Tooth development Flashcards
How are deciduous teeth different to permanent ones.
A, B, C = 1, 2, 3
E = a small 6
D = unique in morphology.
Crowns are more bulbous
Teeth are smaller
Roots are more flared (so perm teeth can grow under)
Roots show more resorption
Occlusal/incisal surfaces show more attrition
Larger pulp chamber (and smaller dentine layer)
Whiter enamel bc is less mineralized.
The time frame for a developing deciduous tooth (until root completion)
Crown calcification = 12 months before eruption (E-12)
Crown completion = 6 months before eruption (E-6)
Eruption/roots half formed = E
Root completion = 18 months after eruption (E+18)
Order of deciduous teeth eruption
A, B, D, C, E
The time frame for a developing permanent tooth (until root completion)
Crown calcification begins = E-6 years
Crown completion = E-3 years
Eruption = E
Root completion = E+3 years
Order of eruption for permanent teeth
6, 1, 2, 4, 5, 3, 7, 8
Development of the canines/eruption
Canines/ 3’s don’t erupt until roots are complete so eruption and root completion both occur 6 years after crown completion/around 11 years of age.
Do maxillary or mandibular teeth erupt first
Mandibular
When are the teeth germ present for permanent dentition
Present at birth apart from for the 7’s and 8’s.
What are the stages of tooth development
Initiation Further development Morphodifferentiation Cytodifferentiation Root formation
What are the stages of initiation
- ~7 weeks after fertilization and after the maxillary arch has developed.
- Ectoderm band thickens= primary epithelial band
- Primary epithelial band grows and proliferates into the underlying lamina propria.
- The formation of the primary epithelial band induces the condensation of ectomesenchyme cells around the thickened band.
- The primary epithelial band splits into the dental lamina (w/ the ectomesenchyme cells) and the vestibular lamina. Both continue to grow deeper.
- The deep part of the dental lamina proliferates = a ball/bud stage. Superficial cells of the vestibular lamina die and cause a groove to form.
Growth factors/genes needed for the initiation stage of tooth development
Bone morphogenic proteins and fibroblast growth factors expressed from the ectoderm interact w/ ectomesenchyme = right number of tooth germs.
DLX gene coding = tissue differntiation and positioning
Homeobox genes at specific places on arch = type of tooth.
What is the result of initiation being disrupted
Initiation causes the right number of teeth in the right place, =
adontia (no teeth)
Hypodontia (not enough teeth, 8>5>2)
Hyperdontia (too many teeth, can be accessory or supplemental)
What happens during further development
Ectoderm = enamel organ
Ectomesenchyme = dental papilla
Enamel organ covers the dental papilla = called a tooth germ now.
Stages of morphodifferentiation
Needed to produce the correct shape of the crown.
- Changes are lead by the dental papilla/ectomesenchyme (not enamel organ/ectoderm, like in initiation)
- BMP and FGF induce selective mitosis of the internal dental epithelium of the EO = change in shape.
- The enamel knot does the same thing but only refines the shape e.g. determines if 2nd or 3rd molar.
- The enamel knot disappears.
- The permanent tooth bud grows from the enamel organ.
- The dental lamina disintegrates.
- The dental follicle surrounds the tooth germ (makes the cementum and PDL)
The enamel organ layers
Internal and external dental epithelium (cervical loop where they meet/are continuous)
Stellate reticulum
Stratum intermedium.
(CT layer under the internal dental epithelium)
Function/structure of the external dental epithelium
Cuboidal cells
Regulates entry of nutrients into the EO
Function/structure of the stellate reticulum
Star shaped cells joined by desmosomes.
Space packing w ECM which provides vital nutrients to the avasuclar enamel organ.
Function/structure of the stratum intermedium
2-3 layers of squamous cells needed for enamel production.
Function/structure of the internal dental epithelium
Differentiates into ameloblasts which secrete enamel.
What happens during cytodifferentiation
- Internal dental epithelium induces the dental papilla cells to differentiate into odontoblasts (odontoblasts look more columnar, dental papilla looks like fibroblasts)
- Oodontoblasts secrete dentine
- The dentine induces the internal dental epithelial cells to differentiate into ameloblasts.
- The ameloblasts secrete enamel.
Root formation
Happens as the crown is completing the formation
- The cervical loop where the internal and external dental epithelium are continuous grows (mitosis happening at the tip) = the epithelial root sheath.
- The root sheath grows between the dental papilla and the dental follicle and forms a cylinder around the dental papilla (and divides if its a multi-rooted tooth)
- As it grows, it stretches out causing islets of cells/rests of malassez to occur meaning the root sheath is in contact w the dentine/dental follicle
- As the dentine and dental follicle are both derived from ectomesenchyme, they cant induce each other. The root sheath (derived from ectoderm) induces the dental follicle to differentiate into cementoblasts and fibroblasts (to make cementum and PDL) by secreting a thin hyaline layer of cartilage onto the root dentine
Dentine features
70% mineralized (if wasn’t mineralized it would be less resistant to abrasion and erosion)
30% Collagen type 1 (and ECM + proteins)
Organic matrix = compressable and high tensile strength so acts as a shock absorber and compensates for brittle enamel.
Vital and v sensitive (but doesn’t have many nerves)
Odontoblasts in quiet state at the pulp-dentine border and their processes extend w dentine forming around them = tubules.
Dentinogenesis
- Dental papilla cells differentiate into pre-odontoblasts (not fully differentiated yet) due to signals from the internal dental epithelium (BMP, FGF)
- Preodontoblasts secrete a mantle dentine layer (not mineralised dentine matrix) which stays as a layer under the future ADJ.
- Preodontoblasts fully mature to odontoblasts (cuboidal cells to polarised columnar)
- As the odontoblasts retreat they extend their processes and dentine forms around them = tubules.
- Pre-dentine begins to mineralize = dentine.
What is mantle dentine
A layer under the ADJ.
The first dentine secreted (by preodontoblasts).
Unmineralised dentine matrix - contains less collagen and more ECM.
How does pre-dentine calcify/mineralise
As it is primary calcification (enamel and cementum are laid down next to tissue that’s already being mineralised) it needs to be initiated.
- Initiation happens via matrix vesicles that contain HAP crystals in a cell derived triluminar membrane.
- Calciospherites merge to form uniform structures around the dentine tubules. If this process is destrupted then you get interglobular dentine where the calciospherites havent fully merged.
What is in the dentine matrix
Collagen
Dentine sialoproteins
Dentine matrix proteins
(The proteins are needed to make dentine what it is because without them the odontoblasts become more like osteoblasts and secrete bone)
What is circumpupal dentine
All dentine formed after the mantle dentine.
What are enamel spindles
As dentinogenesis happens before amelogenesis, sometimes the odontoblasts will get trapped in the enamel as they are retreating. They still extend their processes into the enamel = enamel spindles.
Features of a cross-section of dentine
Black circles (air where the odontoblast processes would have been) Surrounded by white circle = 90% mineralized peritubular dentine In a pink background = 70% mineralised circumpupal dentine.
How does dentine become translucent
As you get older, peritubular dentine becomes more mineralized until it’s translucent.
This process begins from the root apex and travels in and up.
Amount of translucency = age so can be used forensically.
primary, secondary and tertiary dentine
Primary = development Secondary = reduces size of pulp chamber Tertiary = reactionary or reparative
How can dentine incremental lines be seen
Add tetracycline antibiotic - attaches to mineralizing tissue and stains it brown and fluorescent.
Dental pulp
Leftover dental papilla + nerves, vessels, fibrovascular CT
Vital, v sensitive and vascular = reacts by inflammation if exposed.
Features of nerves in pulp
A myelinated (x2) - mechanosensitive
C unmyelinated
Only transmit pain
Lots of convergence at brain stem and in teeth = hard to localise the pain.
Types of treatments done to the pulp (e.g. if infected)
Pulpectomy = remove all the pulp Pulpotomy = remove some of the pulp Endodontics = treatment
How does the dentine get exposed
Caries or fractures from enamel or root
Recession
Ename eroded away
Why/ how is the dentine sensitive
Doesn’t contain many nerves so only theories about how it can be sensitive:
- Has some nerves
- The odontoblast processes act as neurons.
How can sensitivity in the dentine be reduced
Encouraging the dentine to block the tubules.
Hardening the dentine e.g. using fluoride varnish.
How does dentine react to exposure
Self-seals tubules using dentine
Odontoblast processes shorten
Odontoblasts reactivated
Reactivated odontoblasts retreat and secret tertiary dentine as they do
How can large dentine cavities be restored
Amalgam fillings = mechanically lock into the cavity
Dentine bonding agents = chemical lock
Types of tertiary dentine
(Also called irregular secondary)
Reparative/Irritation/Reactive
Reactionary/regenerative
Reparative dentine features
Caused by aggressive stimuli e.g. infection
Secreted by newly differentiated odontoblasts (from proginators)
Irregular e.g. has few tubules.
Reactionary dentine features
Caused by mild stimuli e.g. slow erosion of enamel.
Secreted by re-activated odontoblasts
Physiological structure but different direction of tubules.
What name is given to the apical 1/3 dentine
Radicular dentine
What is radicular dentine
Dentine in the apical 1/3rd
Enamel features
96% CaHAP, 2% proteins, 2% water. Very strong but brittle and translucent HAP in rod structures, places where orientation changes = rod boundaries and this is seen as prisms. Acellular so can't repair itself. Derived from ectoderm.
Cementum features
Bone-like layer (yellow, soft) covering the root of the tooth.
PDL insert into it.
Cellular and acellular parts - cellular is thicker and closer to the apex. It contains cementocytes.
55% mineralized so doesn’t remodel if a load is applied to it (e.g. like bone).
Derived from ectomesenchyme.
Grows throughout life e.g. cellular parts get thicker w age.
Collagen fibers embedded in the calcified matrix.
Alveolar bone development
1, 222, 3, 4, 5
Forms as the tooth forms/erupts and if tooth removed, it is resorbed.
Alveolar process forms the buccal and lingual cortical plates (compact bone). As these get taller, crypts/bony septa form between the teeth and when the tooth erupts, PDL supports these.
Interradicular bone forms between the roots of multi-rooted teeth.
Forms sockets that the teeth sit in and PDL insert into.
Reversal lines show where new/changes in deposition occurred.
What do PDL contain
Dense fibrous connective tissue contains:
- Fibroblasts
- Collagen bundles
- ECM = hydrophilic and can’t be compressed so pushes n alveolar walls to increase the pressure/tension in the PDL so they can withstand the forces.
- Undifferentiated ectomesenchyme cells
- Immune cells during inflammation
- Neurovascular bundles
- Cell rests left from ERS
Amelogenesis
Odontoblasts secrete BMPs and FGFs into the dentine matrix which induces the internal dental epithelium to differentiate into ameloblasts.
Ameloblasts = have protein secreting structures e.g. RER and also have absorption features so can absorb the proteins from the enamel as it is mineralizing.
Ameloblasts = columnar polarised, w nucleus at the basal end.
Mineralisation begins at certain points, e.g. under the cusps.
Some aprismatic enamel secreted first to make tome’s process which dictates the rod boundaries.
Mineralisation/ making of the prisms in enamel structure
A thin layer of aprismatic enamel secreted first = Tome’s process.
CaHAP crystals laid down in rods (keyhole shaped- the result of 4 neighboring ameloblasts).
Rod laid down at right angles to the surface so a change in orientation = a rod boundary. Seen as prisms.
Rod boundaries coincide with Tome’s process.
Keyhole-shaped rods run in layers and the layers run at angles to each other.
Ameloblasts retreat (in a wave shape) as this is happening and use up the nutrients in the enamel organ until only the reduced enamel epithelium is left.
What is the reduced enamel epithelium
All that is left of the enamel organ after it has been used up to make the enamel.
Consists of external dental epithelium and ameloblasts.
Covers/ protect the tooth until it erupts after which it gets worn away.
Histology of enamel viewed on a decalcified sample
Mature enamel can’t be seen because not enough organic material. Immature enamel can be seen as a dark area as it is 70% organic.
Benefits of the keyhole shape of the rods
More interlocking = stronger
Why is dentine important for enamel
High tensile strength and compressible = supports and cusions the enamel rods so stops them fracturing
Why are rod boundaries visible histologically
Gaps caused by the uneven packing of the rods contain more matrix so change in light diffraction/change in optical density = visible.
What direction/orientation/shape do the enamel rods run in
From the ADJ to the surface, in a wave.
What are incremental lines and give 3 examples
When the enamel temporarily stopped mineralising.
Daily incremental lines - finest
Brown striae of retzius - darker
Neonatal line - only in teeth that were mineralising at birth e.g. 6, 1, 2, primary teeth.
What are enamel lamellae
Fractures of the enamel. Travel in the same direction as the prism boundaries.
What are enamel spindles
Where the processes of the trapped odontoblasts continued to grow into the enamel.
What are enamel tufts
Areas of hypomineralisation by the ADJ
Enamel clinical applications
- Restorations
- Fluorides effect on enamel
- Saliva on enamel
- Need to create a rough surface on enamel so that the amalgam can mechanically attach. Adding phosphoric acid = the acid dissolves the surface of the rods with a greater surface area/at more of an angle than the verticle one = an uneven surface.
- Fluoride reduced the critical pH and makes the crystal lattice tighter.
- Exchange of ions from saliva to the enamel (e.g. Ca and PO4) allows some remineralization of early caries.
- The best time to add fluoride to the tooth is when the enamel is maturing.
Development defects of enamel
- Due to fluoride e.g. fluorosis = too much fluoride kills the enamel matrix proteins and they don’t get removed making the enamel less mineralised/more porous.
- Hypomineralisation = less mineralised
- Hypoplasia = less enamel
- Intrinsic discolouration
Components of un-mature enamel matrix
Amelogens = Get destroyed and taken out and replaced w water which CaHAP crystals grow into.
Enamelin proteins = become mature enamel proteins.
In a 20:1 ratio.
30% mineralised.
Pulp and tooth response to trauma - potential outcomes
Necrosis = pulp death but breakdown products not removed so it goes black.
Fracture = Infection can track in via now-empty tubules.
Pulpitis = Due to excessive heat, toxins, chemicals, infections.
Avulsion = tooth can be reinserted if PDL and fibroblasts still alive. Vessels can be reinserted through the apical foramen surgically if it is large enough.
Tertiary dentine - reparative or reactionary.
Pulp and tooth trauma treatments
Pulp cap
- Dentine bridge
- Reparative dentine
- Add sodium hydroxide to kill bacteria and stimulate odontoblasts to reactivate.
- Biodentine stimulates pulp cells to differentiate.
- MTA alkali forms a strong layer on the tooth when it sets.
Remove the pulp +/- the tooth = to allow the bone to repair.
Prevention of trauma
- Filling the cavity so pulp not exposed = less chance of pulpitis.
- Gum shield
- Effective cooling system to prevent trauma due to heat.
Progression of toothache/pain due to pulpitis
- Irreversible pulpitis
- Pulp necrosis
- The pain goes away as pulp dies
- Formation of an abscess
- Pain returns
- Removal of the pulp
Cementum innervation, vascular-ness
Not innervated and avascular so not labile e.g. hormones don’t reach it so doesn’t usually remodel, resorb, etc.
Development of cementum
Epithelial root sheath secretes a thin hyaline (of Hopewell-Smith) layer = intermediate/primary cementum.
This induces the dental follicle cells to differentiate into cementoblasts and fibroblasts.
Cementoblasts make acellular cementum first, then alternating cellular/acellular layers.
Acellular cementum features
Produced by cementoblasts
Thinner layer, found in cervical/middle 1/3.
Featureless but may be able to see thin lines where PDL/Sharpay’s fibers insert.
Intrinsic fibers lay parallel to root surface.
Cellular cementum features
Contains cementocytes (trapped cementoblasts) which are dynamic and communicate w each other via canal network
Apical 1/3 of the tooth.
Gets larger with age.
Forms faster than acellular because tooth erupts faster once it’s in the mouth.
Processes face acellular space.
2 categories of PDL fibers
Main/Sharpey’s fibers = embedded in the calcified matrix and incorporated in cementum
Other = dense irregular network of fibers in the matrix.
Types of cementum problems
Hypercementosis
Cementum resorption
Hypercementosis
Due to pulp disease, excess occlusal stress, or hereditary e.g. Paget’s disease.
Cementum lumps form on PDL making it harder to extract the tooth (bc wider apex)
Cementum resorption
Excess occlusal stress or orthodontic movement.
Vitamin A or D deficiency.
Pressure due to tumor or cysts.
If the cause of resorption is removed, cementum may be deposited again.
Ankylosis
Cementum and bone mix so tooth bound to the alveolar bone (PDL disappear)
Cementum callus
Irregular/ disorganized laying of cementum e.g. after a fracture
Alveolar bone features
Outer cortical plates = compact bone, with cancellous bone between them.
Different from normal compact bone because lacks Haversian’s systems and has collagen bundles.
Inner cortical plate/bundle bone is perforated so PDL inserts into it and vascular/neural communication bw PDL and trabecular space.
Has alveolar crests and neurovascular bundles.
Changes in bone
Always remodeling e.g. responds to mechanical stress - needs Pi and Ca ions.
Remodels if a load is applied to it because it is highly mineralized.
PDL features
Insert from cementum to the gingiva, alveolar bone or adjacent tooth to support the tooth and absorb masticatory loads.
Many orientations to absorb the maximum load.
Derived from ectomesenchyme.
A reservoir of cells that bone and cementum are derived from so used to repair and maintain them = allows remodeling.
Varying thickness:
- thinnest around level of rotation
- thicker around apex and mouth of the socket
- Get thinner with age
- gets thicker if under more tension
3 Types of gingival fibres
Dentogingival
Alveologingival = alveolar crest to gingivae.
Circular = goes all around the tooth.
CT/ fibre structure of gingiva
Soft CT = gingival corium.Gingival fibres insert into this and attach gingiva to the neck of the tooth.
PDL CT
Collagen fibres in gingiva run into the cementum or merge with the PDL.
CT/ fibre structure of gingiva
Soft CT = gingival corium.Gingival fibres insert into this and attach gingiva to the neck of the tooth.
PDL CT
Collagen fibres in gingiva run into the cementum or merge with the PDL.
Types of gingivae
Attached = stops the free gingiva coming away from the tooth
Free gingiva.
Interdental = concave and site of stagnation.
Gingival papilla = cone-shaped and fill the space between the interdental space.
Marginal.
The dental follicles role in eruption
- Stellate reticulum signals to the dental follicle to release growth factors to begin tooth eruption.
- Monocytes invade the coronal part of the DF and differentiate into Osteoclasts which degrade the bone above the crypt, forming an eruption pathway.
- The basal part of the DF releases BMPs = formation of osteoblasts = alveolar bone growth = a force to push the tooth up.
What is a crypt
A bony cavity enclosing a developing tooth, formed by the dental follicle. Has an opening at the so dental follicle fibers can communicate w oral mucosa.
Pre-eruptive movement
Happens in the jaw, and begins during crown formation.
Crown moving all the time as Mx, Md, crypts, adjacent teeth and roots form.
Eruptive movement
- Crown needs to be in the right position
- Roots begin to form - dentine, pulp, more fibrous tissue.
- Occlusal movement of crown within the crypt, until it reaches the mucosa. REE fuses with the epithelium.
- Crown penetrates through the fused epithelium layers.
- Intraoral occlusal movement, until the crown reaches the opposing tooth.
Alveolar bone and roots are growing.
Post-eruptive movement
To maintain occlusion e.g. as jaws develop, or to compensate for erosion or tooth wear.
What types of orthodontic tooth movements are there?
Tipping
Bodily movements
Rotation
Intrusion/extrusion
How does orthodontic tooth movement occur
Cycles of movement and rest.
Pressure applied to the bone on the side we want to move it to causes the activation of Oc which resorb the bone = clearing a path.
The tension in PDL on other side causes the activation of Ob so new bone gets made.
What are the general types of post-eruptive tooth movements
Exfoliation
Approximal drift
Orthodontic movement
Why does approximal tooth movement occur
- Force applied e.g. the anterior component of masticatory force.
- Loss of the opposing tooth = supraocclusion/super-eruption or drifting.
- Naturally, all teeth move towards the midline = crowding
How does exfoliation occur
As the underlying bone develops, it puts an upward pressure on the tooth causing resorption of the root cementum and dentine + loss of PDL = a wobbly tooth.
What are the disadvantages of approximal tooth movement
Aesthetic reasons
Loss/reduction in function
Harder to clean/poorer oral health
What happens if too much force is applied during orthodontic movement
- The rate of PDL broken > rate of new fibres made = inflammation and resorption of the tooth apex.
- Hyalinization of the PDL = avascular and translucent.
Why is it necessary to wear a retainer after orthodontic treatment.
To allow the cells to recover and consolidation of the bone in the new socket.
What are 2 types of alveolar bone loss resulting in root exposure.
Bone fenestration = a hole in the bone e.g. not coronally.
Bone dehiscence = loss of the bone covering the root, starting/inc coronally.
Treatment options for severe diseases of the periodontium
Smoking cessation advice.
Scaling and other general treatments.
Regenerative therapy e.g. encouraging ectomesenchyme cell to differentiate by using proteins and growth factors etc.
Using bone materials e.g. mineralized part of bovine bone or collagen from porcine bone (Bio-Oss, Bio-Gide, Emdogain)
Types of PDL fibre groups
Principle Horizontal Interradicular Apical Dentogingival Alveolodental Trans-septal
Principle PDL fibers features
Oblique orientation
Bone to cementum
Axial load bearing
Horizontal PDL fibers features
Horizontal orientation
Bone to cementum
Tilting load bearing
Trans-septal PDL fibers features
Horizontal orientation
Cementum to cementum
Hold teeth together
Interradicular PDL fibers features
Radial orientation
Cementum to bone
Space packing
Apical PDL fibers features
Radial orientation
Cementum to bone
Protect the apical nerves and vessels
Dentogingival PDL fibers features
Oblique orientation
Cementum to gingiva corium
Keep gingivae attached
Alevolodental PDL fibers features
Oblique orientation
Bone to gingiva
Keep gingivae attached
