland.
Speaker 1: The source material really emphasizes the timing of a pituitary
Speaker 1: tumor secreting excess growth hormone. Why is the timing so incredibly.
Speaker 2: Critical because it dictates the entire architectural outcome of the body.
Speaker 2: It all hinges on whether the growth plates in the
Speaker 2: long bones the epiphysis have fused yet.
Speaker 1: Okay, so it's like a factory's production line. If the
Speaker 1: growth hormone machine gets stuck on high before the structural
Speaker 1: scaffolding of the body is finished, you get a giant
Speaker 1: building exactly.
Speaker 2: That is gigantism.
Speaker 1: But if that machine gets stuck on high after the
Speaker 1: building is already done, like in a middle aged adult,
Speaker 1: the existing walls just bulge out.
Speaker 2: That's acromegaly. And you see it right there in the
Speaker 2: dental chair. The mandible literally expands, causing an underbite or prognifism.
Speaker 2: The teeth spread apart and the tongue enlarges.
Speaker 1: Wild And conversely, if there's a severe lack of growth hormone,
Speaker 1: you see dwarfism like achondriplasia, which again gives you delayed
Speaker 1: tooth eruption and a really crowded dental art.
Speaker 2: Right, it's all connected.
Speaker 1: Let's talk about the biological materials themselves for a second.
Speaker 1: Osteogenesis in perfecta riddle bone disease. I know this is
Speaker 1: a genetic collagen defect, and you might notice a blue
Speaker 1: tint to the whites of the patient's size, But how
Speaker 1: does faulty collagen actually affect the teeth?
Speaker 2: Well, because dentin, the layer just beneath the tooth and
Speaker 2: anmel is absolutely packed with collagen. So osteogenesis imperfecta is
Speaker 2: tightly linked to type one dentiogenesis imperfecta oh ICEE Yeah,
Speaker 2: the teeth often have these bulbous crowns, and on an
Speaker 2: X ray the pulp chambers inside the teeth look completely obliterated,
Speaker 2: just filled in with faulty dentin.
Speaker 1: It's fascinating how a single genetic misfire just cascades like that.
Speaker 1: Ectodermal dysplasia is another one that caught my eye. The
Speaker 1: notes say these patients are often missing teeth and missing hair.
Speaker 1: I had to think about that for a second, but
Speaker 1: it makes perfect sense, right, because.
Speaker 2: Both teeth and hair developed from the ectoderm, the outermost
Speaker 2: tissue layer of the embryo.
Speaker 1: Exactly the foundational blueprint is flawed. We also see congenital
Speaker 1: impacts in down syndrome or trisomy twenty one, which often
Speaker 1: presents with missing teeth in a thickened tongue, or pure
Speaker 1: robin syndrome in neonates.
Speaker 2: Oh purebent is critical for airway management. The infant has micrognathia,
Speaker 2: an incredibly small jaw right and.
Speaker 1: Because the jaw is so small, there's just no room
Speaker 1: for the tongue, so it falls back into the airway.
Speaker 1: That's a condition called glossoptosis.
Speaker 2: Right spot on glossoptosis.
Speaker 1: Okay, So We've tracked how the whole body sets off
Speaker 1: alarms in the mouth, But what happens when the systemic
Speaker 1: engine is running totally fine and you just have one
Speaker 1: highly localized alarm, like a single strange spot on a
Speaker 1: jaw radiograph.
Speaker 2: This is where we move from systemic medicine into localized
Speaker 2: diagnostic imaging. You really have to learn the visual vocabulary
Speaker 2: of dental anomalies here.
Speaker 1: Some are pretty obvious, I guess, like attrition.
Speaker 2: Right attrition where a patient who severely grinds their teeth
Speaker 2: leaves flat polished ware of facets on the enamel, or
Speaker 2: a Messiodander's, which is just an extra supernumerary tooth popping
Speaker 2: up right between the upper front teeth.
Speaker 1: And you have densin dente, which sounds like a total
Speaker 1: horror movie but is literally just a tooth developing within
Speaker 1: a tooth, usually in the upper lateral incisors, and a
Speaker 1: hypersomintosis an overgrowth of root tissue, which, wait, that ties
Speaker 1: right back to Paget's disease, doesn't it.
Speaker 2: It absolutely does. The unorganized bone growth of pagets often
Speaker 2: triggers that excess cementum on the roots. But the real
Speaker 2: diagnostic tests are the cysts and tumors.
Speaker 1: Visual clues are everything here, but honestly, looking at these notes,
Speaker 1: some of them seem basically impossible to tell apart. For example,
Speaker 1: a globular maxillary cyst is an inverted pear shape between
Speaker 1: the upper lateral incisor and the.
Speaker 2: Canine right very distinct shape.
Speaker 1: And an analobe blustoma is this aggressive tumor that looks
Speaker 1: like a cluster of soap bubbles in the bone. But
Speaker 1: then I'm looking at a periapical syst versus a dental
Speaker 1: granuloma on an X ray. They both just look like
Speaker 1: dark circles at the root tip of a dead tooth.
Speaker 1: How am I supposed to know which is which?
Speaker 2: Well you can't wait, really, not just by looking the radiograph. No,
Speaker 2: they're radiographically identical. The only definitive way to distinguish them
Speaker 2: is to biopsy the tissue under a microscope. Oh wow, Yeah,
Speaker 2: If the lesion has an epitheal lining, it's a cyst.
Speaker 2: If it's just a solid mass of fibrous connective tissue,
Speaker 2: it's a granuloma.
Speaker 1: Good to know. I'm not just missing something obvious. But
Speaker 1: here's a dangerous one. I saw in the material the cementoma,
Speaker 1: it shows up as a dark radiolucent spot at the
Speaker 1: root apex of the lower front teeth. If it looks
Speaker 1: exactly like a periodical abscess from an necrotic tooth, how
Speaker 1: do you prevent a well meaning dentist from drilling in
Speaker 1: and doing a totally unnecessary root canal.
Speaker 2: By understanding the mechanism of where the lesion actually comes from.
Speaker 2: A cementoma or a periapical cemental dysplasia arises from the
Speaker 2: bone itself, not from a dead nerve inside the tooth.
Speaker 1: Aw.
Speaker 2: Okay, do you just perform a simple cold or electrical
Speaker 2: pulp vitality test if the tooth reex normally the nerve
Speaker 2: is alive. That tells you it's a cemon tuna. And
Speaker 2: the most important clinical step here, what's that? Do absolutely nothing?
Speaker 2: It requires zero treatment and will eventually calcify and turn
Speaker 2: white on the X ray all by itself.
Speaker 1: Man, a quick vitality test saves a lot of unnecessary drilling.
Speaker 1: Speaking of those X rays, the notes heavily emphasize the
Speaker 1: rule of occult diseases. What's the protocol there?
Speaker 2: It's a very strict rule of radiation safety. You never
Speaker 2: expose a patient to radiation just to go fishing for
Speaker 2: hidden or a cult cysts or tumors if they have
Speaker 2: zero clinical symptoms.
Speaker 1: So no random X ray is just to check exactly.
Speaker 2: The only exception is screening for cavities because decay is
Speaker 2: just so universally common. However, once you take an X
Speaker 2: ray for a valid reason, you are legally and ethically
Speaker 2: obligated to meticulously evaluate the entire image for those hidden lesions.
Speaker 1: Right and remember, for anyone studying this, the dentist, not
Speaker 1: the hygienis, not the assistant, is the only one who
Speaker 1: can legally prescribe those radiographs.
Speaker 2: Absolutely, and doing it digitally cuts the radiation exposure by
Speaker 2: fifty to eighty percent anyway, Plus, if you want to
Speaker 2: actually see the crystal bone to check for period dombal disease,
Speaker 2: you have to take vertical bite wings.
Speaker 1: Okay, getting the diagnosis is only half the battle. Right now,
Speaker 1: you have a living, breathing, potentially medically compromised human sitting
Speaker 1: in your chair. How do we safely manage them?
Speaker 2: You rely on physiological protocols. If a patient goes into
Speaker 2: cardiac arrest, it's caab compressions airway breathing thirty compressions to
Speaker 2: two breaths.
Speaker 1: And what if a diabetic patient becomes hypoglycemic, like there
Speaker 1: are blood sugar crashes, they get confused, cold, sweaty.
Speaker 2: You need fast acting carbs immediately, a third of a
Speaker 2: cup of orange juice every five minutes until they stabilize.
Speaker 1: Got it. For seizure patients, the priority is preventing self harm,
Speaker 1: so you use bite blocks. For pregnant patients, if they
Speaker 1: need elective work, you aim for the second and third trimesters.
Speaker 1: But the protocols for radiation patients this is incredibly heavy.
Speaker 2: It is very serious.
Speaker 1: The notes say you absolutely must extract any unsalvagable teeth
Speaker 1: before radiation therapy begins to the head and neck. Why
Speaker 1: is the timing so rigid.
Speaker 2: Because radiation fundamentally and permanently damages the blood vessels in
Speaker 2: the bone, particularly in the dense mandible. If you pull
Speaker 2: a tooth after radiation, the bone just has no blood
Speaker 2: supply to heal the extraction socket.
Speaker 1: Oh man, So it just doesn't heal at all.
Speaker 2: It doesn't. The bone simply dies and gets infected. That's
Speaker 2: called osteo radiotocrosis. And you face a very similar risk
Speaker 2: with patients taking ivy bisphosphonates for us zeoporosis or cancer.
Speaker 2: The bones healing mechanism is zerrely compromised.
Speaker 1: You really have to understand the microscopic mechanisms to keep
Speaker 1: patients safe, which actually brings us to pharmacology. Drugs binding
Speaker 1: to receptors to make things happen. I know we have
Speaker 1: different bonds electrostatic, ionic bonds, hydrogen bonds, Drugs that open
Speaker 1: ion channels or use g proteins for second messengers.
Speaker 2: Right, and some even bypass all of that and act
Speaker 2: as nucleus receptors to alter DNA transcription directly. And at
Speaker 2: those receptors, drugs act as either agonists which trigger an
Speaker 2: effect or antagonists which block it.
Speaker 1: Right, And if an antagonist is competitive, it means it's
Speaker 1: just fighting for the exact same parking spot as the agonist.
Speaker 1: So if you flood the system with enough of the
Speaker 1: agonist drug, you can overpower.
Speaker 2: The blocker perfectly stated.
Speaker 1: But I'm looking at the adrenergics, the drugs that mimic
Speaker 1: our fight or flight sympathetic nervous system. I get how
Speaker 1: isoproteronal is a powerful agonist that dilates the bronchioles and
Speaker 1: the lungs. But how does methyl dopo work for high
Speaker 1: blood pressure? The notes say it creates a false transmitter.
Speaker 2: Mythyl dopa is brilliant. Actually, it essentially acts as a
Speaker 2: trojan horse. It gets taken up by the nerve endings
Speaker 2: and converted into a fake version of neropine.
Speaker 1: Front wait, a fake version.
Speaker 2: Yeah, And this fake neurotransmitter gets stored in the nerve
Speaker 2: so when the nervous system fires to raise blood pressure,
Speaker 2: it releases this fake inactive chemical instead of the real thing.
Speaker 2: It effectively keeps the blood pressure lowered. It's heavily used
Speaker 2: for hypertension, especially in patients with kidney damage.
Speaker 1: That is a wildly elegant mechanism. Now contrast that with
Speaker 1: something blunt, like a neuromuscular blocker. Yeah, sucunal coline oh signalochline.
Speaker 2: It's a depolarizing blocker used for endotracheal intubation. It forces
Speaker 2: the muscle receptor to fire once, causing a brief twitch,
Speaker 2: and then completely paralyzes it.
Speaker 1: But there is a massive danger there, huge.
Speaker 2: Danger if a patient genetically lacks the enzyme's pseudocolon esterrays
Speaker 2: to break that drug down, they will suffer from prolonged
Speaker 2: respiratory paralysis. They won't be able to breathe on their
Speaker 2: own for a very long time.
Speaker 1: Terrifying, but essential to know if you're taking the boards.
Speaker 1: Let's talk about pain management and drug interactions. We know
Speaker 1: mixing alcohol with certain drugs causes the disulfuum ethanol reaction,
Speaker 1: severe vomiting, headache, plunging blood pressure. But in dentistry we
Speaker 1: constantly combine drugs intentionally for pain, like hydro codone and ibuprofen.
Speaker 1: Why give two different.
Speaker 2: Pills because you are attacking the pain pathway at two
Speaker 2: completely different anatomical locations.
Speaker 1: So it's like a military flank attack like that. Exactly,
Speaker 1: the narcotic, the hydrocodone, crosses into the central nervous system
Speaker 1: to hit the brain and just you know, shut off
Speaker 1: the alarm bells. Meanwhile, the nsaid the ibuprofen stays in
Speaker 1: the peripheral nervous system, traveling to the actual site of
Speaker 1: the surgery to put out the inflammatory fire at the
Speaker 1: tissue level.
Speaker 2: That's a great way to visualize it, and a clinical bonus,
Speaker 2: narcotics do not affect blood clotting. Go if you have
Speaker 2: a patient on blood thinners like warker and narcotics are safe,
Speaker 2: and if an overdose occurs with a narcotic, you immediately
Speaker 2: use a reversal agent like mel mephine or nultrexone to
Speaker 2: knock the drug off the receptors.
Speaker 1: Okay, the patient is stabilized, their numb they're safe. Now
Speaker 1: we put on our engineering hats to rebuild the teeth.
Speaker 1: Let's jump into prosodontics and operative dentistry.
Speaker 2: Let's do it. When designing a removable partial denture or RPD,
Speaker 2: the foundation is applegates rules for Kennedy classifications. One major
Speaker 2: rule is you always classify the arch after any planned
Speaker 2: extractions are completed. It completely dictates the design makes sense.
Speaker 2: And if you are building a maxillary major connector using
Speaker 2: ap straps across the roof of the mouth, those straps
Speaker 2: must be at least fifteen millimeters apart for structural integrity,
Speaker 2: and they must never cross onto the vibrating soft palette
Speaker 2: where the patient just won't tolerate it.
Speaker 1: What about complete dentures? The primary support comes from the
Speaker 1: residual bony ridge and the hard palette, but the notes
Speaker 1: say you must provide relief over the median palatal raph.
Speaker 1: I'm trying to picture this. Why would a perfectly fitted
Speaker 1: denture suddenly start rocking like a bad restaurant.
Speaker 2: Because the medium pelladal raft is the suture line running
Speaker 2: right down the middle of the roof of the mouth.
Speaker 2: The tissue there is paper thin over solid bone. Oh
Speaker 2: I see yeah, whereas the tissue everywhere else is squishy
Speaker 2: and resilient. So when the patient bites down, the denture
Speaker 2: sinks into the squishy tissue but bottoms out hard on
Speaker 2: that middle raft, causing it to rock. You have to
Speaker 2: carve out a relief space in the denture base to
Speaker 2: accommodate that difference in tissue yield.
Speaker 1: That makes perfect sense. You have to account for the
Speaker 1: tissue dynamics under pressure. This also brings up the VDO,
Speaker 1: the vertical dimension of occlusion. Why is losing that vertical
Speaker 1: height such a disaster for patient?
Speaker 2: If the VIDO decreases, meaning the patient's upper and lower
Speaker 2: jaws are overclosing because the teat or dentures are worn down,
Speaker 2: the facial mechanics just collapse. The lips lose their border,
Speaker 2: and the face scrunches up. That sounds uncomfortable, It is
Speaker 2: mechanically the patient will chronically bite their cheeks. Chemically, the
Speaker 2: overclosure creates deep folds at the corners of the mouth
Speaker 2: where saliva pools, causing a constant, painful fungal infection called
Speaker 2: angular kilitis.
Speaker 1: Form truly dictates function. This is exactly why over dentures
Speaker 1: are so prized. Right If you can keep just a
Speaker 1: few retained tooth roots in the bone underneath the denture,
Speaker 1: it preserves the alveolar bone and stops that vertical collapse exactly.
Speaker 2: And when we're picking the fake teeth, we use the
Speaker 2: golden proportion one point six eight to one point zero
Speaker 2: to zero point six, so the teeth look mathematically natural
Speaker 2: as they fade into the smile.
Speaker 1: And we use plastic teeth, not porcelain, so they chemically
Speaker 1: bond to the acrylic base.
Speaker 2: Right now, when we shift to fixed partial dentures bridges
Speaker 2: that are cemented in booth, even the temporary plastic bridge
Speaker 2: has to do two critical jobs. It must insulate the
Speaker 2: living pulp from hot and cold, and it must hold
Speaker 2: positional stability with tight inter proximal contacts so.
Speaker 1: The adjacent teeth don't drift While you're waiting for the
Speaker 1: lab to make the final ceramic bridge exactly and the
Speaker 1: design of the pontic, the faked tooth suspended in the
Speaker 1: middle of the bridge can make or break the tissue health.
Speaker 1: The material says to never use a saddle pontic, but
Speaker 1: it looks natural because it straddles both sides of the gumbridge.
Speaker 1: So why is it banned?
Speaker 2: Because it creates a microscopic concave cave underneath it. It is
Speaker 2: physically impossible for the patient to run floss under saddle pontic.
Speaker 2: Plaque accumulates instantly, causing massive chronic tissue inflammation.
Speaker 1: So what do you use instead?
Speaker 2: In non esthetic zones like the lower molars, use a
Speaker 2: hygienic or fish belly pontic. It leaves a three millimeter
Speaker 2: open gap above the tissue, so a toothbrush can sweep
Speaker 2: right under it.
Speaker 1: We see that same demand for exact geometry and operative
Speaker 1: dentistry like filling cavities, But first you have to understand
Speaker 1: the decay itself carries happens in zones. Zone one is
Speaker 1: normal dentin, Zone two is subtransparent, dentin. Zone three is
Speaker 1: transparent dentin right.
Speaker 2: And the key here is that zones two and three
Speaker 2: are demineralized but they do not contain bacteria.
Speaker 1: And because they are bacteria free, if you seal them up,
Speaker 1: they are entirely capable of remineralizing. You don't actually have
Speaker 1: to drill them away. When you do d say for
Speaker 1: a class two silver amalgam, the microscopic geometry is vital.
Speaker 1: You only bevel the deep gingible floor of the prep.
Speaker 1: If that margin sits on enamel, why what does the
Speaker 1: bevil actually do well.
Speaker 2: Enamel is made of millions of tiny crystalline rods. If
Speaker 2: your drill leaves short, unsupported rods at the edge of
Speaker 2: the filling, the moment the patient bites down on that amalgam,
Speaker 2: those rods will shatter, breaking the seal.
Speaker 1: Ah, So the bevel sweeps away the fragile, unsupported rods exactly.
Speaker 2: And if you are deeper down on the root cementum,
Speaker 2: there are no rods, so no bevel is needed.
Speaker 1: And while you are cutting that prep, you have to
Speaker 1: use water as a bird coolant. If you just blast
Speaker 1: it with air, you dehydrate the dentin. The fluid inside
Speaker 1: the microscopic dentin tubules evaporates, creating a vacuum that literally
Speaker 1: sucks the nerve endings. The odonto blasts up into the tubules.
Speaker 2: Which it causes massive post operative hypersensitivity.
Speaker 1: Sounds brutal, which perfectly sets up our final foundational concept.
Speaker 1: You can engineer a mathematically flawless amalgam or bridge, but
Speaker 1: it means absolutely nothing if the ground underneath it is sinking.
Speaker 1: We have to discuss periodontics.
Speaker 2: The biological bedrock. When a patient had deep periodontal pockets,
Speaker 2: surgery is often the answer, and a foundational cut is
Speaker 2: the internal bevel incision.
Speaker 1: I've always thought of this like tailoring a fine suit.
Speaker 2: That's a highly accurate analogy with an internal bevel incision.
Speaker 2: Your blade removes the diseased, frayed lining on the inside
Speaker 2: of the pocket, but it completely concerns the healthy, pristine
Speaker 2: outer fabric of the gums. It creates a sharp, clean
Speaker 2: margin that you can stitch tightly back against the bone.
Speaker 1: And if the tissue contours are bulky and uncleansible, then
Speaker 1: we reshape.
Speaker 2: We use a gingy voplasty to recontour the soft tissue
Speaker 2: for physiological form. Note this doesn't eliminate pockets, it just
Speaker 2: improves the shape. And for bone, if the bone itself
Speaker 2: is bulky, we use an osteoplasty to reshape the non
Speaker 2: supporting alveolear bone, being very careful not to damage the
Speaker 2: bone actually attached to the tooth root.
Speaker 1: But before when we make a single cut, we have
Speaker 1: to measure the damage. The periodonal probe is arguably the
Speaker 1: most important instrument in the tray because it calculates clinical
Speaker 1: attachment loss right.
Speaker 2: Pocket depth alone is deceptive. If a patient has a
Speaker 2: four milimeters pocket, but their gums have receded three millimeters
Speaker 2: down the route, their total clinical attachment loss is actually
Speaker 2: seven millimeters. You have to add the recession to the
Speaker 2: pocket depth to see exactly how much foundation has been destroyed.
Speaker 1: And sometimes the patients are destroying it themselves. You see
Speaker 1: toothbrush abrasion constantly, right deep notches worn into the prominent
Speaker 1: teeth like canines and premolars because they scrub with a
Speaker 1: hard bristled brush.
Speaker 2: All the time, and switching to a soft brush doesn't
Speaker 2: just stop the damage, it actually allows the exposed roof
Speaker 2: surface to naturally remineralize over time, which shuts down cold sensitivity.
Speaker 1: During professional scaling, we often use ultrasonic instruments to clear
Speaker 1: that tartar, but you must respect the contraindications. You never
Speaker 1: use them on unshielded pacemakers. You never use them on
Speaker 1: chalky demineralized enamel because of vibration will just blast it.
Speaker 2: Away, and you avoid them in young children because their
Speaker 2: pulp chambers are so large. The heat can damage the nerve.
Speaker 1: And if an adult patient feels a sinralizing of heat
Speaker 1: during ultrasonic scaling, the.
Speaker 2: Clinician needs to immediately adapt. You move the instrument faster
Speaker 2: so it doesn't linger, decrease the power setting, or turn
Speaker 2: up the water spray to cool the tip.
Speaker 1: We also have to be on the lookout for acute swellings.
Speaker 1: If a patient comes in swollen, you have to determine
Speaker 1: if it's a periontal abscess in the gums or an
Speaker 1: endodontic abscess from a dead nerve, and if it's a
Speaker 1: combined lesion, you have to treat both, usually starting with
Speaker 1: the root canal, otherwise it will never fully heal exactly
Speaker 1: and all.
Speaker 2: Of this complex care is organized into rigid treatment planning phases.
Speaker 2: You have a preliminary phase to hander immediate pain and emergencies.
Speaker 2: Phase one is initial therapy, which includes your deep scaling
Speaker 2: and root planning. Phase two is the surgical phase. Phase
Speaker 2: three is restorative, putting in the crowns and fillings, and
Speaker 2: finally phase four is maintenance, keeping it all healthy.
Speaker 1: I want to point out the ultimate irony here. We
Speaker 1: just talked about surgical incisions, complex pharmacology, and mathematically precise
Speaker 1: tooth preparations, but the absolute most important aspect of all
Speaker 1: of this therapy, specifically phase one, is oral hygiene instruction.
Speaker 1: It really is, after all the drilling and prescribing, the
Speaker 1: most critical factor for success is just teaching the patient
Speaker 1: how to brush and floss effectively at home. If they
Speaker 1: can't do that, the surgery is destined to fail anyway.
Speaker 2: It's the absolute truth of clinical dentistry. The most advanced
Speaker 2: knowledge is only valuable when the patient can apply it daily.
Speaker 1: Okay, let's take a breath. We have covered an intense
Speaker 1: amount of ground on this deep dive. To reinforce what
Speaker 1: you've learned, I want you to viotalize that opening scenario
Speaker 1: one more time.
Speaker 2: Let's test your clinical instincts. If you have a patient
Speaker 2: who presents with a cottonwool appearance on their cranial radiograph
Speaker 2: and complains that their dentures no longer fit, what systemic
Speaker 2: disease should you suspect, and what specific dental anomaly involving
Speaker 2: the roots might you find?
Speaker 1: Have you connected the dots the hat and dentures point
Speaker 1: to Paget's disease, and because the bone is going crazy,
Speaker 1: you'd likely find hypersamentosis thickening those tooth roots. This brings
Speaker 1: us right back to where we started. The human body
Speaker 1: isn't a car. You can't just plug in a computer
Speaker 1: to get an aero code. The mouth is flashing the
Speaker 1: check engine light. But it takes a brilliant diagnostition to
Speaker 1: read the subtleties, connect the systemic chaos to the local pathology,
Speaker 1: and treat the whole patient. Keep reviewing these mechanisms, keep
Speaker 1: looking for the why behind the symptoms, and keep diving deeper.
Speaker 1: See you next time.