CTB Theme 2 Flashcards
what are the 3 phases of tooth development
initiation
morphogenesis
histogenesis
what is determined in initiation and how is it characterised
the tooth position
appearance of tooth germs
what is determined in morphogenesis and how is it characterised
tooth shape
cell proliferation and movement
what is formed in histogenesis and how is it characterised
dental tissues
cell differentiation and specialisation (e.g. odontoblasts and ameloblasts)
what occurs firstly in tooth initiation
primary epithelial band forms
thickening of oral epithelium
condensation of mesenchymal cells
when is the primary epithelial band formed
6 weeks in utero
what causes the thickening of the oral epithelium
the cells divide downwards thickening the epithelial band
what are the 2 types of lamina formed in tooth initiation
dental and vestibular lamina
in what direction do dental and vestibular lamina form
dental - lingually
vestibular- buccally
how is vestibular lamina formed
epithelial cells proliferate and the central cells subsequently enlarge and degenerate to produce the sulcus of the vestibule
what occurs in tooth morphogenesis
formation of the tooth bud
when is the tooth bud formed
8 weeks in utero
what occurs in the bus stage of tooth morphogenesis
elongation of dental lamina
formation of localised swellings
condensation of mesenchymal cells surrounding the tooth bud
what occurs in the early cap stage
enamel organ develops
cap not completely formed
when does the early cap stage occur
11 weeks in utero
when does the late cap stage occur
12 weeks in utero
how does the enamel organ form
dental epithelium forms a cap shaped structure, the enamel organ
what forms the enamel knot
a group of non-dividing epithelial cells
what is the function of the enamel knot
a transient molecular signalling centre. can send instructions to surrounding cells to induce changes in shape
what forms the dental papilla
condensed mesenchymal cells underlying the enamel organ
what forms dental follicle
mesenchymal cells surrounding the enamel organ
what does the dental papilla form
pulp
what does the dental follicle form
periodontal tissue
when does the early bell stage form
14 weeks in utero
what is the enamel organ distinguished by
outer enamel epithelium
with cuboidal epithelial cells
what is the stellate reticulum
group of star shaped cells in the centre of the enamel organ and synthesise glycosaminoglycans
what are the intracellular spaces filled with when epithelial cells get separated in morphogenesis
glycosaminoglycans and collagens I, II, III (ECM)
what are the characteristics of inner enamel epithelium
columnar
the epithelial cells differentiate into ameloblasts later
what happens to the mesenchymal cells of the dental papilla and dental follicle in morphogenesis
they continue proliferating
what is the stratum intermedium
2-3 layers of flat epithelial cells that form between inner enamel epithelium and stellate reticulum
what does the stratum intermedium produce
alkaline phosphatase
- mineralisation of enamel matrix
what is the stratum intermedium involved in
protein synthesis, transport of substances to and from inner enamel epithelium (epithelium)
-ameloblasts supporting function
what happens to the dental papilla in tooth morphogenesis
generates fibroblasts and mesenchymal stem cells of the pulp, and odontoblasts
what happens to the dental follicle in tooth morphogenesis
it supports the enamel organ with nutrients and generates tooth supporting tissues
when does the late bell stage occur
18 weeks in utero
what happens to the tooth in the late bell stage
its acquired its future shape
what happens to the stellate reticulum in the late bell stage
it moves downwards which helps protect the cellular area of the developing tooth
what is the cervical loop
the growing end of the enamel organ (cell interactions)
where is the cervical loop located
where the IEE and OEE meet and is later involved in root formation
what happens when the dental lamina breaks down in the late bell stage
enamel organ loses contact with oral epithelium
what are odontoblasts and what do they do
they’re dental papilla cells and secrete predentine that mineralises and forms dentine
what are ameloblasts and what do they do
they’re inner enamel epithelial cells that secrete preenamel that mineralises and forms enamel
what does the stratum intermedium produce
alkaline phosphate and support the enamel
what does the stellate reticulum do
protects and maintains tooth shape
what does outer enamel epithelium do
maintains tooth shape and exchanges substances with dental follicle
what are the reciprocal tissue interactions in crown formation
- inner enamel epithelium (IEE) separated from dental papilla cells by a cell-free zone
- IEE cells become elongated and secrete signalling molecules to induce odontoblast differentiation from dental papilla cells.
- odontoblasts align and produce predentine
- Signals from odontoblasts (in the predentine) induce differentiation of pre-ameloblasts into ameloblasts that start producing pre-enamel.
Dentine produced first and enamel later due to this interaction
how is the IEE separated from the dental papilla cells
by a cell free zone
how is odontoblast differentiation induced from dental papilla cells
IEE cells become elongated and secrete signalling molecules to induce odontoblast differentiation from dental papilla cells
how is differentiation of pre-ameloblasts into ameloblasts induced
by signals from the odontoblasts in the predentine
what do ameloblasts do
produce pre-enamel
is dentine or enamel produced first? why?
dentine, as signals from odontoblasts are what cause ameloblast formation
how is the crown protected after completion
root formation begins
reduced enamel epithelium(REE)
how is REE formed
from flattened ameloblasts and remnants of the enamel organ
how does REE protect the tooth crown after completion
protects enamel of erupting tooth from being attacked by osteoclasts which remodel the jaw bone once the tooth erupts
how is enamel space caused
by demineralisation of enamel during tissue processing
pre-enamel is only partially mineralised, what does this mean for the enamel proteins after demineralisation
they remain afterwards
in which direction do successional tooth germs of the permanent teeth bud off from the dental lamina, and what happens to them
lingually (not molars)
they stay dormant until further tooth development is initiated
how are permanent molars formed since they have no primary predecessors
they are formed by posterior growth of the dental lamina
what does the backward extension of dental lamina give off in the formation of permanent molars
gives off epithelial buds which form the molars
when are the first molars formed
4 months in utero
when are the second molars formed
6 months in utero
when are the third molars formed
4-5 years after birth
what are the components of the tooth germ
enamel organ
dental papilla
dental follicle
what are the cells of the enamel organ
cervical loop outer enamel epithelium stellate reticulum stratum intermedium inner enamel epithelium
what are the cells of the dental papilla
odontoblasts
undiff. mesenchymal cells
fibroblasts
what are the cells of the dental follicle
cementoblasts
fibroblasts
osteoblasts
what are ex of ectodermal appendages
mammary glands salivary glands teeth hair tongue papillae
what is the function of the enamel knot
signalling centre determining the shape of the tooth
what does the number of enamel knots correspond to
the number of cusps
how can an experiment be carried out to determine the odontogenic potential
- dissection of mandibular arch
- enzymatic digestion to isolate epithelial and mesenchyme
- recombination of epithelium and mesenchyme followed by in vitro culture
- transplantation of tooth germ into kidney capsule and in vivo culture for 2-3 weeks
- tissue analysis
what is meant by the odontogenic potential
capability of a tissue to induce gene expression in an adjacent tissue and to initiate tooth development
where is the odontogenic potential at the initiation stage
its on the epithelium (epithelial signalling)
where is the odontogenic potential at the bud stage
is on the mesenchyme
mesenchymal signalling
how do we know that the odontogenic potential for the initiation stage is on the epithelium
because after 11 days there is no tooth formation when dental mesenchyme instructs non-dental epithelium, however there is tooth formation when the dental epithelium instructs the non-dental mesenchyme
how do we know that the odontogenic potential for the bud stage is on the mesenchyme
because after the 13 days, when the bud has formed, the dental epithelium cannot instruct the non-dental mesenchyme to form a tooth, however after 13 days the dental mesenchyme can instruct the non-dental epithelium
how is a transcriptional response induced in the dental mesenchyme
by overlapping gradients of the morphogens: FGF, BMP in the dental epithelium
what does the initiation stage signalling determine
tooth position
which cells will form a tooth
only those that express PAX 9
what does mesenchymal signalling by the dental mesenchyme in the bud stage secrete and induce
secretes signalling molecules (FGF, BMP) and induces the formation of the enamel knot in the dental epithelium
what signalling occurs in the cap stage
enamel-knot signalling
what does enamel knot signalling induce
cell cycle arrest within the enamel knot but induces cell proliferation in surrounding cells
which signalling molecules induce cell cycle arrest & proliferation (2 separate molecules)
BMP- cell cycle arrest
FGF- cell proliferation in surrounding cells
where does FGF bind in the cap stage
to epithelial cells bordering the enamel inducing cell proliferation directed downwards
in which key genetic regulator would tooth development be arrested at an early stage to give rise to Ectodermal dysplasia
EDA1/EDAR
in which key genetic regulator would tooth development be arrested at an early stage to give rise to hypodontia
PAX9 and MSX1
what is the odontogenic homeobox code tell
a hypothesis for specification of tooth identity
what is the evidence for an odontogenic homeobox code
mandibular molars will still form if you remove the DLX gene for maxillary molars as they have different genes which can compensate for the loss of DLX 1 and 2
Also an expressed molar gene Barx 1 in the incisor region will transform the incisor into a molar as it overrides the Msx1 incisor gene
what do defects during initiation affect
tooth number and identity
what are examples of defects that have occurred during initiation
ectodermal dysplasia, hyperdontia
what do defects during morphogenesis affect
tooth number, shape and size
what are examples of defects that have occurred during morphogenesis
hypodontia, hyperdontia
what do defects during cell differentiation and histogenesis affect
hard tissue formation
what are examples of defects that have occurred during cell differentiation and histogenesis
amelogenesis imperfecta, dentinogenesis imperfecta
what other dental anomalies can various cellular defects cause
eruption
replacement
tumours
what are examples of defects that have occurred as a result of various cellular defects
osteopetrosis
eruption cysts
odontomes
what are characteristics of early defects (development)
missing teeth
supernumerary teeth
abnormalities of tooth shape and size
what are examples of late defects (cell differentiation)
anomalies in structure of teeth-dentine
anomalies in structure of teeth- enamel
anomalies of teeth eruption and/or resorption
what are syndromic defects
dental defects seen in combination with other anomalies
what are non-syndromic defects
dental defects are not associated with other anomalies (only the dental tissue is affected
what is associated with non-syndromic hypodontia and oligodontia
missing teeth e.g.
premolars, lateral incisors, peg shaped tooth
what is associated with syndromic oligodontia
Hypohidrotic ectodermal dysplasia (→ Eda1) Rieger syndrome(→ Pitx2) Oligodontia-colorectal cancer syndrome (→ Axin2)
which teeth are most likely to be missing caused by MSX1 mutation
5s and 8s
which teeth are most likely to be missing caused by PAX9 mutation
7s and 8s
what is the multidisciplinary team approach to manage hypodontia
Orthodontist Child Dental Health dentist Restorative dentist Maxillofacial Surgeon Psychologist Geneticist
what are treatment options for hypodontia
open spaces for bridges or implants
close spaces using orthodontic devices
what gene mutation causes hyperdontia (supernumerary teeth)
RUNX2
what occurs in hyperdontia
bone defects and craniofacial malformations
enamel hypoplasia, delayed eruption, malocclusion
Dentigerous cysts
normally, what happens to the dental lamina at the bell stage
it breaks down
what happens if there is incomplete removal of epithelial remnants
supernumerary teeth
eruptions cysts
odontomes (bening tumours)
what do eruption cysts do
they block the eruption pathway
what happens if remnants of dental lamina are not removed
they can receive signals from the dental follicle and abnormal cysts can form
what is an odontome composed of
bone, dentine, soft tissue
what is hypoplasia
affects enamel matrix formation- reduced enamel thickness
what is hypomineralisation
normal enamel thickness but decreased enamel thickness
what is hypomaturation
normal enamel thickness but mottled and softer
what are the inheritance patterns for amelogenesis imperfecta
autosomal dominant
autosomal recessive
x-linked forms
what are the gene mutations in amelogenesis imperfecta
AMELX, ENAM, MMP20, KLK4, DLX3, FAM83H, WDR72
what is dentinogenesis imperfecta
defects in dentine formation (odontoblasts)
what do teeth look like in dentinogenesis imperfecta
Blue-gray or amber brown, opalescent teeth
Bulbous crowns and short narrow roots; obliterated pulp chambers
what is the dentine like in dentinogenesis imperfecta
Soft dentine => Enamel chipping => Teeth wear down rapidly
what are the inheritance patterns for dentinogenesis imperfecta
autosomal dominant
what are the gene mutations in dentinogenesis imperfecta
DSPP (DSP, DGP, DPP)
how can dentine be classified
by time of development or by anatomical location/histology
what are the types of dentine that develop over time
pre-dentine
primary dentine
secondary dentine
tertiary dentine
what is pre-dentine
an unmineralised dentine matrix secreted by odontoblasts
what is primary dentine
all dentine until the completion of root formation
when does secondary dentine form and what is it associated with
after root completion/eruption
ageing- in time it will reduce the pulp chamber and root canal size
when is tertiary dentine produced
in response to an external stimuli (attrition, caries, cavity preparation etc).
what is tertiary reactionary dentine
when original odontoblasts function in dentine deposition , produce few tubules (slow response=weak stimuli/injury)
what is tertiary reparative dentine
when odontoblasts die and are replaced by newly recruited odontoblast-like cells induced from pulp stem cells. deposit dentine with very little structure (rapid response=severe injury)
what are the types of dentine that can be classified by anatomical location/histology
coronal dentine
root dentine
what are the types of dentine classified by anatomical location
coronal dentine (in crown) root dentine
what are the types of coronal dentine
mantle dentine
circumpulpal dentine
what is mantle dentine
outermost layer of crown dentine, forms first
what is circumpulpal dentine and what are its 4 types
forms the bulk of the crown
- interglobular dentine
- intertubular dentine
- intratubular/peritubular dentine
- sclerotic dentine
what is interglobular dentine
a type of circumpulpal dentine- it forms when dentine is mineralised rapidly
what is intertubular dentine
a type of circumpulpal OR root dentine - it forms between dentinal tubules
what is intratubular/peritubular dentine
a type of circumpulpal OR root dentine- forms inside dentinal tubules
what is sclerotic dentine
a type of circumpulpal OR root dentine - caused by complete obliteration of dentinal tubules
what are the layers of root dentine
Hyaline layer
Granular layer of Tomes
what is the Hyaline layer
the outermost layer of root dentine
what are the chemical properties of dentine (by weight)
70% inorganic: calcium hydroxyapatite crystals
20% organic: mainly collagen fibrils
10% water
its less mineralised than enamel
where do hydroxyapatite crystals form and how do they appear (inorganic matter)
form between type 1 collagen fibrils
appear as uniform small plates (smaller than those in enamel)
what type of collagen forms in the organic matrix
mainly type 1 collagen (90%) and some type III- rest are traces of type V and VI
how do type I and type III collagen form a network
type I are linear and type III are reticular which link them together
what makes up the organic matrix
collagen fibrils proteoglycans glycoproteins phosphoproteins growth factors
what are the glycoproteins involved in the mineralisation process of dentine
osteonectin, osteopontin and dentine sialoprotein (DSP)
what are the phosphoproteins in the organic matrix of dentine
dentsialoprotein
dentoglyco protein
dentphospho protein
what gene makes the 3 phosphoproteins in the dentine organic matrix and how
dentine phosphoprotein gene (DPP) via proteolytic cleavage
what are the growth factors in the dentine organic matrix and what is their function
transforming growth factors (TGF)
bone morphogenic proteins (BMP)
released and travel down tubules and stimulate repair in caries
what are the properties of dentine
softer than enamel higher tensile strength than enamel more resilient (elastic) than enamel (supports brittle enamel) porous (dentinal tubules) sensitive (pulp innervation) reactive to damage (tertiary dentine)
how can pulp dentine respond to structure and physical properties especially changes with age
its a living organ
how does dentine appear on a radiograph compared to enamel
its less radiopaque
how does the dental pulp appear on a radiograph
radiolucent
when does dentine formation begin
at the late bell stage at the cusp tip
what are odontoblasts
mesenchymal cells derived from dental papilla (form dental pulp), they differentiate when receiving molecular signals from pre-ameloblasts
what is a sub odontoblast cell
a daughter cell from the division of ectomesenchymal which HAS NOT been exposed to epithelial influence to differentiate into an odontoblast
what is the first step in the formation of pre-dentine
formation of large von Koff’s fibres (type III collagen) at 90 degrees angle to the EDJ
what occurs after the formation of von Koff’s fibres in dentinogenesis
odontoblasts odontoblast secrete smaller type 1 collagen fibres parallel to the EDJ
what occurs after smaller type 1 collagen fibres are secreted in dentinogenesis
the odontoblasts secrete matrix vesicles (mv) than contain highly concentrated calcium phosphate ions (mineralisation)
what is the unmineralised area between the odontoblast layer and mineralising front termed
pre-dentine
what do odontoblasts develop in dentinogenesis
cell processes
where does initiation of mineralisation in dentinogenesis occur
within the matrix vesicle
how is the mineralising front formed in dentinogenesis
mineralisation occurs within the matrix vesicle secreted by odontoblasts, causing crystallites to burst out and form the mineralising front
what are matrix vesicles and where are they secreted
small (25-250nm) membrane bound vesicles produced by odontoblasts, its secreted into the dentine matrix surrounding odontoblasts
what do matrix vesicles contain
phospholipids that bind to calcium
alkaline phosphates
what do the alkaline phosphates from matrix vesicles do
increase phosphate concentration and destroys the inhibitor of mineralisation (pyrophosphate)
are matrix vesicles involved in the mineralisation of circumpulpal dentine
they have only been observed during mineralisation of mantle dentine. Therefore, they may or may not be involved with mineralisation of circumpulpal dentine
what suggests that collagen is not responsible for initiating mineralisation
there is no mineralisation in or near the collagen fibres
why does the thickness of predentine remain constant
because the amount that calcifies is balanced by the addition of new unmineralised matrix
what are the 2 patterns of dentine mineralisation
linear or globular depending on the speed of dentine formation
where is globular calcification found
in the mantle dentine, where the mineralisation occurs by the matrix vesicles
what type of calcification is found in the circumpulpal dentine
linear and globular calcification both occur depending on the rate of dentine deposition
when dentine deposition is fast, what mineralisation occurs in circumpulpal dentine
globular
when dentine deposition is slow, what mineralisation occurs in circumpulpal dentine
linear
what forms within the collagen matrix in globular calcification
calcospherites (globular masses of mineralised dentine)
they form within collagen matrix and increase in size until they fuse to form a single calcified mass
what happens if globular calcification proceeds fast
incomplete fusion of calcospherites results in formation (of the hypomineralised) interglobular dentine
where can interglobular dentine be found
in the upper third of circumpulpal dentine
what are enamel spindles
formed from an odontoblast process that has intercalated between two ameloblasts and extends into the enamel (it doesnt follow the path of enamel prisms)
what is enamel tuft
hypomineralised region in the enamel which follwos he
what does the scalloping of dentine allow for
increased surface area of the EDJ which enables a tighter interlocking between enamel and dentine
what does the excessive branching of dentinal tubules at the EDJ allow for
increased sensitivity as the odontoblast processes are involved in sensation of whats going on outside of the tooth
what are the types primary curvature of dentinal tubules
s-shaped
linear
where do s-shaped dentinal tubules occur and why
in coronal dentine due to the crowding of the odontoblasts because they are pushed apically as dentine grows inwards towards the pulp
where do linear dentinal tubules occur and why
in the cervical dentine of the crown and in root dentine because little or no crowded results from decrease the surface areas, and tubules run in a straight course
what is the secondary curvature of dentinal tubules
slight changes in tubule direction during dentine deposition creating wavy tubules
what are the 2 types of dentine incremental growth lines
von Ebner lines -short period/daily
Adresen lines - long period
what are the characteristics of von Ebner lines
daily equivalent to cross striations in enamel weakiler defines with a closer spacing dentine deposited daily each line is 3-4 microm
what are the characteristics of Andresen lines
long period equivalent to striae of Retzius in enamel more sharply defined with wider spacing each line 20 micrometers 6-10 short period lines
when does a contour line of Owen form in dentinal tubules
when secondary curvature is pronounced and coincides in adjacent tubules
what causes a contour line of Owen form
metabolic stress during dentine formation
what are owen lines
accentuated incremental growth lines (von Ebner lines) and are hypomineralised
what is the most prominent incremental growth line
the neonatal line due to the disturbances of dentine formation by the birth process
what do the accentuated owen lines correspond to
accentuated lines in enamel
where is secondary dentine found
mostly on roof and floor of pulp chamber
what is intratubular dentine (peritubular)
forms within the dentinal tubule and lines the inner surface as a hyper mineralised layer of dentine (40% more mineralised than the surrounding dentine)
what is intertubular dentine
can be any primary or secondary dentine
dentine between the dental tubules
contains a dense network of type I collagen fibrils in which HA are deposited
less mineral than intratubular dentine
what is sclerotic dentine
continued formation of intratubular dentine leads to obliteration of the dentinal tubules. if complete the dentine is termed sclerotic dentine
why does sclerotic dentine appear transparent in ground sections
due to increased mineralisation
what are dead tracts
when dentinal tubules have lost their odontoblast processes following death of odontoblasts or retraction of processes, the tubules become empty and air-filled, and appear as a dark lines in ground sections
why does sclerotic dentine increase with age
in areas of attrition & caries of the enamel => Protection of the pulp against invading microorganisms.
what are the two explanations for Tomes’ granular layer
- extensive branching and backward looping of odontoblast processes
- incomplete fusion of calcospherites
when does amelogenesis occur
at the late bell stage, morphological changes occur in the enamel organ
how do Inner enamel epithelium cells differentiate into ameloblasts
receive signals from odontoblasts (in the predentine)
once ameloblasts are formed what do thy do
secrete enamel matrix which forms the aprismatic initial enamel layer
what 2 events can amelogenesis be characterised by
enamel secretion
enamel maturation
what occurs in enamel secretion in ameolgenesis
enamel matrix secreted by ameloblasts is partially mineralised (30%)
what occurs in enamel maturation in amelogenesis
When enamel is fully formed, the mineral content increases to about 96%. Enamel crystals grow wider & thicker at the expense of the organic content and water which is gradually removed
wha are the 3 stages for the life cycle of ameloblasts
presecretory
secretory
maturation
what can the presecretory stage be divided into in amelogenesis
morphogenetic stage
histodifferentiation stage
what can the secretory stage be divided into in amelogenesis
Initial secretory stage without Tomes’ process
Secretory stage with Tomes’ process
what can the maturation stage be divided into in amelogenesis
Ruffle-ended ameloblasts
Smooth ended ameloblast
Protective stage
what occurs in the morphogenetic phase in amelogenesis
IEE cells have a cuboidal shape
basal lamina produced by IEE separates IEE from the dental papilla
late bell stage: predentine produced by odontoblasts, ameloblast differentiation
what occurs in the differentiation phase
in amelogenesis
IEE cells differentiate into ameloblasts
what happens to the pre-ameloblasts in the differentiation phase of amelogenesis
Preameloblasts elongate and become columnar; cell nuclei are located proximally towards the stratum intermedium (→ establishment of polarity)
when ameloblasts are fully differentiated what do they do
synthesise enamel proteins
what happens to the basal lamina in the differentiation phase of amelogenesis
Basal lamina between ameloblasts and odontoblasts is removed as its where dentine and enamel have formed
what occurs in the initial secretory stage of amelogenesis
Ameloblasts elongate and secrete enamel matrix, form an (aprismatic) initial layer of enamel
Enamel has lines, not enamel prisms (as its produced by ameloblasts without tomes process)
what occurs in the secretory stage of amelogenesis
the ameloblasts form tomes’ process (proximal and distal portion)
what does the proximal portion produce in the secretory stage of amelogenesis
interprismatic enamel (‘interrod’ enamel)
what does the distal portion produce in the secretory stage of amelogenesis
produces prismatic enamel (‘rod’ enamel)
what happens when the outermost layer of enamel is formed in the secretory stage of amelogenesis
Ameloblasts become shorter, lose the distal portion of Tomes’ process → form a thin aprismatic enamel layer (similar to the initial enamel layer)
what happens as the enamel thickness increases in the secretory stage of amelogenesis
Distal portion of Tomes’ process develops from proximal portion. It elongates, becomes thinner and is located between prismatic & interprismatic enamel
what are the enamel matrix components
amelogenins
non-amelogenin proteins
what are the characteristics of amelogenins
90% matrix component
Low molecular weight
roles in regulating growth and thickness of enamel crystals
Form nanospheres
Selectively removed by proteolytic enzymes
provides scaffolding allowing controlled mineralisation of enamel
what proteolytic enzymes are amelogenins removed by
enamelysin (MMP20) and kallikrein 4
what are the characteristics of non-amelogenin proteins
secreted first but rapidly processed by proteolytic enzymes
10% of matrix content
Form the enamel sheath
Larger proteins: Ameloblastin (70 kDa), Enamelin
amelotin
what is the function of ameloblastin
facilitates adhesion of ameloblasts to enamel matrix
what is the function of enamelin
promotes and guides formation of enamel crystals; least abundant protein
what is amelotin
basal lamina protein; involved in adhesion of junctional epithelium to enamel
how is the maturation stage of ameolgenesis characterised
by growth in width and thickness of pre-existing crystals (hardening of enamel)
what are the phases of the maturation phase in amelogenesis
transitional phase
maturation proper (phase)
cyclic modulation of ameloblasts
what occurs in the transitional phase of maturation
After the enamel layer has been fully formed:
- Decrease in height & volume of ameloblasts
- 50% ameloblasts die by apoptosis
what occurs in the maturation proper phase of maturation
Removal of water and proteins from the enamel matrix
Transport of ions is required for the increase in mineral content
what occurs in the cyclic modulation of ameloblasts in maturation
ruffle-end and smooth-ends alternate
this increases mineral content (ruffle ended) and removal of organic matrix (smooth-ended)
how do ruffle ended (80%) ameloblasts allow selective transfer of calcium ions into the enamel and prevent material in interstitial space
there leaky junctions between ameloblasts at proximal (basal) end; tight junctions at distal (enamel) end;
what are the characteristics of smooth ended ameloblasts
20%
leaky junctions at distal end
enamel protein fragments and water leave the maturing enamel
trace elements
where does the ISF travel in smooth ended ameloblasts
leaks into enamel layer – when cells pump positive ions into a place this is accompanied by H+ which decrease the pH
what do the trace elements in the ISF do (smooth ended ameloblasts)
e.g. strontium and fluoride enter the enamel layer and increase hardness
where is the enamel layer most mineralised
at the occlusal surface
mineralisation decreases towards the EDJ
why are primary teeth less mineralised than permanent
because the maturation phase is shorter
what contributes to the dynamic cycle of enamel demineralisation and remineralisation
acid (from food, stomach or of bacterial origin) causes mineral loss
bicarbonate ions from saliva cause remineralisation (pH buffering), allows other ions like fluoride to incorporate into the tissue
what occurs in the protective stage of amelogenesis
reduced enamel epithelium(REE) forms inactive (cuboidal) ameloblasts and remnants of the enamel organ (‘papillary layer’)
what does the REE do
it covers the tooth crown and protects the enamel from being resorbed by osteoclasts that resorb bone as part of the eruption process or from abnormal cementum deposition
what is the additional function REE has in tooth eruption
forms the junctional epithelium
what are the clinical issues of fluoridation? how is this seen histologically
excessive consumption- “fluorosis”
- faint white opacities/severe pitting and discolouration
- histologically, high porosity in the outer third of the enamel
what are the benefits of water fluoridation
incorporation of fluoride ions into enamel crystals
enamel becomes more resistant to acid so reduction of dental caries
what is etching the enamel surface with acid beneficial for
adhesive dental restorative materials when removing plaque or a thin layer of enamel which would increase the surface area and create a better bonding surface for adhesive materials
what are white spot lesions due to
localised demineralisation of the enamel surface near the gingival margin or fissures
(can be arrested or progress to cavity formation)
when would abnormal enamel formation affect all teeth
ameogenesis imperfect, fluorosis
when would abnormal enamel formation affect individual teeth
- local (non-systemic) causes e.g. trauma or unknown aetiology.
- systemic causes affecting the teeth developing at time of this disturbance e.g. chronological /linear enamel hypoplasia, molar-incisor hypoplasia
how does enamel hypoplasia appear
as a groove or pit on the enamel surface
what does enamel hypomineralisation appear as
smooth surface but abnormal colour (less mineral; abnormal maturation)
what enamel defects affect all teeth caused by enviro/systemic factors
febrile disease
treatments with tetracycline
a chronic ingestion of fluoride ions
how does treatment with tetracycline cause enamel defects
it can be incorporated into mineralising tissues resulting in band or total brown pigmentation
what are enamel defects that affect all teeth caused by genetic factors
syndromic vs non-syndromic
pattern of inheritance: autosomal or x-liked, dominant or recessive
what is molar hypomineralisation (MIH)
associated with opacities and loss of enamel affecting teeth in the first year of life, the molars are fragile and can develop caries easily
when MIH more common
in children who have taken amoxicillin in the first year of life , usually for otis media
how does amoxicillin interfere with enamel
amoxicillin interferes with ameloblast function at the secretory stage and the temporal sequence of amelogenesis events.
what is linear enamel hypoplasia
It is a disruption to enamel formation that causes deep grooves forming on the surface of the tooth. Generally caused by poor nutrition during tooth development
what is the general structure of enamel
highly mineralised
96% inorganic contain
4% organic content and water
what origin is enamel
epithelial
what are the 2 steps in amelogenesis
1st formed enamel is only partially mineralised (30%)
the crystals grow whilst the organic matrix and water are lost
how does the thickness of enamel vary
it varies in thickness over different locations (thickest in . cusps, thinnest over cervical margin)
it varies in thickness between different teeth (increase from 1st to 3rd)
enamel is thicker in primary vs permanent
what are the properties of enamel
translucent extremely hard lacks resilience brittle resistant to abrasion resistant to sharing and impact forces low tensile strength
what are the components of enamel
96% mineral- calcium hydroxyapatite (HA)
3% organic - proteins
1% water
what do the HA crystallites combine to form
prisms separated by the inter-prismatic region
why is it clinically important to be aware that enamel is brittle and it is supported by the underlying dentine
when considering caries and cavity preparation
what is the orientation of the crystals in enamel like
not entirely uniform and differ for the prism and interprismatic region
wha are enamel prisms
the structural unit of enamel, millions in enamel (each prism=1 ameloblast)
where do enamel prisms grow from
the EDJ to the crown surface in layers
what are the three enamel prism patterns in cross section
- prisms circular
- prisms stacked
- keyhole pattern
which enamel prism pattern predominates in humans
3- keyhole
what is pattern 1 of enamel prisms
form with discrete rods surrounded by interprismatic enamel
what is pattern 2 of enamel prisms
discontinuities- rods in vertical rows with interrow sheets of interprismatic enamel
what is pattern 3 of enamel prisms
horseshoe shaped (keyhole); interprismatic attached to the tail below the head of the prism when seen in cross section
what does the keyhole pattern look like in cross section
a wide head towards coronal/occlusal surface
a narrow tail towards cervical
how many ameloblasts is each keyhole rod formed by
4
1- head
3- tail
what is the orientation of the crystals within the prism
parallel to the long axis of prism in head
oblique to the long axis of prism in tail (angled)
what does the prism sheath form
the boundary between rod and interprismatic enamel
what does the prism sheath contain
organic material
what is the prison direction (except from in cervical region)
from the EDJ to the surface like spokes of a wheel but with a 3D curve
what is the prism direction in cervical enamel in primary teeth
obliquely oriented towards the oral cavity
what is the prism direction in the cervical enamel in permanent teeth
obliquely oriented toward the alveolar crest
why is the direction of the rods important in cavity preparation
cavity prep must be done in the same direction as the rods
what is prisms decussation
bundles of enamel rods cross eachother as they travel from EDJ to the surface
what path do groups of enamel rods follow
sinusoidal
what is the benefit of prism decussation
it strengthens the enamel structure, prevents propagation of cracks into deeper areas of the enamel, and improves the resistance to fracture
what are Hunter-Schreger Bands
an optical phenomenon occurs in the inner two-thirds of enamel, as an alternating light and dark bands
what is the underlying mechanism responsible for Hunter-Schreger Bands
prism decussation
what are parazones
prism bands that are cut longitudinally (light zones)- reflective zones
what are diazones
prism bands that are cut transversely (dark zones)- transparent zones
what is gnarled enamel
an area with exaggerated prism decussation (extremely angular) over cusp tips
what causes gnarled enamel
the ameloblasts adapt to the rapidly expanding enamel surface and as the crown becomes larger, cohorts of ameloblasts are displaced apically by their own enamel production
where does scalloping occur
on the EDJ
what does scalloping do
increases the surface area for accommodating more ameloblasts where there is a large difference between EDJ area and crown surfaces area
what is the benefit of a scalloped enamel dentine junction
strengthens the attachment of enamel to dentine
prevents the shearing of enamel during function
less scalloped in primary vs permanent
what does prism decussation result in
hunter-schreger bands and gnarled enamel
what is the neonatal line
an incremental line that occurs at birth resulting from stress
how can the neonatal line be identified
its darker than other incremental lines
how does daily enamel secretion rate vary
it increases from the EDJ to the enamel surface in both permanent and primary teeth
how many micrometers is the inner, mid and outer enamel in permanent cuspal
2-3 inner
3-4 mid
4-5 outer
how many micrometers is the enamel from the EDJ to the surface in lateral primary enamel
2.5 to 4.5
by how much do daily enamel secretion rates drop by per day across the neonatal line in primary teeth
0.5 microns per day
what are cross striations (short daily lines)
DAILY secretion of enamel
how do cross striations form
they are the result of a daily variation in ameloblast secretion rate and mineralisation
what are cross striations (short daily lines) equivalent to in dentine
von Ebner lines however they are weaklier defined with a closer spacing
what are the Striae of Retzius (long period lines )
WEEKLY, wider lines, more defined and result from the ameloblast position at various points of time during development
what are the striae of retzius (long period lines) equivalent to in dentine
Anderson lines
how many short period lines are between 2 long period lines
7-10
what are accentuated striae
neonatal line also produced due to systematic disturbance
what is perikymata
- Perikymata is the outward aspect of internal growth increments
- Visible on teeth to naked eye
- The normal transverse wavelike grooves or lines on the external surface of the tooth
what are the enamel incremental growth lines
cross striations - short daily lines
striae of retzius- long period lines
perikymata
what do the striae of retzius represent
the growth of all the prisms at that increment
what are perikymata surface manifestations of
striae of retzius
what are hunter schreger bands related to
prism orientation
what are the structural defects of enamel
enamel tufts
enamel lamellae
enamel spindles
what are enamel tufts
hypomineralised voids following the direction of decussation
where are enamel tufts and what do they contain
inner third of enamel, start at the EDJ and project outwards
they contain organic material (mainly tuftelin)
how do enamel tufts appear
like lines and only travel for a short distance
what are enamel lamellae
when enamel tufts pass through the entire thickness of enamel (contain organic material)
enamel lamellae appear visually as cracks, how are they different
cracks are still mineralised enamel where as lamellae enamel is hypomineralised and they contain organic material
what are enamel spindles
formed from an odontoblast process embedded into the first zone of enamel, mainly in the cusp tips
why do enamel spindles not follow prism direction
Tomes’ process produces enamel at and an angle
what is enamel erosion
the chemical dissolution of dental hard tissues from acid that does NOT originate from bacteria (extrinsic or intrinsic acid) , resulting in irreversible tooth surface loss
what is the process by which enamel erosion occurs
- hydrogen ions dissociate from the acids & interact with the HA crystal causing dissolution (combine with carbonate/phosphate)
- this releases all ions from that region of the crystals creating the typical honey comb etched surface
- the core of the enamel prisms has been dissolved by the acid and the adjacent interprismatic areas appear more prominent
what is the connective tissue from the dental pulp derived from
mesenchymal cells of the dental papilla
what are the 2 types of pulp
coronal pulp and radicular pulp
what does the pulp open into through the apical foramen
the periodontal ligament
what does the dental pulp provide entry for
blood vessels- nourishment
nerves- sensation
lymphatic vessels- lymph drainage
why may there be 3 roots present instead of 2 and what problems can this cause
accessory canals present- they are the source of infection and inflammation
what is the dental pulp and whats it made up off
loose connective tissue made up of:
- ECM
- different cell types
- blood and lymphatic vessels
- nerves
what does the dental pulp contain
75% water
25% organic material
is there hard tissues in the dental pulp
usually no but calcifications and pulp stones can be found in the pulp of aged teeth
what are the histological zones of the dental pulp
odontoblast cell layer
cell free zone
cell rich zone
pulp core
where do nerve endings terminate
cell free zone
what is the shape and structure of odontoblasts
coronal are columnar
cellular processes reaching into the dentinal tubule
cuboidal in root
what happens to the odontoblast layer as the tooth matures
it becomes flatter and the number of cells is reduced by apoptosis
what does secondary dentine do
its laid at a slower rate after root completion and reduces the size of the space occupied by the dental pulp
how can tertiary dentine be produced
in response to external stimuli, odontoblast-like cells can differentiate from progenitor cells in the pulp
what are the types of junctions between odontoblasts
- tight junctions
- desmosomes
- gap junctions
what are tight junctions and desmosomes , what is there function
mechanical union between 2 cells
maintain spatial relationship
restrict substances in the pulp from entering the dentine
what do gap junctions allow for
openings allowing exchange of small molecules and cell-to-cell communication
what are fibroblasts most abundant
within the dental pulp (particularly in coronal & cell rich zone)
what do fibroblasts produce
the collagen fibres and ground substance of the pulp matrix
what can fibroblasts also do to collagen
degrade collagen (collagen turnover)
what are the characteristics of a young pulp
large, centrally located nucleus
multiple cellular processes
what are the characteristics of an aged pulp
smaller, spindle-shaped fibroblasts
fewer organelles
what are the cell types in the dental pulp
fibroblasts
undifferentiated mesenchymal cells
dental pulp stem cells
immune cells
what can undifferentiated mesenchymal cells do
differentiate into odontoblast-like cells and fibroblasts
the number reduces with age
what can dental pulp stem cells differentiate into
Multipotent: odontoblasts, chondrocytes, osteoblasts, adipocytes and neurones depending on the tissue they’re formed in
what are the immune cells of the dental pulp
macrophages
t and b lymphocytes
neutrophils and eosinophils
dendritic cells
what do macrophages do in the dental pulp
patrol the pulp and remove dead cells/ bacteria (innate and adaptive immunity)
what do neutrophils and eosinophils do in the dental pulp
they respond to infection and mediate inflammation
what do dendritic cells do in the dental pulp
present foreign antigens to T cells
what do t and b lymphocytes do in the dental pulp
adaptive (antibod-driven) immune system
what makes ip the ECM of the dental pulp
collagen fibres ground substance (non-fibrous protein matrix)
what collagen is in the ECM of the pulp and what does it do
type I and III (creates meshwork by linking type 1)
forms a scaffold providing stability to the pulp
what are the ground substances in the ECM of the pulp
- glycosaminoglycans
- hydrophilic molecules (swell and form hydrogel that fills most of the extracellular space)
- growth factors (cellular process regulation)
where do the collagen fibres type I and III form
as bundles at the roots area not the coronal
what is the vascular supply of the pulp
blood vessels originating from periodontal ligaments (enter pulp via apical fo)
-peripheral blood vessels branching out towards the odontoblast
what controls capillaries
nerves
what are the lymphatic vessels in the dental pulp involved in
the drainage of tissue fluid
what is the difference between blood vessels and lymphatic vessels
have thinner walls and no red blood cells
how many nerve axons enter through the apical foramen
2,500 nerve axons
what are the types of nerve fibres in the dental pulp
myelinated afferent nerve fibres (25%)
unmyelinated C fibres (75%)
what are the myelinated afferent nerve fibres and what do they do
schwann cells forming the myelin sheath
transmit pain sensation to the CNS; cell bodies in trigeminal ganglion
what are the unmyelinated C fibres and what do they do
afferent (main) or efferent (minor)
sense changes in extracellular environment
what do the afferent unmyelinated fibres do
terminate at odontoblast layer or in the dentinal tubules to transmit any noxious stimulus (pain)
what do the efferent unmyelinated fibres do
terminate on smooth muscle cells of the aterioles to regulate capillary blood flow
what is the plexus of raschkow
extensive nerve plus that terminates in the cell-free zone, just below the odontoblast layer of the crown
(axons can pass between odontoblasts & enter dentinal tubules)
where is the nerve plexus
coronal, not in root canals
what is the main function of the dental pulp
provide vitality to the tooth and nourishment of odontoblasts via blood vessels/capillaries
how does the dental pulp have a protective function
- sensation of external stimuli via nerves and their endings
- barrier/defence- tertiary dentine triggering an inflammatory response
what are the clinical issues with the pulp
age changes infection spread and inflammation RCT calcifications and pulp stones dentine sensitivity
what is the challenge associated with a young tooth
large pulp chamber so challenge for cavity/crown preparation (thin dentine layer and pulp exposure can easily occur)
what is the challenge associated with an old tooth
narrow pulp chamber and narrow root canal so challenge for RCT, secondary dentine also accumulates
how can caries spread
from the dental pulp into the surrounding periodontal tissues (abcess)
how can periodontal disease spread
from the surrounding periodontal tissues into the dental pulp e.g. through accessory root canal
what do calcifications and pulp stones form in response to
a chronic stimulus (e.g. caries infection or as an age related change
why does an older pulp form calcifications and pulp stones
less vascular
what can false pulp stones be formed from
calcifying blood vessels and contain bone-like material (inflammation then healing)
what are true pulp stones formed from
detached odontoblasts and contain dentine
how does dentine sensitivity occur
afferent nerve endings terminating in the dentine or near odontoblasts sense pain, mechanical, thermal and tactile stimulus
what are the 3 theories for dentine sensitivity
- neural theory- dentine directly innervated
- odontoblasts act as receptors
- hydrodynamic theory- fluid movement in dentinal tubules is sensed directly/indirectly by nerve endings
when is HERs formed in root formation
after the formation of the crown
how is HERs formed
epithelial cells of the IEE and OEE initially proliferate downwards from the cervical loop of the enamel organ to form a double layer of epithelial cells
what does HERs define when it extends around the pulp
the shape of the future root
what is the difference of HERs to the cervical loop
there is no stratum intermedium and no stellate reticulum
epithelial: PTHrP and enamel proteins
mesenchymal: TGF-β, BMP, RUNX2 (cementoblast differentiation and periodontal regeneration)
how is odontoblast differentiation initiated in the root
the IEE of HERS induces it
what is the difference between odontoblast induction at HERS in the root over the differentiation at the cervical loop
no ameloblast differentiation in root
predentine secreted which forms dentine
primary apical fo forms
HERS becomes stretched
what term is used to describe the curved end of HERS that outlines the primary apical fo
epithelial diaphragm
what is the role of HERS in tooth eruption
cell proliferation of epithelial cells- its position remains stationary and the dentine at the bottom moves the tooth upwards
why was the growth displacement theory disproved
teeth can still erupt of the root is blocked
how are the PDL involved in tooth eruption
rearrangement of collagen fibres and contraction, tooth is pulled up and the bone is removed to create the space
what are the layers of root dentine
cementum
hyaline layer
tome’s granular layer
root dentine
what are the two explanations of Tome’s granular layer
- extensive branching and backwards looping of odontoblasts processes
- incomplete fusion of calcospherites (similar to interglobular dentine)
what are the differences of root dentine compared to coronal dentine
- collagen fibres are deposited parallel and at a distance from the basal lamina of HERS
- root dentine is less mineralised and mineralises faster
- less phosphophoryn
what is phosphophoryn
dentine phosphoprotein- it binds calcium and regulates dentine mineralisation
how does HERS enclose the pulp and appear
as a ‘curtain’ hanging from the crown
how does the primary apical foramen divide
by the fusion of epithelial folds from HERS
at eruption the roots is only at what percentage of its final length
roughly 65%
wide open root apex
when does the root complete for primary and permanent teeth
1.5 years after eruption for primary
3 years after eruption for permanent
cementoblasts differentiate from what cells
undifferentiated mesenchymal cells of the dental follicle
what occurs before the differentiation of dental follicle cells occur
odontoblast induction from dentine formation
stretching and disintegration of HERS
what do dental follicle cells differentiate into
osteoblasts (alveolar bone)
fibroblasts (PDL)
cementoblasts (cementum)
what are the two theories of cementoblast differentiation
inductive signals from gaps in disintegrating HERS/predentine sent to undifferentiated dental follicle cells
epithelial-mesenchymal transmission (EMT) of HERS to cementoblasts
is cementum vascular or avascualr
avascular
what is the function of cementum
attachment of root dentine to PDL
what is the % of hydroxyapatite in cementum
40-50%
what is the benefit of the hydroxyapatite in cementum
allows the resistance to root resorption
what are the types of collagens in cementum
type I- 90%
type III
type XII
what are the non -collagens in cementum
alkaline phosphotase, bone sialoprotein, dentine matrix protein matrix protein 1, dentine sialoprotein, osteocalcin, osteonectin, osteopontin
what do you classify cementum according to
the absence or presence of cells : acellular (primary) or cellular (secondary)
the origin of collagen fibres in cementum : extrinsic or intrinsic
how is cementum distributed in most people at the cementoenamel junction
cementum overlaps enamel- 60%
cementum meets enamel - 30&
cementum and enamel dont meet - 10%
where is acellular cementum found
covering the root adjacent to dentine (primary attachment)
where is cellular cementum found
in apical and interradicular (in between roots)
what is the function of cellular cementum
adaption and repair
thickeness increases with age
what are the cells in cellular cementum
lacunae and canaliculi containing cementocytes and their processes
in which cementum is the development relatively fast
cellular
in which direction are the calnaliculi directed
towards the PDL
where do cementoblasts align in the early formation of accellular cementum
along newly formed hyaline layer
what is the fibrous fringe
extension of cementoblast cell process into predentine and deposition of collagen fibres that intermingle with un-mineralised predentine matrix
how do the PDL stitch to the fibrous fringe
by the extension of collagen fibres
how do collagen fibres become trapped in predentine causing strong connection of cementum to dentine
it mineralises and spreads through the cementum
what are the incremental growth lines in cementum
lines of salter
what are cementicles and where do they sit
a group of cementoblast that become detached
in PDL
what are the epithelial rests of malassez
clusters of epithelial cells on PDL (potentially regenerate periodontal tissue) that have been left behind during the apoptosis of HERS
where do enamel pearls occur
where the root bifurcates (of maxillary molars)
how can enamel pearls cause plaque accumulation and PD
the distrust of attachment of the tooth creates an entry point for bacteria
what are the mechanisms of enamel pearl formation (hypothesises)
- attachment of Epithelial Cell Rests (ECR) to predentine (caused by absence of cementum deposition) which may receive signals from predentine and initiate ameloblast differentiation
- stellate reticulum and stratum intermedium cells of the cervical loop become trapped in a subset of ECRs when HERS/rot development is initiated
why does there need to be combination of hypothesises for the development of enamel pearls
you need to the molecular signals from the pre-dentine for but you need the relevant cells that support ameloblast differentiation
what are the clinical considerations during root development
concrescence
dilacerated roots
roots and canals multiple
hypercementosis
what is concresence
union of two teeth after eruption resulting from a fusion of their cementum surfaces
what are the causes of concresence
trauma and tooth crowding
what are the clinical considerations for concresence
radiography and surgery
what are dilacerated roots (causes and clinical considerations)
curved or bent roots
caused by developmental trauma (playground accidents)
CC: radiographs and careful extraction
how do multiple roots or root canals form
abnormal folding of HERS
what are the clinical considerations when there are multiple roots or root canals formed
radiograph and variation of extraction technique
careful cleaning of extra root canal during endodontic treatment
what is the difference between a lateral and accessory root canal
lateral - connections between root canals
accessory - form in the apical foramen
what is the mechanisms of lateral root canal formation
continuity of HERS is interrupted too early during root dentin formation
this affects local formation odontoblasts resulting in a canal in the dentine connecting the dental pulp and the PDL of the mature tooth
what is hypercementosis
abnormal production of cellular cementum (produced after the root is completely developed)
what are the causes of hypercementosis
age change paget's disease idiopathic occlusal trauma patients that grind their teeth - tooth moves up so space is filled with cementum
what are the clinical considerations for hypercementosis
increased distance from CE junction to root apex (imp in endodontic treatment)
how does coordinated root and periodontal tissue formation occur
odontoblast induction and dentine formation
stretching and disintegration of HERS
differentiation of dental follicle cells
what do dental follicle cells differentiate into
cementoblast (cementum)
fibroblasts (PDL)
osteoblasts (alveolar bone)
what are FGFs thought to regulate
cell proliferation and migration in the formation of periodontal tissue
what are BMPs thought to regulate
cell differentiation and bone formation in the formation of periodontal tissue
what growth factors stimulate periodontal regeneration
FGF2, BMP2
what are stem cells in PDL a source of
regenerative therapies in periodontal disease e.g. mesenchymal cells
what are the functions of the PDL
- tooth attachment
- withstand forces of mastication
- sensory receptor
- remodelling function
- nutritive function
how does PDL aid tooth attachment
PDL fibres insert into cementum and alveolar bone to form fibrous joint with little/no movement (gomphosis, synarthrosis)
how does PDL act as a sensory receptor
sensation of pain and tension/compression
repositioning of teeth to achieve occlusion
how does the PDL have a remodelling function (tooth movement)
high turnover of extracellular matrix and collagen fibres (source of progenitor/stem cells)
how does the PDL have a nutritive function
high vascularised tissue; connected to dental arteries, bone marrow and gingiva. blood vessels needed to perform remodelling function
how does timing of PDL development and differentiation vary
among species
between tooth types
between primary and permanent teeth
what is involved in the initiation stage of PDL development
- ligament space between cementum and bone consists of an unorganised connective tissue (fibroblasts and ecm)
- short fibre bundles are formed near cementum and bone and extend a short distance into the ligament space
how do fibre bundles gradually extend from bone to cementum in PDL formation
fibroblasts produce more collagen fibrils that assemble as fibre bundles
how does the thickness of fibres bundles vary from the bone side and cementum side
bone side: thick fibre bundles
cementum side: thin fibre bundles
where are alveolar crest fibres first formed
at cemento-enamel junction (fibres form apically as the root forms)
what orientation are the alveolar crest fibres
initially oblique, then parallel, then oblique
when do thick alveolar fibre bundles only form
when teeth occlude and function - this is bc mechanical sensation induces the completion of PDL development
what are the principle fibre groups of the PDL
alveolar crest group horizontal group oblique group apical group apical group interradicular group
where is the alveolar crest group and whats it function
below CEJ- rim of alveolus
resists extrusive forces (must overcome when extracting the tooth)
where is the horizontal group and what is its function
below the alveolar crest group, at right angles to tooth axis
resists horizontal forces (tipping)
what is the function of the oblique group
resists intrusive (‘compressive’) forces - mastication
where is the apical group and whats its function
radiates around tooth apex
resists intrusive forces
where is the interradicular group and whats its functiojn
connects to crest of interradicular septum; only in mutli-rooted teeth
resists extrusive forces- overcome when extracting tooth
what are the principle fibre groups of the PDL that need to be overcome when extracting a tooth
alveolar crest group
interradicular group
what are the elastic fibres of the PDL and where do they run
oxytalan fibres and fibrillin (no elastin)
run perpendicular to collagen fibres in cervical region
what is the function of elastic fibres
associated with neurovascular bundles; form 3D meshwork surrounding root and REGULATE vascular flow
what is the function of sharpey’s fibres
mineralised PDL fibres in alveolar bone and cementum
what are the cell types in the PDL
fibroblasts osteoblasts and osteoclasts cementoblasts and cementoclasts rests of malassez immune cells blood vessels nerve fibres
what is the function of fibroblasts in the PDL
produce collagen fibres, growth factors and ground substances (ecm)
perivascular and endosteal fibroblasts surround the blood vessels
what is the collagen half life
3-23 days (highest turnover at tooth apex)
what cell to cell contacts do fibroblasts in the PDL form
adherens junctions and gap junctions
how is the activity of fibroblasts in the PDL induced
by mechanical/masticatory forces
how do fibroblasts have a dual function in remodelling in the PDL
synthesis and degradation of ECM and collagen; matrix metalloproteases
why are matrix metalloproteases (MMPs) the therapeutic target in periodontal disease
they’re the enzyme involved in collagen turnover and are highly active periodontal disease
what is the composition of the PDL
60% ground substance (mainly collagen fibres, blood vessels and nerves)
fibres: 90% collagen, 10% oxytalan(microfibrils without elastin)
collagen types: I(80%), III(15%), IV, V, VI, VII, XII
when are type XII collagen fibres present and what is there function
usually not during development , only after eruption
fibril-associated: link other collagens. expressed on pressure side following mechanical loading
what is the ground substance in the PDL composed of
complex composition of glycosaminoglycans: hyaluronic acid, dermatan surface, chondroitin and heparin sulfate) ,proteoglycans and glycoproteins
what is the function of the ground substance
ion and water binding
70% shock absorber
orientation of collagen fibres
what does the ECM control
the hydration of the tissues and increases the strength of collagen fibrils
how does the composition of the ground substance vary according to developmental state
hyaluronan decreases during development of PDL from dental follicle
proteoglycans increase during tooth development
what does the fibronectin in ground substance do
mediates attachment of cells to collagen fibrils - influence on cell migration and differentiation
clinically promotes wound healing
what growth factors and cytokines does he ECM bind in the ground substance
FGF TGF-beta (BMP) IGF PDGF VEGF interleukins prostaglandins
what is the function of the rests of malassez in the PDL
they’re remnants of HERS and a source of all mesenchymal cell types e.g. fibroblasts, osteoblasts, cementoblasts
what are the immune cells of the PDL
macrophages
mast cells
eosinophils
how does the vascularisation of the PDL vary
between species, tooth types, erupting teeth
what arteries supply the PDL
branches of superior and inferior alveolar arteries
branches of the lingual and palatine arteries entering through the gingiva supplying the PDL
how do the superior and inferior alveolar arteries enter the PDL
enter the pulp at apex
interalveolar vessels pass through the alveolar process (perforating arteries)
more abundant in posterior and mandibular teeth to supply PDL
what do the interalveolar vessels do
form interstitial areas
enable PDL function after endodontic treatment- nutrients needed through interalveolar vessels
extractions wounds: formation of blood clot and invasion of cells involved in healing
what are neurovascular bundles in PDL
pass through perforations in the alveolar bone and form the interstitial areas in the PDL - contain blood vessels and nerves
where are interstitial areas in the PDL usually located
closer to the alveolar bone
where do blood vessels form a capillary plexus in PDL
near the root surface and a postcapillary plexus from which venules pass into the alveolar bone
what directions do blood vessels run in
apical occlusal direction and form arteriovenous anastomoses
where does venous drainage in the PDL occur
at apex, removal of waste products
what does the circular plexus surround
the root surface
what does the crevicular plexus surround
the tooth in the region beneath the gingival crevice
what are fenestrated capillaries
pores in endothelial cells that surround blood vessels - special feature of the PDL and not seen in other connective tissue
what do fenestrated capillaries do
increase diffusion capacity which is consistent with the high metabolic rate in the PDL (esp during tooth eruption)
how is PDL innervation distributed
follows pattern of vasculature
perforating nerve fibres divide into an apical and gingival branch
what is the regional variation for PDL innervation
more nerve endings at the tooth apex
upper incisors have denser innervation throughout the PDL compared to molars
related to masticatory response
what are the types of nerve fibres in the PDL
sensory - nociception and proprioception
autonomic - blood flow regulation
myelinated- sensory only
myelinated and unmyelinated- sensory and autonomic
what are the types of nerve endings in the PDL
free-ending, tree like
ruffini’s corpuscles
coiled type
encapsualted spindle type
where are free nerve endings and what is there function
-Evenly distributed across the PDL
Unmyelinated fibres (enveloped by one Schwann cell; inset)
Extend up to the cementoblast layer
Sense pain and pressure
where are ruffuni’s corpuscles and where are they found
in PDL at root apex
myelinated fibres with dendritic endings
associate with collagen fibres
sense pressure
where are coiled nerve endings found
middle of PDL
where are encapsulated spindles found
in PDL at root apex
surrounded by fibrous capsule
what is the general thickness of the PDL
0.15-0.38mm thinnest in middle of root
what is the PDL thickness for 11-16 years
0.21mm
what is the PDL thickness for 32-52 years
0.18mm
what is the PDL thickness for 53-67 years
0.15mm
what does mastication induce
periodontal remodelling increasing PDL width by 50% including thicker fibre bundles and increased alveolar bone size
where is PDL thicker
in areas are tension rather that compression
what results in periodntal tissue loss
reduced function
how does Capacity for PDL remodelling form the basis for orthodontic treatment
Excessive force can cause localised necrosis of the PDL by cutting off the normal bloody supply to the cells. E.g. too much pressure
how can Damaged PDL be repaired from cells in vital parts
Failure of repair causes localised resorption and tooth ankylosis (fusion of tooth to alveolar bone;) problem extracting
how can Accidentally lost teeth can be replanted
- If portions of the ligament are permanently damaged, external root resorption and ankylosis could occur. Progenitor cells in the PDL can restart the process and reintegrate the toot into the socket
why is PDL is a target of therapies for periodontal disease
- Prevention of undesirable wound healing (guided tissue regeneration – prevent undesired wound healing in PD treatment)
- Growth factors, cytokines or stem cells to stimulate PDL regeneration
what forms of the tooth sockets
the alveolar process of the mandible
what are 3 mechanisms of bone formation
endochondral ossification
intramembranous ossification
sutural ossification
what is involved in endochondral ossification
bone made from a cartilage model - chondrocytes produce cartilage that is replaced by osteoid/bone produced by osteoblasts
what are examples of bone produced by endochondral ossification
long bones(epiphyseal growth plate), base of skull (synchondrosis) mandibular condoyle (secondary cartilage)
what is involved in intramembranous ossification
bones are made by osteoblasts that have differentiated from mesenchymal stem cells and lay down the bone directly
it is determined by the spaces around where the bone forms
what are examples of bones produced by intramembranous ossification
flat skull bones
facial bones: mandible, maxilla and alveolar bone
what is involved in sutural ossification
similar to intramembranous o. but with fibrous connection
provides stability during growth
what are examples of bone enabled by sutural ossification
postnatal growth of flat skull bones
what makes up bone composition
mineralised living connective tissue
non-collagenous proteins
what is mineralised living connective tissue
organic matrix is permeated by hydroxyapatite (deposited between type I collagen fibrils)
what are non-collagenous proteins and what is their fucntion
bone sialoprotein, osteocalcin, osteonectin, osteopontin (all of these bind to ca or HA)
control of mineralisation, proteoglycans, cytokines, growth factors, serum proteins
what is the main function of bone
support, protection, locomotion, mineral reservoir
what hormones is bone physiology controlled by
(-)PTH (+)Calcitonin (+)Vitamin D (+)Estrogen (decreased after menopause) (+)Leptin
what growth factors and cytokines does bone secrete
GF: BMP, TGF-ß, PDGF, IGF
Cytokines: Interleukins, TNF, RANKL
(bone also secretes neuroendocrine factors)
what is meant by ‘woven’ bone
bone formed during development characterised by randomly orientated collagen fibrils. it becomes replaces by lamellar bone
when else is ‘woven’ bone formed except from during development
bone fracture repair
- forms as part of the wound healing response but eventually replaced by lamellar bone
what is adult bone composed of
compact (denser outer area) and trabecular bone (cancellous, spongy)
what is trabecular bone
cavity filled with bone marrow interrupted by a network of bone plates (trabeculae), leaving spaces in between where the bone marrow sits
what are examples of adult bone
mandible
long bones
what are bone lamellae
different types of bone layers
what are the 3 types of bone lamellae
circumferrrential lamellae
concentric (Haversian) lamellae
Interstitial lamellae
what is circumferrential lamellae
encloses the entire outer and inner perimeter of the bone
what is concentric lamellae
forms the basic unit bone (osteon) and makes up the bulk of the compact bone
what is interstitial lamellae
interspersed between adjacent osteons (remnants of remodelled osteons
are osteons transient or static
they’re transient so are constantly resorbed and formed
wha are osteons
cyclinder of bone (generally parallel to the long axis of he bone)
what is the osteon composed of
central canal (haversian canal) including a blood capillary lined by a layer of osteoblasts volkmann's canals - interconnect adjacent central canals
how can osteblasts remodel osteons from inside
they can enter through blood vessels
what is the periosteum
connective tissue membrane consisting of two layers
what are the two layers of the periosteum and what are they composed of
outer fibrous layer- dense collagen fibres
inner cellular layer- osteoblasts and their precursors, highly vascularised
what is the endosteum and what is its composition
the internal surface
not well demarcated, loose connective tissue including osteoblasts; separates bone surface from marrow; less active in bone formation than periosteum
what are the bone cells
osteoblasts
osteocytes
osteoclasts
what are the characteristics of osteoblasts
cuboidal cell shape
inactive: flat, bone lining cells
where are osteoblasts derived from and what do they synthesise
mesenchymal stem cells
synthesise organic bone matrix
what do osteoblasts produce
osteoid (mainly collagen type I)
alkaline phosphatase- cleaves inorganic phosphate to initiate and promote mineralisation
growth factors- : IGF1, TGF-ß, PDGF which increase bone repair (dental therapy - implants)
what are osteocytes
osteoblasts that become trapped in unmineralised or mineralised matrix
what is a lacunae and how is it produced
spaces in the matrix produced by
osteocytes becoming smaller in size
what are canaliculi and how do they form
canals between lacunae
formed from a network of cellular processes that connect adjacent osteocytes
what do osteocytes function as
sensors of changes in the bone environment
signalling centres to maintain bone integrity (induce bone remodelling)
what are osteoclasts
large multinucleated cells; derived from haematopoietic cells
what do osteoblasts produce
Howship’s lacunae (resorption bays -holes in bone)
acid phosphates and lysosomal enzymes
what occurs in the resorption sequence
- attachment of osteoclasts to bone
- creation of acidic microenvironment for demineralisation
- degradation of exposed matrix by enzymes
- endocytosis of degradation products
what occurs in intramembranous ossification
mesenchymal cells in the cellular periosteum differentiate to become osteoblasts which produce woven bone (irregular)
gradual turnover/remodelling of woven bone to lamellar bone - formation of primary osteon
continued bone replacement produces highly organised mature bone with fewer cells, secondary and tertiary osteons and circumferential lamellae
what does the mature bone space consist of
mineralised bones and very few osteocytes
outline the development of the alveolar process
mandible takes the shape of a trough underneath the inf. alveolar nerve. the alveolar process begins to grow towards the tooth germ and will start surrounding it
alveolar process almost surround the incisor tooth germ. the inferior alveolar nerve is enclosed in a bony canal
to accommodate the growing tooth germ, the alveolar bone must be resorbed on the inner wall of the alveolus and new bone must be deposited on the outer wall
what cells are involved in bone remodelling
osteoblasts- area of bone formation
osteoclasts- area of bone resorption (lacunae)
osteocytes- osteoblasts embedded in bone
bone lining cells- flat area of no bone activity
what is the function of bone lining cells
protection from resorption by osteoclasts
initiating bone remodelling
mineral metabolism
source of progenitor cells
what are the stage of bone remodelling
resorption- osteoclasts
reversal- cessation of resorption, disappearance of osteoclasts
formation- recruitment, migration and differentiation of osteoblasts (bone formation)
resting- bone in tact but remodelled, cessation of bone formation, surface covered by flat bone-lining cells
what are the structural lines in bones
resting lines- pause in bone deposition, osteoblasts stop producing bone- parallel
reversal lines- change from bone resorption to deposition (position of howships lacunae)- scalloped
what is involved in the life cycle of an osteon
resting
formation
reversal
resorption
what are the components of the tooth socket
buccal cortical plate lingual cortical plate cribiform perforations in bone for blood vessels and nerves to enter PDL interdental septum (between teeth) interradicular septum (between roots)
what is the structure of alveolar bone
- outer compact layer: cortical plate
- central trabecular layer: spongiosa
- inner compact layer: alveolar plate, perforated to allow access to blood vessels connecting PDL
- alveolar crest (1.5-2mm below CEJ)
what is the cortical plate- where is it thickest and thinnest
surface layer of lamellar bone supported by osteons
thinner in maxilla than mandible
thickest on buccal aspect of mandibular premolars and molars
what is spongisa composed of
trabecular (cancellous) bone
-bone marrow spaces rich in adipose tissue which is an energy storage
where is spongisa absent
in anterior teeth; cortical and alveolar plate fused
what is the alveolar plate composed of
lamellar bone and bundle bone
- contains sharpeys fibres
what is bundle bone
The innermost layer of the alveolar plate (directly lining the socket) is referred to as bundle bone because the collagen fibre bundles of the PDL are embedded
what is the function of bundle bone
Provides the attachment for PDL fibres
Where fibres are inserted is bundle bone
how does remodelling: tooth drift (to the right) occur in orthodontic treatment
Resorption by osteoclasts on the right side of the alveolar plate creates the space that the tooth can move into
To compensate for this bone loss new bone must be formed onto the cortical plate on the opposite side. Keeps thickness constant
Because the tooth moves to the right, the space in the socket on the left must be filled by bone deposition onto the alveolar plate
The excess bone must then be resorbed by osteoclasts from the cortical plate on the opposite side
through what stage does alveolar bone remodelling procees
resorption, formation, resting
what is mesial drift
- Unworn teeth have very few interproximal contact points
- Attrition cause hard tissue loss on occlusal and interproximal surfaces
- Increase in interproximal distance is compensated by mesial (forward) drift of teeth to fill the gap
- Broader interproximal contact points
what is intraocclusion
During trauma or infection can cause tooth ankylosis (fusion of tooth root to alveolar bone ) toot cannot move anymore, can no longer erupt and exfoliate
Most common in primary molars e.g. partial root resorption
what are the consequences of intraocclusion and what should be done
- Prevents exfoliation; leads to impaction of successor tooth
- Further growth of alveolar bone results in “submergence” of ankylosed tooth
- Extraction to prevent malocclusion or periodontal problems
what is lamina dura (clinical consideration)
alveolar plate on the dental radiograph is lamina dura
An interrupted lamina dura in the apical region indicates a periapical abscess.
what is alveolar bone resorption and when does this occur. what are the consequences of this
Following tooth extraction or chronic periodontitis, the alveolar process can resorb:
- Placement of dental implants will be difficult
- Implanting soon after tooth loss decreases the rate of alveolar ridge resorption. Should not but implant soon after bone resorbed
- Bone loss impacts on construction of removable prostheses
what is maxillary sinus perforation
the Close proximity of premolar/molar roots and alveolar bone to maxillary sinus flow means
During tooth extraction, maxillary floor can rupture (bone can fracture) (oro-antral connection/fistula; infection)
what is alveolar osteitis and what does it lead to
After tooth extraction, socket fills with blood and forms blood clot: Important step in wound healing- detachment of blood clot and it falls out- ‘dry socket’.
leads to painful bone inflammation and bad odour
what is the gingiva
the part of the oral mucosa that surrounds and is attached to teeth and alveolar bone - continuum with the oral mucosa or pdl
what creates the dentogingival junction and how
tooth eruption
during eruption the REE fuses with the oral epithelium
what cell type is the REE
simple epithelium: cuboidal cells
what cell type is the OE
stratified squamous
what happens when the REE fuses with the OE during tooth eruption
degeneration of central epithelial cells, this causes a continuum between the 2 epithelia which prevents the tooth from creating a wound
why is there no bleeding when the tooth erupts
there is epithelial continuity at all times between REE and OE which means there is no connective tissue exposure. if there is blood it is the remaining blood from the tooth pulp
what epithelium is formed when the tooth erupts and the DGJ is formed
junctional epithelium (JE)
what does the JE consist of, whats its function and is it keratinised or non keratinised
entirely REE
attaches gingiva to tooth
it is non-keratinised
JE is very simple and primitive
what occurs to the gingiva some time after tooth eruption
gingival epitehlium appears to overgrow and replaces the REE
sulcular epithelium occurs
what types of epithelium are at the gingival sulcus
Junctional epithelium
Sulcular epithelium
Gingival epithelium
what cell type is the junctional epithelium
simple, non keratinised
what cell type is the sulcular epithelium
stratified, non keratinised
what cell type is the gingival epithelium
stratified keratinised
what is the mechanism for epitehial change some time after tooth eruption
gingival cells change to sulcular which is non keratinised
stratification of early REE and rete peg formation
how is the development (depth) of the sulcus induced
by masticatory forces acting on the gingiva
base of the sulcus at the same level as free gingival groove, deeper in disease tooth
why does the junctional epithelium still appear like REE
JE is simple non keratinised and REE is simple cuboidal - very primitive
what occurs in the epithelia 2-3 years after tooth eruption
the gingival epithelium appears to have completely replaced the REE
small epithelial tag remains from the REE (cell remnants and primary enamel cuticle)
what is the primary enamel cuticle (nasmyths membrane)
internal basal lamina that the epithelial cells sit, it covers the tooth once erupted but usually worn away by mastication
what indicates that junctional epithelial cells are different from gingival epithelial cells
molecular markers
REE could become stratified and develop rete pegs
what is evidence that stem cells can form JE
tooth attachment is restored after gingi-vectomy
gingival tissue grafting possible
what 2 enamel matrix proteins are stained in immunohistochemical staining
amelotin (AMTN; A)
odontogenic ameloblast-associated (ODAM:B)
where is ameolotinn expressed
in the basal lamina
normally expressed by the maturation stage ameloblasts forming the REE
where is ODAM expressed
in internal basal lamina and junctional epithelial cells
where is junctional epithelium derived from
REE
its not a downgrowth of the gingiva
what secretes primary enamel cuticle and what does it do
epithelial cells secrete it onto the enamel surface where it bonds with enamel proteins
what is a hemidesmosome
half a desmosome by which cells below the internal lamina attach
what does the external basal lamina attach to
lamina propria
why is the junctional epithelium permeable and what does the allow
there reduced number of desmosomes and larger intracellular spaces
allows the passage of GCF and defence cells into the sulcus
what does the GCF contains
antibodies
complement factors
macrophages (phagocytes)
desquamated sulcular and junctional epithelial cells (5-6 days turnover)
cytokines and metalloproteases (during infection)
what is the function of the GCF
inflammatory exudate which is secreted to cleanse out the gingival crevice
first line of defence against bacteria
what happens if GCF is overproduced
provide subgingival bacteria with excess nutrients potentially allowing harmful bacteria to survive
tissue destruction caused by inflammation
GCF can be an indicator of periodontal health
what are the features of attached gingiva
alveolar mucosa
submucosa
what are the features of free gingiva
free gingival groove(border between free and attached) gingival margin gingival sulcus junctional epithelium sulcular epithelium
what is the mucogingival junction
boundary between the alveolar mucosa and attached gingiva
what are the cells of the masticatory mucosa like
parakeratinised (and partially orthokeratinised)
what are the layers of the gingiva
epithelium
lamina propria
mucoperiosteum (submucosa absent
what are the features of teh epithelium of the gingiva
thick
parakeratinised- live cells in keratin layers
can also be orthokeratinised which occurs when there is a strong masticatory force on gingiva (appears white)
what are the features of the lamina propria
fibres attach with underlying alveolar bone
long, narrow papillae
dense collagen fibres- makes tissue tough to resist masticatory forces
what is the function of the mucoperiosteum
stability
submucosa acts as a cushion
what is the clinical relevance of the mucoperiosteum
difficult to inject and painful for patients
doesn’t require suturing
why is the mucoperiosteum present in gingiva instead of submucosa
submucosa provides mobility- acts as a cushion e.g in lining mucosa . contains loose connective tissue and salivary glands or adipose tissue.
however in order to withstand masticatory forces the lamina propria is directly joined with the periosteum of bone in e.g. masticatory mucosa to provide stability
where do the transseptal fibre groups run and what is their function
interdentally from CEJ over the alveolar crest to the CEJ of neighbouring tooth
controls mesio-distal spacing
what is the clinical relevance of the transseptal fibre group
when braces come off, teeth move back into their original position due to these fibres
what does the dentogingival fibre group do
(largest group)
connects cervical cementum to lamina propria of free and attached gingiva
what does the alveogingival fibre group do
connects the alveolar bone crest to lamina propria of free and attached gingiva
what does the dentoperiosteal group do and where does it run
runs from the cementum over the outer surface of the alveolar process and insert either into the alveolar process or the vestibular muscle and floor of the mouth
what does the circular group do
(smallest group)
forms bands around the neck of the teeth and interlaces with other fibres in the free gingiva. binds free gingiva to the tooth
which gingival fibre is in the gingiva and has the same structure as the junctional epithelium
denal col- depression
doesnt attach to any teeth
what occurs when mild periodontal inflammation causes gingivitis
the inflammatory response in connective tissue attracts immune cells- 70% of collagne fibres are destroyed by this. as a response the sulcular epithelium grows downwards to comepensate for the loss of connective tissue here
how do the sulcular and gingival epithelial tissue appear when connective tissue is inflamed
deep in growth of both epithelium
what occurs if there is persistent inflammation
further destruction of connective tissue by inflammatory cells causes apical migration of junctional epithelium- forming a gingival pocket
if advanced: loss of PDL and alveolar bone
what is the mechanism of epithelial down growth
growth until intact connective tissue is reached, compensation for the loss of mechanical stability
what occurs in periodontal surgery
insertion of membrane which prevents cells from growing down (guided tissue regen) formation of fibrin clot against root surface
what occurs in guided tissue regeneration
the insertion of membrane allows new tissue regeneration, bone can regenerate and connective tissue reformed with new fibroblasts and collagen
what is the depth of gingival sulcus in health gingiva
0.5-2mm
what is the depth of pocketing in diseased gingiva
> 3mm
what is the oral mucosa
continuum from the gingiva and lines the whole mouth
where are the oral epithelium and epidermis derived from
embryonic ectoderm
what is the buccopharyngeal membrane
early structure where the epithelial from the ectoderm meet the epithelia from the endoderm
where do oral cancers occur more commonly
in the pharyngeal region (inside) formed by endoderm
what are the landmarks in the oral cavity
oral vestibule
oral cavity proper
what is the oral vestibule
the space between the lips, cheeks, alveolar bone and gingiva. Slit-like space between lips/cheeks and alveolar bone/teeth
what are the features of the oral vestibule
vestibular fornix
upper labial frenlum
frenlum near maxillary molars
how is a midline diastema caused between the maxillary central incisors and how can this cause problems clincally
a large labial frenlum with an attachment site near the alveolar crest
can affect the stability of dentures
how is the oral vestibule separated from the oral cavity proper
by alveolar bone/teeth
what are the features of the oral cavity proper
anterior pillar of the fauces (palatoglossal fold)- formed by glossopalatine muscle
posterior pillar of the fauces (palatopharyngeal fold) - formed by pharyngopalatine
palatine tonsil
uvula
soft palate
hard palate
what is oral mucosa made from
epithelium-mesenchyme
what are the functions of the oral mucosa
mechanical protection-masticatory forces barrier to microorganisms and toxins immunological defence (immediate and adaptive) lubrication and buffering sensation
what are the regional variations of the oral mucosa and functional adaptations
epithelial thickness degree of keratinisation interface with connective tissue composition of connective tissue presence or absence of a submucosa
how much of the oral mucosa consists of lining mucosa
60%
floor of the mouth, cheeks etc.
how of the oral mucosa consists of masticatory mucosa
25%
mainly the hard palate
how much of the oral mucosa consists of specialised mucosa
15%
dorsal surface of the tongue
what is the basic architecture of oral mucosa and skin
oral epithelium (epidermis) lamina propria (dermis) submucosa (hypodermis)
what does the oral epithelium (epidermis) consist of
stratified squamous epithelium
- epithelial ridges
- epithelial projections
- keratinocytes
what does the lamina propria (dermis) consist of
connective tissue
- papillae
- fibroblasts, macrophages, lymphocytes
- collagen (I, III) and elastic fibres
- blood vessels and nerves
what does the submucosa (hypodermis) consist of
loose connective tissue: fibroblasts
- larger blood vessels and nerves
- fat deposits
- salivary glands
- found in cheeks, lips, lateral palate(no clear boundary with lamina propria)
- much looser than the lamina propria to provide tissue mobility
where about does the submucosa provide mobility and act as a cushion
in lining mucosa
where is mucoperiosteum found
masticatory mucosa in the middle of the hard palate or the gingiva
what is the regeneration cycle time for the skin and oral mucosa
skin- 27 days
oral mucosa- 9-14 days
what does the stratified squamous epithelium of the oral mucosa consist of
basal cell layer
prickle (suprabasal) cell layer
granular layer
keratinised layer
what are the characteristics of the basal cell layer -stratum besale
Cuboidal cells; proliferating
single cell layer; basal lamina attached to lamina propria;
contains stem cells and transit-amplifying cells (regeneration);
expresses keratins 5 (Type II, Basic) and 14 (Type I, Acidic)
what can keratins be used as
molecular markers e.g. to diagnose cancer
what are the characteristics of the prickle (suprabasal) cell layer - stratum spinosum
round, “spiny” cells (increase in desmosomes);
several layers;
differentiating;
only parabasal cells proliferate;
expresses keratins 1 and 10, loricrin and involucrin
what are the characteristics of the granular layer- stratum granulosum
Larger, flatter cells; several layers
maturating
loss of cell organelles and cytoplasm filled with keratohyaline granules (contain profilaggrin and lipids; secreted)
what are the characteristics of the keratinised layer (stratum corneum)
- Very flat cells; ~20 cell layers;
- cornified (dead); no cell organelles (nucleus)
- filaggrin binds keratin filaments together (“keratin”);
- crosslinking of involucrin→ cornified envelope (barrier);
- cell shedding (desquamation)
Cornified envelope forms a barrier against microorganisms
what are the types of keratinisation and where are they found
orthokeratinised- hard palate, tongue
parakeratinised- gingiva
nonkeratinised- lining mucosa
what is orthokeratinised
cornified layer: dead cells, no cell nuclei
what is parakeratinised
cornified layer: dead cells,
cell nuclei present
what is nonkeratinised
superficial layer: live cells
no keratohyalin granules
what are they other cell types (“clear cells”) in oral mucosa
melanocytes- basal; produce melanin pigment and transfer it to keratinocytes via dendritic processes
Merkel cells: Basal; sensory receptor cells => sense light touch
Langerhans cells (immune cells) : Suprabasal; dendritic cells; antigen processing & presenting to immune system
Lymphocytes: Often associated with Langerhans cells; Inflammatory response
what is the mucosa for the hard palate
masticatory mucosa
what are the features of the hard palate
Incisive papilla: Prominence overlying nasopalatine foramen (→ denture fitting).
Palatine raphe: Midline epithelial ridge; directly attached to bone
Palatine rugae: Unique epithelial folds; food transport towards pharynx
Alveolar bone: Submucosa present at junction with lateral hard palate
Fovea palatini (openings of the ducts of minor salivary glands; posterior border for an upper denture)
what are the landmarks in the hard palate important for denture fitting
incisive papilla
fovea palitini
what are the histological features of the masticatory mucosa
thick epithelium
can be OC or OC+PK
lamina propria
- long, narrow papillae
- dense collagen fibres
mucoperiosteum (submucosa) absent
what type of mucosa is buccal mucosa
lining mucosa
what are the features of buccal mucosa
fordyce’s spots
parotid papilla- level of 2nd max molar, opening of parotid duct
linea alba- parakeratinisation of buccal mucosa at moar occlusal plane
what are fordyce’s spots and what is their production and function
Ectopic sebaceous gland without associated hair follicle
Sebum (oily substance) lubricates the buccal mucosa or the lips
what is present on the skin of lip epithelium
keratinised epidermis
hair follicle
sebaceous gland
dermis
what mucosa is on the floor of the mouth
lining mucosa
what are the features on the floor of the mouth
Lingual frenum
Sublingual papilla- opening of the submandibular salivary ducts
Sublingual folds- openings of the sublingual salivary ducts
Fimbriated folds- irregular folds; remnants of tongue development
Deep lingual veins
outline the histology of lining mucosa: labial and buccal
Epithelium: -Thick; Nonkeratinised Lamina Propria: -Dense; Long and slender papillae Submucosa: -Dense; firmly attached to muscle; minor salivary and sebaceous glands -Function: Mobility and Stability
outline the histology of lining mucosa: ventral tongue;floor of mouth
Epithelium: -Thin; Nonkeratinised Lamina Propria: -Thin; Short papillae Submucosa: -Thin and irregular -Function: Mobility
outline the features of the lips(lining mucosa) and gingiva (masticatory mucosa)
- Vermillion zone: Lining mucosa
- Intermediate zone; parakeratinised
- Labial mucosa: Lining mucosa; nonkeratinised
- Alveolar mucosa: Lining mucosa; nonkeratinised
- Gingiva: Masticatory mucosa; parakeratinised (+ orthokeratinised)
- Mucogingival junction: Junction between alveolar mucosa and gingiva
what is the vermillion zone of lining mucosa and what are its characteristics
Transition zone between skin and labial mucosa
Keratinised. Thin epithelium; numerous capillaries => red colour; contains no salivary glands, only a few sebaceous glands in corner of the mouth.
what are the functions of the tongue
Mastication, swallowing, speech, taste, immune function
what are the ectodermal appendices on the tongue
filiform papillae- masticatory
fungiform papillae-taste
foliate papillae- taste circumvallate papillae - taste
where is the epithelium derived from on the anterior 2/3 of tongue
ecotoderm
where is the epithelium derived from on the posterior 1/3 of tongue
endoderm
what is the histology of the specialised mucosa: dorsal surface of the tongue and what is its function
Epithelium:
- Thick
- Orthokeratinised (filiform papillae)
Nonkeratinised (taste papillae and interpapillary regions)
Lamina Propria:
- Long papillae
- Nerves, minor salivary glands
Submucosa:
-Absent (lamina propria attaches directly to muscle)
Function: Stability & Taste
what are the age changes of the oral mucosa
Smoother and dryer surface (→ ‘dry mouth’)
Thinner epithelium, flattening of epithelial ridges (arrow)
Decreased cellularity of lamina propria and increase in fibrous tissue (asterisk; fibrosis)
Fewer Langerhans cells (reduced immunity)
- Systemic disease
- Medication (decreasing salivary flow)
Increase in Fordyce’s spots (buccal, lips)
Atrophy of minor salivary glands
what are the age related changes of the tongue
Epithelial atrophy (loss of FF papillae)
- smooth, often fissured surface
(e. g. nutritional deficiencies; medication)
Burning sensations; loss of taste – poorly understood
Development of nodular, varicose veins on underside of tongue (‘caviar tongue’)
what is black hair tongue
Hypertrophy of filiform papillae - TOO MUCH FILLIFORM PAPILLAE
The papillae trap food, accumulation of food debris and microorganisms
what is geographic tongue
(Benign migratory glossitis)
Atrophy (loss) of filiform papillae; migrating depapillated patches with white border; inflammation (arrows)
occurs in children
what is recurrent aphtous stomatitis
Painful lesions in the mouth
Recurrent mouth ulcers
20% of population (familial history)
starts in childhood or adolescence
what are other types of ulcers
Virus infections (e.g. Herpes, HIV) Iron and vitamin B deficiency Crohn’s disease
what is candida albicans infection
- Fungal hyphae (stained purple)
- Older ages
- Shows up at white spots
- Fungal hyphae in the stain
what are the common diseases of the oral mucosa
recurrent aphtous stomatitis
lichen planus- reticular patches (autoimmune disease)
white sponge naevus- spongy
leukoplakia- white patches
what are the solutions to the problems of tissue regeneration e.g. there is incomplete tissue function regeneration
cellular therapy- stimulate bodys own stem cells into repairing defect
tissue engineering - collagen netword to modulate tooth shape
biomedical engineering
gene therapy- altering genome
what are stem cells and what is their function
Unspecialised (undifferentiated) cells that:
- can self-renew
- can differentiate into other cell types
Function: Development and Regeneration (become active in an injured tissue)
what are totipotent stem cells
all cell types (e.g. fertilised egg)
what are pluripotent stem cells and where are they found
all cell types of the three embryonic germ layers (e.g. embryonic stem cells)
rare, not accessible in the adult body.
what are multipotent stem cells
many cell types (e.g. haematopoietic stem cells; mesenchymal stem cells)
what are oligopotent stem cells
few cell types (e.g. Myeloid precursors -Five blood cell types)
what are quadripotent stem cells
four cell types
(e.g. mesenchymal progenitor cells: cartilage, bone, stroma, fat)
Unipotent: one cell type (e.g mast cell precursors)
what are the 4 tissues of tissue regeneration
- Stem cell-mediated regeneration
- Epimorphosis
- Morphallaxis
- Compensatory regulation
what is involved in stem cell mediated regeneration and what are examples
Replacement of lost tissue by stem cell activity. Production of new progenitors
Examples: Hair growth from follicular stem cells in the hair bulge.
what is involved in epimorphosis and what are examples
Dedifferentiation of cells at the wound site and formation of undifferentiated cells that redifferentiate to form the lost structure.
Example: Planarian flatworms; Amphibian limbs
what is involved in morphallaxis and what are examples
Repatterning of existing tissue with little new growth.
Example: Hydra (freshwater polyp- if you cut across middle)
what is involved in Compensatory regulation
Differentiated cells divide and maintain their differentiated functions
Example: Liver regeneration- liver injury, the cells start to divide again and maintain their function
what are the 4 stages of wound healing in the oral mucosa
Hemostasis
Inflammatory response
Reparative phase (epithelial response)
Reparative phase (connective tissue response)
what occurs in stage 1- Hemostasis
- Vascular damage causes hemorrhaging into the tissue defect and results in the formation of a blood clot (Coagulation: fibrin deposition & aggregation of platelets)
- Forms barrier that unites the wound margins and protects the exposed tissue; provides provisional scaffold for subsequent colonisation by reparative cells.
what occurs in stage 2- inflammatory response
Cell activation, migration and function
Microorganisms and toxins have likely entered through the wound and induce an acute inflammatory response
Leakage of plasma proteins and platelet-derived cytokines and growth factors
leukocyte migration towards the wound
Neutrophils- kill bacteria (appear within a few hours)
Monocytes- remodelling
lymphocytes- humoral
(appear after 24hrs)
what occurs in stage 3: reparative phase
epithelial response
Mobilisation of epithelial cells
within 24 hours
Increased basal cell proliferation and epithelial cells adjacent to the wound margin start to migrate beneath the blood clot (24-48 hours). basal lamina deposition facilitates movement and epithelial sheet formation (stratification- squamous stratified ep produced)
Migration stops when cells reach opposing wound margin and increased cell proliferation and differentiation leads to stratification
what occurs in stage 4: reparative phase
connective tissue response
Fibroblasts proliferate and migrate into wounded connective tissue within 24- 48 hours and deposit disorganised collagen fibres
Formation of new blood capillaries from existing vessels (angiogenesis) at the wound margin ECM (fibronectin, laminin, collagen) formed by new fibroblasts provides scaffold for forming blood vessels.
scar tissue formation-Increased collagen deposition between days 5 and 20 but reduced tensile strength
what is fibroblast deposition of collagen regulated by
TGF-β
what is the Formation of new blood capillaries from existing vessels (angiogenesis) at the wound margin regulated by
VEGF, FGF and TGF-β
what does the formation of new capillaries provide
nutrients and oxygen, enable access of inflammatory cells, stimulate connective tissue formation
what happens to the scar tissue
its remodelled and converted into better alignment of collagen fibres in around 5 months
outline what occurs in wound contraction
First fibroblasts to enter the wound site are contractile myofibroblasts and Pull the wound together
Different from connective tissue fibroblasts
Pericytes implemented in the formation of myofibrocytes- pull wound together
Form connections with each other and with collagen fibrils → alignment
Contraction draws edges of the wound together
what are the features of scar tissue
inferior quality
deposition of disorganised collagen leads to immobilisation and rigidity at repair site
remodelled in oral mucosa - wound regenerates to normal function
why do injuries during development result in scarless healing
they do not involve the inflammatory response
how does wound healing occur following tooth extraction
repair:
tooth socket fills with a clot
epithelial response:
epithelialisation of socket (by day 10)
inflammatory response:
polymorph and macrophage response
osteogenic precursors migrate into blood clot
proliferation phase:
osteoblasts differentiate and form bone
how does wound healing occur at the dento-gingival junction
Day 3: Colonisation of gingival wound by epithelial cells and formation (regeneration) of the junctional epithelium
Day 5-7: Expansion and down-growth of the junctional epithelium. Re-establishment of dento-gingival junction
what is the difference in the restoration of a fucntional unit to the oral mucosa
PDL fibres must insert into cementum and bone
Coordinated repair requires complex regulation at cellular and molecular level
what are the cell types involved in the repair of periodontal tissue and what is their function
Fibroblasts- remodelling collagen fibres
Endothelial cells- form new blood vessels from existing vessels
Cementoblasts- perivascular and endosteal fibroblasts
Osteoblasts- mesenchymal progenitor cells in the endosteum or periosteum
what occurs in the normal process of periodontal tissue repair
No inflammation, e.g. tooth movements
what occurs in injury process of periodontal tissue repair
Inflammatory response required to combat infection and initiate repair
why can endogenous repair not be restored if the tissue is chronically inflamed
chronic inflammation inhibits stem cell activation, cell recruitment, cell proliferation and differentiation so cannot restore tissue function
what occurs in mild periodontal inflammation
Dental plaque accumulation causes inflammatory response in connective tissue.
-70% of collagen fibres destroyed within 3-4 days!
what does persistent inflammation cause in PD
Further destruction of connective tissue by inflammatory cells
causes apical migration of junctional epithelium (arrow)
Formation of gingival pocket.
Advanced: Loss of PDL and alveolar bone.
how far does epithelial down growth go
Growth until intact connective tissue is reached
Compensation for loss of mechanical stability.
whats involved in periodontal surgery
Insertion of membrane (physical barrier).
Guided tissue regeneration
preventing abnormal wound healing by inducing the clot
what are the molecular approaches in periodontal repair in PDL and cementum
EGF, FGF, IGF, PDGF, TGF-ß
what are the molecular approaches in periodontal repair in bone and cementum
BMP
what does fibronectin do
Forms a link between the fibroblasts and collagen fibres
what does enamel matrix (emdogain) do
Cementum formation may stimulate periodontal repair. Loss of bone in PD- reinduction if new bone in the area required to save the tooth
what is the physio-chemical repair process of enamel
Remineralisation by calcium, phosphate and fluoride ions in saliva
what is the dynamic process of early caries lesions
can be reversed
WSL reversible if surface enamel intact (underlying body may contain destroyed enamel prisms) and acid producing bacteria are removed
remineralisation by ion precipitation from saliva
what does the dentine reparative process depend on
Extent and duration of stimulus
Structural variations in dentine:open or occluded dentinal tubules
Age of tooth:Smaller pulp chamber, diminished blood and nerve supply
how does dentine reparative process occur after slow onset due to prolonged insult (attrition, early caries )
Occlusion of dentinal tubules: Collagen plug or sclerotic dentine – closes up tubules
Reactionary dentine in the pulp: formed by existing odontoblasts (slow, tubular)
how does dentine reparative process occur rapid onset due to severe insult (late stage caries, cavity prep)
Reactionary dentine: could form if odontoblasts survive (slow, tubular)
Reparative dentine: formed by newly differentiated odontoblast-like cells if original odontoblasts have died (rapid, amorphous, less collagen
what are the dental stem cell sources for dental regeneration
e. g. from 3rd molars; primary teeth:
- Dental pulp (DPSC)
- Dental pulp from exfoliated primary teeth (SHED)
- Dental follicle of unerupted teeth
- Periodontal ligament (PDLSC)
- Root apical papilla (SCAP) Tooth germs
- Epithelial rests of Malassez
what are the opportunities in dental tissue engineering and regeneration
- Tissue engineering:
a) Biodegradable scaffolds for cell seeding; 3D printing
b) Bioengineering, material sciences and nanotechnology:
- Nano)materials with novel properties that can be stimulate biological tissues
c) Implants with bioactive surfaces allowing for better tissue integration. - Gene therapy: Ex vivo or in vivo
• CRISPR/Cas9 genome editing tools; RNAi; novel viral delivery vectors
• May not be applied well in dental practice
what is the potential impact of tissue engineering and regeneration on future clinical practice, what are the limitations
Conventional: amalgam, composites, metallic implants, tissue grafts.
Limitations: non-biological, immune rejection, pathogen transmission, lack of remodelling with recipient tissue, donor site morbidity.
Novel: Engineering of precise tissue shape using biodegradable scaffolds onto which cells can grow and re-establish morphology and function.
when force is applied to the crown, where is the force transmitted to
to the root and then to the cementum in the PDL and to the bone.
what is the anatomy of the PDL
Collagen
Vascular supply
Nerve endings – pain & proporioception
Fluid – shock absorber
contains undifferentiated mesenchymal cells → fibroblasts & osteoblasts
what is the anatomy if bone
osteoblasts
osteoclasts
osteocytes
when force is applied to the crown, where is the force transmitted to
to the root and then to the cementum in the PDL and to the bone.
what is the anatomy of the PDL
Collagen
Vascular supply
Nerve endings – pain & proporioception
Fluid – shock absorber
contains undifferentiated mesenchymal cells → fibroblasts & osteoblasts
what is the anatomy of bone
osteoblasts
osteoclasts
osteocytes
what is the response of the PDL and bone to normal function e.g. a force of very short duration
PDL doesn’t compress, alveolar bone bends which sends a piezoelectric signal
what is the piezoelectric function
force applied to crystalline structure (bone/collagen)
movement of electrons
short flow of current
what is the response to forces of 1-2 seconds
PDL fluid expressed
Tooth moves in socket
what is the response to forces of 3-5 seconds
PDL fluid redistributed
Tissue compressed- pain
what is the response to forces of longer duration
tooth moves in socket
bone changes occur
what are the electrical signals and pressure tensions that occur in response to orthodontic forces
Piezoelectric effect
Streaming potential- movement of ground substance
Change in blood flow- increase in tension, decrease in compression
Microfractures- hyalinisation
- Chemical signals- e.g. prosdaglandins, IL-1, Leukotrienes, MMPs
- Cellular response- osteoblasts, osteoclasts, osteocytes
- Systemic response- PTH, VitD, Calcitonin etc.
what is the effect at duration and level of force
force tooth
PDL and bone biological electricity & pressure-tension
osteoblasts (tension) and osteoclasts (compression)
bone resporption/deposition
What happens when heavy ‘orthodontic’ forces are applied after 3-5s
blood vessels in PDL occluded on pressure side
What happens when heavy ‘orthodontic’ forces are applied after a few Mins
blood flow cut off to compressed PDL area
What happens when heavy ‘orthodontic’ forces are applied after a few Hours
Cell death in compressed area- hyaline layer. Bone adjacent to squashed PDL doesn’t have a blood supply
What happens when heavy ‘orthodontic’ forces are applied after 3.5 days
Cell differentiation, undermining resorption starts
What happens when heavy ‘orthodontic’ forces are applied after 7-14 days
undermining resorption removes lamina dura, tooth movements
What happens when light ‘orthodontic’ forces are applied after 3-5s
blood vessels in PDL
- Pressure side- partially compressed on pressure side
- Tension side- dilated
What happens when light ‘orthodontic’ forces are applied after a few mins
blood flow altered, this allows release of cytokines
What happens when light ‘orthodontic’ forces are applied after a few hours
metabolic changes
- Chemical messengers- cellular activity
- Enzymes
What happens when light ‘orthodontic’ forces are applied after 4 hrs
cell differentiation in PDL e.g. osteoclasts and osteoblasts
What happens when light ‘orthodontic’ forces are applied after 2 days
tooth movement more gradual by remodelling
outline the ways in which teeth can move
Tipping Translation/ Bodily Movement Rotation Extrusion Intrusion
what occurs in tipping
Simple movement
Around centre of resistance
Tips the tooth 1/3 from apex
Forces greatest furthest from CoR- forces on the tooth are greatest at the apex.
Can be achieved by any appliance
Force 50-75g
what occurs in translation
Harder to achieve- moving tooth through the bone
All PDL uniformly loaded
Force 100-150g
what occurs in Rotation
Theoretically need high force BUT
Tipping occurs → Excessive compression of PDL
Force – 50-100g
Not too hard to achieve with fixed appliance
what occurs in Extrusion
Pull out the bone
Produce tension in PDL fibres- don’t want too high of a force or risk of loss of vitality of tooth
Force 50-100g
what occurs in Intrusion
Push into the bone
Forces concentrated at root apex
Fairly low force Force 15-25g
Missing part of tooth- tooth moved with too heavy of force, damage to cementum, osteoclasts get to the dentine and caused root resorption
what are the Risks Orthodontics to the pulp
Transient inflammatory response
Can cause loss of vitality
what are the Risks Orthodontics to the root
Root resorption inevitable
Commonly decreased 1-2mm root length
Some repair – however only ever filled in by cementum (rest periods)
Increased with: Distorted apices (roots bend) , Thin roots, Compromised teeth, Excess force, History of root resorption, Asthma
what are the Risks Orthodontics to the bone
Minimal transient damage
BUT : lose ½-1mm of alveolar crest
what are the Risks Orthodontics to the PDL
Minimal transient damage
Unless: Excess force maintained, Existing periodontal disease, Important in relapse- teeth go back to where they were
what are the Risks Orthodontics to the Cementum
Protects tooth from root resorption
Limited capacity to repair
what occurs in Ankylosis and why
Tooth won’t move
In growing patient causes infraocclusion
Root fused to the bone
Periodontal ligament lost, bony union between tooth and bone
Tooth sounds ‘tinny’ on percussion.
Aetiology often trauma
why is consent for orthodontic treatment important
- Root resorption
- Ankylosis
- Decalcification
- Retention / relapse
what occurs in Overeruption of teeth and what are the problems associated with this
teeth tend to continue to erupt if no occlusal contacts- Tendency for teeth to erupt to maintain contact
Problems: gingival trauma , restoration difficult, occlusal problems
Not inevitable- within limits bone/growth
Importance: restorations
Anterior wear- continue to erupt and maintain contact
what occurs in mesial drift and why might this occur
Teeth drift mesially
Maxilla > mandible
Early loss of primary teeth- space loss so posterior teeth drift
Importance to space maintain
Mesial drift can be useful- if early loss of first molars, second molars can erupt mesially
why might Late lower incisor crowding occur
Mandible continue to grow after maxilla stops, mandibular teeth don’t have anywhere to go so stay crooked.
other theories
pressure from Third molars? Mesial drift?
what occurs in the discolouration of teeth due to age changes
progressive thinning of enamel due to tooth wear and thickening of dentine produces yellowish teeth
stains become trapped in microscopic pits of enamel during enamel remineralisation
what might tooth staining result in (in terms of enamel development)
pronounced striae of retzius
how do whitening agents work
produce free oxygen radicals that penetrate through the enamel pores and reduce large chromogenic molecules to smaller molecules that might diffuse out of the pores or absorb less light.
why are older people less susceptible to caries
over time the enamel surface becomes more mineralised by incorporation of fluoride present in saliva- this forms fluorapatite rather than hydroxyapatite, which is more resistant
what is involved in the physio-chemical repair process of enamel
Remineralisation of enamel by re-incorporation of calcium, phosphate and fluoride ions that are present in saliva
what occurs when there is an imbalance in the de-/re- mineralisation cycle
Shift towards demineralisation causes caries. Earliest sign on teeth: ‘White spot lesion’
what is the difference clinically between a chalk-white lesion and hypomineralised lesion of developmental origin
hypomineralised lesions have a shiny appearance, whereas chalk-white lesions don’t (they’re active and non cavitated)
what does the dark zone and translucent zone represent
Dark zone: enamel remineralisation is ongoing
Translucent zone: enamel demineralisation
how do the enamel colours for: surface zone body of lesion dark zone translucent zone
differ in transmitted light and polarised light
transmitted v polarised
Surface zone:
Greenish/brown → Blue
Body of lesion: Orange → ‘Light’ black
Dark zone: Black → ‘Dark’ black
Translucent zone: Not visible here
what might the dark colour of enamel in ground sections represent
may represent a combination of enamel staining and hypomineralised enamel undergoing remineralisation, or where a WSL has developed, but has been arrested over time.
where does secondary dentine accumulate and what does this lead to
lines the pulp and root canals after the completion of tooth roots
more common on the roof and floor of pulp chamber (masticatory forces directly act in the cusp region)
pulp recession
what are the histological features of secondary dentine
continuous with primary dentinal tubules but fewer in number due do odontoblast death
contour line of owen- tubules can bend between primary and secondary dentine
where does peritubular dentine form
on the walls of dentinal tubules
Begins to form in outermost dentine
what are the characteristics of peritubular dentine
About 90 % mineralised
Usually does not contain collagen
Can fill whole dentinal tubules
what occurs when peritubular dentine completely occludes dentinal tubules
formation of sclerotic dentine
outline the physiological and pathological formation of sclerotic dentine
Physiological:
- Ageing process
- Found mostly in roots
Pathological:
- Response to caries
- It is Found between carious lesion and pulp- in the dentine directly affected by progression of caries lesion
when is tertiary dentine produced
Reactionary dentine: slow response mediated by existing odontoblasts lining the dental pulp, fewer tubules. => response to tooth wear (attrition)
Reparative dentine: rapid response mediated by new odontoblast-like cells induced from dental pulp stem cells (existing odontoblasts have died), less structure. => response to caries or cavity preparation
what can stimulate peritubular dentine formation
slow, natural wear of the crown
what is the response by dentine to tooth wear(attrition)
peritubular dentine formation
dentine becomes less permeable and insensitive if exposed
reactionary dentine forms in the pulp to compensate for dental tissue loss
what are the differences between old and young teeth due to reactionary dentine
Young tooth: • Little tooth wear • Larger pulp volume • Defined pulp horn • Pulp volume large Old tooth: • Worn cusp • Smaller pulp volume • Pulp horn filled in with reactionary dentine to compensate for tissue loss • Narrowed root canal – due to ageing as well
how do dead tracts form
Group of odontoblasts die due to continuous, strong stimulus
Results in reparative dentine formation that acts to seal off the pulp from invading micro- organisms
The tubules do not contain odontoblast processes anymore
Empty dentinal tubules contain air causing a dark appearance on ground sections
what are the age changes in the dental pulp
Decreased number of cells (e.g. odontoblasts)
size reduction of the pulp chamber
Calcified structures in pulp
what is the difference between the calcified structures in the pulp:
- false pulp stones
- true pulp stones
- diffuse calcifications
False pulp stones: Have not been produced by odontoblasts, they are calcified areas characterised by Concentric layers of calcified degenerated pulp tissue.
True pulp stones (Denticles):
- Produced by true odontoblasts
- Organic matrix and dentinal tubules
Diffuse calcifications:
- Through the pulp
- Usually associated with blood vessels or collagen fibres- as you age blood vessels can calcify
what are the ages changes that occur in cementum
Cementum thickness increases 3x from 16-70 years of age
Cellular cementum- Forms at root apex in response to attrition at the occlusal surface
what is hypercementosis and how does it occur
increase in cementum
- response to physiological process such as attrition
- Pathological process causing excessive build up
what are the age changes in the PDL
Decrease in cell numbers, density and mitotic activity
Fibroblasts have shorter live spans and diminished collagen synthesis and degradative activity
Increased collagen fibrosis, thicker fibre bundles and mineralisation of fibres
Irregular insertions of Sharpey’s fibres
Teeth become less “mobile” (→ decreased remodelling capacity able to move teeth in the jaw)
what are the Age changes that occur in alveolar bone
Loss of teeth => loss of alveolar bone
what are the Age changes in oral mucosa
Thinning of tongue epithelium on dorsal and lateral surfaces (oral cancer)
Reduced taste sensation
Gingival recession – but may be unclear if due to decreased oral hygiene or normal age change
Increasing susceptibility to precancerous lesions and oral cancer
what are the Age changes in salivary glands
Decrease in amount of glandular tissue
Increase in fibrous tissue, fat cells and inflammatory cells.
Dry Mouth (Xerostomia):
- Usually not presented in healthy older people
- Associated with increased use of medications
- Increases the rate of attrition (due to reduced enamel mineralisation
what is Physiological attrition and what does it affect. what type of dentine forms in response
natural process - tooth wear caused by mastication, e.g. contact with food particles
Affects interproximal and occlusal surfaces
Reactionary dentine has formed in response to attrition and blocked off the dentine tubules, which have become dead tracts.
what is pathological attrition
tooth wear caused by chewing with abnormal movement or habitual jaw clenching, e.g. bruxism
what is abrasion
tooth wear caused by frictional contact with foreign objects, e.g. pipe smoking
what is erosion and what are the dietary, environmental and medical causes
progressive loss of hard tissues due to chemical dissolution
Dietary: e.g. carbonated drinks, fruit/citrus juices and other acidic drinks and foods.
Environmental: e.g. competitive swimmers & professional wine tasters
Medication: e.g. Iron tonics, vitamin C and nutritional supplements.
what is bruxism
Pathological attrition
Habitual jaw clenching and tooth grinding:
Flat occlusal plane
Dentine hypersensitivity due to exposed dentine
what occurs in tooth brush abrasion
V-shaped cervical lesions due to:
• excessive tooth brushing
• abrasive toothpastes
how is erosion caused by stomach acid
Regurgitated stomach acid
• Acid reflux or repeated vomiting
• Eating disorders: Anorexia, Bulimia
• After vomiting, tooth brushing should be avoided for one hour
what is the Chemical basis for erosion
Enamel doesn’t dissolve in calcium-phosphate super-saturated saliva (pH 7) but at pH < 6, saliva is under-saturated and cannot efficiently remineralise the acid.
Acidic dissolution initiates erosion and makes the tooth more susceptible to abrasion.
The lower the pH of the oral environment, the higher is the enamel surface loss.
what Factors contribute to dietary erosion
Amount of drink consumed
Frequency & manner of consumption
Timing of consumption
Strength of acid
what are Lesser known risk groups
- Diabetics who consume fruit juice
- People who have low salivary flow (e.g. older people on medication) should avoid acidic drinks
- Children with asthma (Inhaling lowers the pH)
- Consumers of sports drinks (high sugar)
- Ecstasy and cocaine users
what are the 4 parameters that caries needs to occur
host
diet
time
microbes
what are the clinical aspect of the development of caries
subsurface translucent zone
development of dark zone
early WSL
cavitation, spread along ADJ, relative changes in dentine
what is the ‘seal’ and ‘hold’ concept
can arrest the decay if just filled with a sealant
what is the hall technique
caries is arrested as a metal crown is placed over the tooth, which will remove the substrate going to the caries
outline what is involved in the overview of pain diagnosis
dentine hypersensitivity reversible pulpitis irreversible pulpitis apical periodontitis (asymptomatic/symptomatic) peri-apical abscess (acute/chronic)
what is dentine hypersensitivity
short sharp pain arising from exposed dentine in response to stimuli (e.g. periodontitis so dentine exposed due to gum recession)
what are the stimuli for dentine hypersensitivity
thermal, evaporative, tactile, osmotic (e.g. draws fluid through tubules) or chemical
what is hydrodynamic theory
rapid shifts of fluid within the dentinal tubules, following stimulus application, results in activation of sensory nerves in the inner dentine region of the tooth
what are the 3 theories of dentine hypersensitivity
- dentine innervated directly
- odontoblasts act as receptors
- odontoblasts at the base of odontoblasts are stimulated directly or indirectly by fluid movement through the tubules
how can sensitivity be managed
block tubules
de-sensitising agents
adhesive restorations- physically block tubules
elective devitalisation- remove the nerve from the tooth
how can sensitivity occur due to bleaching (hydrogen peroxide)
- removal of dentinal tubule plugs by oxygenating bleaching gels that remove micro debris within the tooth
- outward movement of fluid within the dentinal tubules due to osmosis from bleaching gels
what occurs in cracked cusp syndrome
Tooth with crack or fracture
Exhibits a sudden sharp pain- fluid pushed through the tubules
Usually on mastication and classically on release of pressure.
Non vital teeth/ obturated teeth can give ‘dull ache’ and be sensitive to mastication.
how can cracked cusp syndrome be diagnosed
History
Orthodontic band
Transillumination- shine light through the tooth
Dyes
Magnification
Tooth sloth- specific occlusal force can be place on one cusp
how can Cracked cusp syndrome be managed
Bonded restoration
‘Cuspal coverage’ (crown)
Endodontic treatment
Extraction
what are the causes of pulpal inflammation
caries
defective restorations
trauma
dens investigation
what is pulpitis
chronically inflamed pulp- can be painless
acutely inflamed pulp can be painful with stimuli from hot, cold, sweet
what are the symptoms of reversible pulpitis
pain is short in duration
pain disappears when stimulus is removed
poorly localised
how can reversible pulpitis be managed
remove irritant and restore
preserve pulp
review
what the symptoms of irreversible pulpitis
Pain is longer in duration.
Pain persists (minutes to hours) when stimulus removed.
Cold can reduce pain- dental emergency clinic
Poorly localised
May have percussion sensitivity- sore when pressure applied
Spontaneous pain
how can irreversible pulpitis be managed
Pulpotomy- half of pulp removed
Pulpectomy- all of pulp removed
Extraction
Not antibiotics- not bacterial infection
what should be done in a stepwise excavation in reversible pulpitis
remove the worst, seal and then re-enter
what are the types of apical periodontitis
Symptomatic apical periodontitis
Asymptomatic (chronic) apical periodontitis
Acute apical abscess
Chronic apical abscess
Cyst formation (radicular)- unsure why.
what is the diagnosis for symptomatic apical periodontitis
TTP, can respond to sensibility tests, can have apical widening of periodontal ligament.
what is the diagnosis for Asymptomatic (chronic) apical periodontitis
Not TTP, no response to sensibility tests, usually shows apical radiolucency.
what is the diagnosis for Acute apical abscess
TTP, non- responsive, swelling (intra or extra-oral), febrile, lymphadenopathy.
what is the diagnosis for Chronic apical abscess
As for asymptomatic apical periodontitis but with draining sinus. Can be mildly TTP.
what would be the diagnosis for a toothache for a 10 year old patient, Fit + Well where:
- Nature: sharp pain on stimuli, with lingering aching pain
- Duration: 60 minutes after triggered
- Started: 5 days ago
- Stimuli: hot, pressure, spontaneous. (Cold helps)
and on clinical examination:
- DO caries 55
- Mildly TTP.
- Marginal ridge broken down
Irreversible pulpitis
what would be the provisional diagnosis for
• 10 year old patient, F+W
• Patient has ‘toothache’
Patient history • Nature: Constant dull aching pain • Duration: hours • Started: 7 days ago • Stimuli: pressure, biting.
Clinical examination
• Grossly carious 54.
• TTP
Acute apical periodontitis
Beyond pulpitis- pulp necrotic
what would be the provisional diagnosis for
- 60 year old patient, F+W
- Asymptomatic but has ‘noticed he has a hole in his tooth’.
Patient history • Nature: No pain. • Duration: No pain. • Started: No pain. • Stimuli: No pain. • Just suddenly had a hole in a tooth.
Clinical examination
• 15 buccal abrasion wear cavity.
• 16 buccal abrasion wear cavity.
• Striations
Abrasion, abrasive tooth wear
