Speaker 1: You know, usually when you look at a piece of machinery,
Speaker 1: the engineering is like pretty obvious. You look at a hinge,
Speaker 1: you can see how it opens, right.
Speaker 2: You look at a shock absorber and there's a big
Speaker 2: spring right there exactly.
Speaker 1: But then you look at the human mouth and suddenly
Speaker 1: you're looking at this wild machine that has to crush
Speaker 1: rocks but also sense like a hair's width of.
Speaker 2: Pressure and survive a literal acid bath every single day.
Speaker 1: Yeah, and heal itself from the inside out. So today
Speaker 1: we're taking a deep dive into the dentin nbde Part
Speaker 1: one study guide. Our mission here is to help you
Speaker 1: master the foundational science of dentistry.
Speaker 2: Right. We're going to break down exactly how this biological
Speaker 2: marvel in your head actually works, from the macro anatomy
Speaker 2: of the jaw down to the microscopic cells.
Speaker 1: We're distilling everything down for you, whether you're a dental student,
Speaker 1: a young professional, or just you know, a curious self learner.
Speaker 1: So let's start big. If we open the mouth, we
Speaker 1: see the soft palette in the back.
Speaker 2: Which separates the oral cavity from the NASA fair.
Speaker 1: Yeah, right, But the real star of the show is
Speaker 1: the tongue. I mean, it looks like just a simple
Speaker 1: slab of muscle, but it is wildly complex.
Speaker 2: Oh, it's a massive bundle of intertwining fibers. And if
Speaker 2: you're trying to understand how this whole system is wired,
Speaker 2: the innervation of the tongue is a huge foundational concept.
Speaker 1: Okay, so what's the golden rule there?
Speaker 2: So the rule is that all the muscles of the tongue,
Speaker 2: the intrinsic ones that curl it and the extrinsic ones
Speaker 2: that move it around, they're all powered by one cranial nerve, right,
Speaker 2: the hypoglossal nerve. That's cranial nerve twelve.
Speaker 1: Okay, cranial nerve twelve. But I mean anatomy loves a curveball, right,
Speaker 1: There's always that one rogue element.
Speaker 2: Always, And here the notorious exception is the palatal glossus muscle.
Speaker 1: Even though it has glossus in the name, which.
Speaker 2: Means tongue exactly, it has glosses in the name, but
Speaker 2: it is actually innervated by the vagus nerve cranial nerve x.
Speaker 1: Oh wow, why is that?
Speaker 2: Because it pulls the soft palette down and elevates the
Speaker 2: back of the tongue to start a swallow. So since
Speaker 2: it bridges the throat and the tongue, it takes its
Speaker 2: wiring from the third snerve.
Speaker 1: That makes total sense. Now looking at the surface of
Speaker 1: the tongue, it's covered in these textural bumps, the lingual pipilla.
Speaker 2: Yeah, where your taste buds live. And they are definitely
Speaker 2: not all the same.
Speaker 1: Right, they have specific zones, don't they.
Speaker 2: They do so. At the very tip and along the
Speaker 2: sides you have the funderform pipillae. They look like well,
Speaker 2: little mushrooms, and they handle sweet and salty.
Speaker 1: Okay, sweet and salty on the mushroom yep.
Speaker 2: Then on the far lateral edges you have the foliot pipillae.
Speaker 2: Those look like leaflike folds and they pick up sour tastes.
Speaker 1: And then there's the bitter ones. At the back right.
Speaker 2: Right, drawing a big V shape at the back of
Speaker 2: the tongue are the circumvallet pipilla. These are huge circular
Speaker 2: structures and they sit in these deep trenches.
Speaker 1: Well, wait, if there are deep trenches, wouldn't like food
Speaker 1: just get stuffed down there? You'd be tasting that bitter
Speaker 1: coffee for hours, you'd.
Speaker 2: Think so, But nature solve that with von Ebner's glands.
Speaker 1: Okay, what are those?
Speaker 2: They are these purely serious salav glands right at the
Speaker 2: base of the trenches. Their only job is to constantly
Speaker 2: pump out watery fluid to wash the trench.
Speaker 1: Out like a biological reset button.
Speaker 2: Exactly, they flush the palette so you can analyze the
Speaker 2: chemical makeup of your very next bite.
Speaker 1: That is just brilliant engineering. But okay, tasting the food
Speaker 1: is only step one. Let's talk about the heavy lifters
Speaker 1: that actually crush it. The muscles of mastication.
Speaker 2: So there are four primary ones, and just like the tongue,
Speaker 2: these four are all wired to the same power source,
Speaker 2: the mandibular division of the trigeminal nerve V three. They
Speaker 2: also all get their blood from the maxillary artery.
Speaker 1: Okay, let's meet the big four. Give me the breakdown.
Speaker 2: First up is the temporalis. It's this massive fan shaped
Speaker 2: muscle on the side of your skull. Because of how
Speaker 2: it fans out, it elevates the jaw, but it also
Speaker 2: retracts it pulls it backward.
Speaker 1: Got it. What's number two?
Speaker 2: The massiter sitting right at the angle of your jaw.
Speaker 2: This is your powerhouse. The most powerful elevator of the mandible.
Speaker 1: I mean you can feel that one flecks when you
Speaker 1: clench your teeth.
Speaker 2: Oh. Absolutely. Then third is the medial terrygoid. It runs
Speaker 2: on the inside of the jaw. It basically forms a
Speaker 2: sling with the master to pull the jaw up and
Speaker 2: slightly side to side.
Speaker 1: Now, hold on a second. You just listed temporalis, massiter,
Speaker 1: and medial terrygoid. All three of those pull the jaw
Speaker 1: up right, they close the mouth. So how does it open?
Speaker 1: Like gravity can't do it all on its own.
Speaker 2: Well, the fourth muscle does the opening, the lateral terrygoid.
Speaker 1: So it's like the lone rebel of the group.
Speaker 2: That is the perfect way to describe it. It's the
Speaker 2: only one that depresses or opens the mandible. It also
Speaker 2: protrudes it dragging the jaw forward.
Speaker 1: And because it's the only one doing that job, it's
Speaker 1: a big clinical clue.
Speaker 2: Is a huge clue. If the lateral terarygoid is injured
Speaker 2: on one side, when you ask the patient to open
Speaker 2: their mouth, the jaw will physically deviate toward the side
Speaker 2: of the injury.
Speaker 1: Because the healthy side is pushing forward, but the broken
Speaker 1: side is just dragging behind exactly.
Speaker 2: It essentially anchors the jaw toward the broken side. Simple mechanics,
Speaker 2: but incredibly useful for diagnostics.
Speaker 1: Okay, so we've mapped the oral cavity, we have the crushers,
Speaker 1: but before we crush anything, we need the actual teeth
Speaker 1: we do, so let's shrink down to the microscopic level.
Speaker 1: You start as an embryo. How does a clump of
Speaker 1: cells figure out how to build a rock?
Speaker 2: It starts really early, around the sixth week in utero.
Speaker 2: You get this U shaped band of tissue in the
Speaker 2: developing mouth called the dental lamina.
Speaker 1: Okay, the dental lamina, and it's basically two tissues talking
Speaker 1: to each other, right right.
Speaker 2: It relies on chemical communication between the oral epithelium, which
Speaker 2: is ectoderm, and the underlying connective tissue, the ectome synchime.
Speaker 1: And when they talk, they form the tooth germ, which
Speaker 1: goes through the cap stage and then the bell stage.
Speaker 2: Yeah. And during the bell stage, this tooth germ splits
Speaker 2: into three highly specialized factories. First, you have the enamel.
Speaker 1: Organ, which comes from the ectoderm. Correct.
Speaker 2: It forms a literal bell shape, and it's made of
Speaker 2: four distinct cellular layers.
Speaker 1: Okay, what the four layers. That sounds like high yield
Speaker 1: exam stuff, very high yield.
Speaker 2: On the outside, you have the outer enamel, epithelium, protective
Speaker 2: barrier and blood supply.
Speaker 1: It makes sense. What's inside that.
Speaker 2: Inside that is the stellet reticulum. These cells are star
Speaker 2: shaped and they trap a ton of water. They act
Speaker 2: like a spongy shock absorber to protect the delicate stuff inside.
Speaker 1: Oh nice. And the third layer the.
Speaker 2: Stratum inner medium. It helps nourish the cells that will
Speaker 2: actually make the enamel. And finally, the innermost layer is
Speaker 2: the inner enamel epithelium.
Speaker 1: Those are the ones that actually do the building.
Speaker 2: Yes, those cells ultimately transform into ameloblasts, which are the
Speaker 2: enamel secreting cells.
Speaker 1: Okay, so that's the enamel factory. What about the rest
Speaker 1: of the tooth?
Speaker 2: Well, inside the bell of the enamel organ you have
Speaker 2: the dental papilla that comes from the ectomessen chyme and
Speaker 2: it forms the dentin and the pulp. Okay, and wrapping
Speaker 2: around the whole thing is the dental sac also ectomisenchyme.
Speaker 2: It forms the periodontium you know, the cementum, the periodontal ligament,
Speaker 2: and the bone.
Speaker 1: I always wondered about the timeline here. If enamel is
Speaker 1: on the outside and dentin is on the inside, which
Speaker 1: factory turns on first?
Speaker 2: It's an inductive relationship. One triggers the other. First, the
Speaker 2: cells of the inner enamel epithelium physically elongate. Okay, that
Speaker 2: shape change sends a chemical signal across to the dental papilla,
Speaker 2: telling its outer cells to turn into adentoblasts.
Speaker 1: The dentin making cells.
Speaker 2: Exactly, and those odontoblasts immediately lay down the very first
Speaker 2: microscopic layer of dentin.
Speaker 1: So the dentin goes first.
Speaker 2: Yes, and only after that first layer of denton is
Speaker 2: down do the ammeloblasts finally wake up and lay down
Speaker 2: the first layer of enamel.
Speaker 1: So dentin fires the starting pistol. The inside triggers the outside.
Speaker 1: That's so cool, and that brings us to the materials themselves,
Speaker 1: the big four enamel, dentin, cementum, and pulp. Let's start
Speaker 1: with enamel, the fortress.
Speaker 2: The fortress wall. It is the hardest, most mineralized substance
Speaker 2: in the human body. Ninety six percent in organic, ninety
Speaker 2: six percent yeah, almost entirely tightly packed. Hydroxyapoitatee crystals, zero
Speaker 2: collagen and mature. Enamel is completely acellular, no living cells
Speaker 2: at all, and.
Speaker 1: It's not just a flap block of crystal either. The
Speaker 1: sources talk about lines of Retzius and hunter Sriger bands.
Speaker 2: Right, because ameloblasts don't build in one continuous pore, they
Speaker 2: rest periodically. This creates visible growth rings like a tree.
Speaker 2: Those are the lines of Rhetzius and the hunter Strigger bands.
Speaker 2: That's an optical phenomenon. The ameloblasts weave the enamel rods
Speaker 2: in different directions to stop fractures. When you shine a
Speaker 2: light on it, those alternating directions look like light and
Speaker 2: dark bands.
Speaker 1: It adds incredible fracture resistance. But let me push back here. Sure,
Speaker 1: if enamel is ninety six percent crystal, completely dead, no
Speaker 1: nerves from up, how can my tooth feel pained when
Speaker 1: I drink ice water? A rock doesn't feel cold.
Speaker 2: It's a great question, and it's because enamel is just
Speaker 2: the shell right underneath that dead Cortreus is the dentin,
Speaker 2: and dentin is very much alive.
Speaker 1: So Denton is the sensory system and the shock absorber.
Speaker 2: Exactly, It's only about seventy percent inorganic. The rest is
Speaker 2: mostly organic material, primarily type.
Speaker 1: One collagen, which gives it flexibility. Right.
Speaker 2: It has a lower modulus of elasticity than enamel, so
Speaker 2: it can flex slightly and absorb the crushing forces without
Speaker 2: shattering the enamel on top of it.
Speaker 1: How is it alive.
Speaker 2: Because it's riddled with millions of tiny tunnels called dentinal tubules.
Speaker 2: Reaching up into every single tube is a living piece
Speaker 2: of a cell called a tomes fiber, which.
Speaker 1: Is an extension of the odonta blast.
Speaker 2: Yes, the main cell body sits in the pulp, but
Speaker 2: this long, fluid filled arm reaches up into the dentin.
Speaker 2: Changes in temperature or pressure shift the fluid, which tugs
Speaker 2: on the nerve endings.
Speaker 1: In the pulp, and that registers as pain exactly, And
Speaker 1: since it's alive, it can adapt, right, Yeah, I read
Speaker 1: there are four types of dentin. Yeah.
Speaker 2: Primary dentin forms the initial shape. Secondary dentin is formed
Speaker 2: slowly but continuously for.
Speaker 1: Your whole life, which means the pulp chamber gets smaller
Speaker 1: as we age. Right.
Speaker 2: If there's an attack like a deep cavity, you get
Speaker 2: tertiary or aperative dentin. The odonta blasts rapidly throw down
Speaker 2: this chaotic layer to physically wall off the decay like
Speaker 2: barricading the door exactly, and finally, sclerotic dentin. In older teeth,
Speaker 2: the tubules actually calcify and plug themselves solid to block bacteria.
Speaker 1: That is wild. Okay, moving down, we have cementum on
Speaker 1: the root and the pulp inside.
Speaker 2: Cementum is about fifty percent inorganic. Heavily resembles bone, but
Speaker 2: it's totally a vascular no blood vessels. Its only job
Speaker 2: is attachment.
Speaker 1: And the pulp is the vascular center, packed.
Speaker 2: With blood vessels, nerves, connective tissue. Its primary job is formative.
Speaker 2: It keeps those odonta blasts alive.
Speaker 1: Now, the study guide makes a huge clinical distinction about
Speaker 1: pulp capping, right, saving an exposed pulp.
Speaker 2: Yes, it's way more successful in young teeth than in
Speaker 2: older adults.
Speaker 1: Why is age such a big factor there?
Speaker 2: It's purely about blood supply. In young tooth, the opening
Speaker 2: at the tip of the root, the apical form in
Speaker 2: is wide open. The pulp is bursting with blood.
Speaker 1: Vessels, so it has a massive immune response.
Speaker 2: Right, it can fight inflammation and heal. But as we
Speaker 2: age that secondary dentin shrinks the canal the form and
Speaker 2: narrows and the pulp gets fibrous. It just lacks the
Speaker 2: blood supply to mount a defense.
Speaker 1: That makes perfect sense. Okay, so we've got this living
Speaker 1: sensing tooth. But if you just drop a tooth into
Speaker 1: a hole in the jawbone, it's not going to stay.
Speaker 1: It'd be like setting up a tent with no pegs.
Speaker 2: Right, first bite of an apple and the tooth is gone.
Speaker 1: So what are the tent pigs?
Speaker 2: That's the periodontium, specifically the periodontal ligament or PDL. It
Speaker 2: sits in a tiny space, usually less than point two
Speaker 2: millimeters between the root cementum and the alveolar bone.
Speaker 1: And it's not just passive glue, No.
Speaker 2: It's a highly cellular vascular Hammock type one collagen fibers.
Speaker 2: The terminal ends of these fibers embed directly into the hard.
Speaker 1: Tissue, the sharpiees fibers.
Speaker 2: Yes, they are calcified into the cementum on one side
Speaker 2: and the bone on the other. An incredibly resilient anchor.
Speaker 1: If the tooth is glued into solid bone with calcified ropes,
Speaker 1: how do braces work? Like? How do you drag a
Speaker 1: tooth an inch across the jaw? Without just ripping the
Speaker 1: root out.
Speaker 2: It relies on a fundamental biological discrepancy. Cementum is more
Speaker 2: resistant to being broken down than alveolar bone.
Speaker 1: Is okay, So how does that play out? When you
Speaker 1: tighten the wire.
Speaker 2: When you apply a continuous pressure, you compress the PDL.
Speaker 2: On one side, that's the pressure side, osteoclasts wake up
Speaker 2: there and start dissolving the jawbone to get out of
Speaker 2: the way. And on the other side, the tension side,
Speaker 2: osteoblasts wake up and lay down new bone to fill
Speaker 2: the gap behind the tooth.
Speaker 1: It's literally like dragging a hot wire through a block
Speaker 1: of ice. It melts ahead of the wire and freezes
Speaker 1: right behind it.
Speaker 2: That is a phenomenal visual and because the cementum is
Speaker 2: highly resistant to those osteoclasts, the root stays intact while
Speaker 2: the bone melts and reforms around it.
Speaker 1: Unbelievable and ceiling. The top of this system is the gingeeva,
Speaker 1: the gums.
Speaker 2: Right the biological seal. You have the free gin jieva
Speaker 2: forming a call and the attached gingeeva bound to the bone.
Speaker 2: But the critical barrier is the junctional epithelium. How does
Speaker 2: that attach the soft tissue physically glues itself to the
Speaker 2: enamel using microscopic hemidesmosomes and a basal lamina. It stops
Speaker 2: oral bacteria from diving down into the bone.
Speaker 1: Speaking of the teeth themselves, the sources highlight some specific
Speaker 1: clinical quirks that just ruin a dentist day.
Speaker 2: Oh. Absolutely. The classic trap is the maxillary first premolar.
Speaker 1: What's wrong with it?
Speaker 2: It features a severe mesual root concavity, basically a deep
Speaker 2: trench like groove on the side facing the front of
Speaker 2: the mouth. Biologically, plaque hides deep in there, huge periodontal
Speaker 2: risk and klindically if you have to do a filling there.
Speaker 2: Trying to adapt a flat metal matrix span into that
Speaker 2: deep depression is incredibly frustrating.
Speaker 1: I can imagine. What about the lower jaw.
Speaker 2: The mandipular first premolar is structurally fascinating. It's technically a
Speaker 2: bicuspit meaning two cusps, but its interlingual cusp is so
Speaker 2: tiny and non functioning. It way more like a canine
Speaker 2: than a pre molar.
Speaker 1: It tears food instead of crushing.
Speaker 2: It exactly and moving further back. The maxillary first molar
Speaker 2: is a giant, prominent oblique ridge crossing the surface, and
Speaker 2: it frequently has an extra little mini cusp on the
Speaker 2: inside front corner, called the cusp of carabelly.
Speaker 1: Good to know. Now, if you listening right now, run
Speaker 1: your tongue along your teeth, you'll notice they aren't flat squares.
Speaker 1: There are these triangular spaces between them called embrasures.
Speaker 2: Right.
Speaker 1: Why do we have those? Why not just have a
Speaker 1: perfect solid brick wall of teeth.
Speaker 2: If they were flat squares, every time you bit down
Speaker 2: on tough food, it would be driven straight down like
Speaker 2: a wedge, crushing the delicate gums between your teeth.
Speaker 1: So the embrasers act as like spillways.
Speaker 2: Yes, biological spillways. They direct the crushed food out to
Speaker 2: the sides, away from the gums, makes the teeth self
Speaker 2: cleansing and prevents frictional trauma.
Speaker 1: Which brings us to how the upper and lower arches
Speaker 1: meet cocclusion. The textraws a huge line between maximum intercuspation
Speaker 1: or MIICP and centric relation.
Speaker 2: Okay, so MIICP is purely tooth guided. It is just
Speaker 2: the position where your upper and lower teeth fit together
Speaker 2: the tightest you bite down the gears lock.
Speaker 1: That's MIICP and centric relation.
Speaker 2: Entirely joint guided has absolutely nothing to do with the teeth.
Speaker 2: It's the most superior stable position of the condyle in
Speaker 2: the TMJ socket.
Speaker 1: So a dentist's goal is usually to align the bite
Speaker 1: so your tightest tooth fit naturally happens when the joint
Speaker 1: is in that stable cr position exactly. The text also
Speaker 1: contrasts bilateral balanced decclusion with mutually protected occlusion. Right.
Speaker 2: A bilateral balanced declusion is for complete dentures. If a
Speaker 2: denture patient slides their jaw left, you actually need the
Speaker 2: teeth on the right side to stay in contact.
Speaker 1: Why wasn't that getting the way?
Speaker 2: If they separate, the denture tips up and falls out
Speaker 2: of the mouth, you need simultaneous contacts everywhere to keep
Speaker 2: the acrylic plate stable.
Speaker 1: Ah okay, but you absolutely do not want that in
Speaker 1: a mouth with natural roots.
Speaker 2: Correct for natural teeth, the gold standard is mutually protected occlusion,
Speaker 2: also called canine guidance.
Speaker 1: So if you slide your jaw to the side right now.
Speaker 2: You should feel your upper and lower canines touch and
Speaker 2: physically force all your back teeth apart. Canines have massive
Speaker 2: roots designed to absorb those sideways grinding forces.
Speaker 1: So they protect the back teeth during lateral movements, and
Speaker 1: the back teeth protect the front when chewing straight up
Speaker 1: and down.
Speaker 2: It's an incredibly elegant.
Speaker 1: System, but not invincible. Let's look at pathology. What takes
Speaker 1: this fortress down.
Speaker 2: The primary architect of smooth surface cavities is a bacteria
Speaker 2: called Streptococcus mutants.
Speaker 1: And it doesn't just eat the enamel directly, does it.
Speaker 2: No, it's basically throwing a chemical weapon at the wall.
Speaker 2: S Mutants consumes fermentable carbohydrates, mostly sugar, and it secretes
Speaker 2: lactic acid as.
Speaker 1: A byproduct, which drops the pH.
Speaker 2: Right. Enamel is strong but very vulnerable to acid. When
Speaker 2: the oral pH drops below five point five, the acid
Speaker 2: leaches calcium and phosphate out of the crystals, demineralization exactly.
Speaker 2: If it stays below five point five, the structure collapses
Speaker 2: and you get a cavity and.
Speaker 1: Decay in the mouth rarely stays isolated. Right. The guide
Speaker 1: emphasizes systemic links, especially diabetes melitis.
Speaker 2: The link is absolute. The classic triad of uncontrolled diabetes
Speaker 2: is polydipsia excessive.
Speaker 1: Thirst, polyphagia excessive.
Speaker 2: Hunger right and polyuria excessive urination. But the dental reality
Speaker 2: is severe. Diabetics lose twice as many teeth as non diabetics.
Speaker 1: Twice as many. Why is the bone laws so aggressive?
Speaker 2: It comes down to microvasculature. Chronic high blood sugar causes
Speaker 2: proteins in the blood vessels to glycate. This physically thickens
Speaker 2: the walls of the tiny capillaries feeding the.
Speaker 1: Gums, so it restricts blood flow severely.
Speaker 2: Oxygen and immune cells can't reach the periodontium to fight
Speaker 2: off normal plaque. The immune response becomes dysfunctional, inflammation runs rampant,
Speaker 2: and the alveolar bone is rapidly destroyed.
Speaker 1: Wow, and this vulnerability isn't just an adulthood. The text
Speaker 1: notes problems can begin in the first trimester of life with.
Speaker 2: Teratogea teratogens or external agents like drugs or viruses that
Speaker 2: disrupt fetal development. The first trimester is the critical window
Speaker 2: of organogenesis when the dental, lamina, and facial structures are forming.
Speaker 1: So what happens if there's exposure then.
Speaker 2: The consequences are permanent. For instance, if a pregnant mother
Speaker 2: takes the antibiotic tetracyclan, then the drug physically binds to
Speaker 2: the calcium in the forming tooth.
Speaker 1: Germ, resulting in that permanent dark intrinsic staining of the dendsins.
Speaker 2: Yes or exposure to the Rubella virus during that exact
Speaker 2: window can drastically alter the shape of the teeth and jaw.
Speaker 2: The timing dictates the defect.
Speaker 1: It is all profoundly connected from the first trimester right
Speaker 1: through to old age. We've covered an immense amount of
Speaker 1: ground today. We mapped the tongue's nerves, watched the lateral
Speaker 1: terigoid pull the jaw open, saw a dent and trigger
Speaker 1: enamel formation.
Speaker 2: We covered a lot of biology today.
Speaker 1: We did. We felt the living denin under the Dead
Speaker 1: Crystal Fortress, watched bone meld for orthodontics, and explored how
Speaker 1: I would drop in pH where a spike in blood
Speaker 1: sugar can tear it all down.
Speaker 2: It really just emphasizes that dentistry is not just mechanics,
Speaker 2: it's an applied mastery of histology, neurology, and microbiology.
Speaker 1: Now, to fulfill our mission today of helping you master
Speaker 1: this material, I have a repidfire review question for you
Speaker 1: the listener.
Speaker 2: Oh, let's hear it.
Speaker 1: Imagine you are in the clinic, if a patient presents
Speaker 1: with a severe mesial root concavity that is notoriously difficult
Speaker 1: to clean and restore. Which permanent tooth are you most
Speaker 1: likely looking at and what is its primary nerve supply?
Speaker 2: Well, you are looking at the maxillary first premolar and
Speaker 2: because it's in the upper job, the heavy lifting of
Speaker 2: mastication there is powered by the maxillary division of the
Speaker 2: trigeminal nerve.
Speaker 1: V two nailed it to wrap us up today. What
Speaker 1: is a final provocative thought our listeners can take away
Speaker 1: from this deep dive?
Speaker 2: Think back to the mmeloblasts. Those are the cells that
Speaker 2: build the enamel fortress. Biology dictates that once they finish
Speaker 2: building the crown, they degenerate completely. They vanish, so they're
Speaker 2: just gone on forever. Human enamel has zero capacity to
Speaker 2: heal itself biologically. The enamel on your teeth right now
Speaker 2: is basically a historical fossil of your embryonic development.
Speaker 1: That is wild right.
Speaker 2: It raises a fascinating question as we advance in stem
Speaker 2: cell research, how might future therapies figure out a way
Speaker 2: to chemically wake up the oral epithelium and force it
Speaker 2: to regenerate what nature designed to be a one time
Speaker 2: only factory.
Speaker 1: We were literally walking around with an irreplaceable set of
Speaker 1: crystal armor that hasn't changed since before we were born.
Speaker 1: Next time you look at a dentle X ray, remember
Speaker 1: you weren't just looking at a jagged white line. You
Speaker 1: are looking at a living, breathing marvel of engineering fighting
Speaker 1: to hold its ground. Thanks for taking the deep dive
Speaker 1: with us.