L11 Flashcards
The periodontium: “Around the tooth” - The support system for the tooth
Cementum
Alveolar bone
Periodontal ligament (PDL)
Gingiva: Tooth-associated and gingival ligaments
Hertwig’s epithelial root sheath (HERS)
what is it?
Extension of enamel organ, transforms from cervical loop
Bilayer structure of IEE and OEE
Hertwig’s ERS
What does it do?
“Architect” of the root defining size and shape (morphogenesis)
Induces root odontoblast differentiation
But how do you get multiple roots?
Epithelial growth – epithelial interradicular process(es) = tongues of epithelium growing toward one another
Apical foramina (plural
Hertwig’s epithelial root sheath (HERS):
Differentiation of the root
Differentiation of root odontoblasts
Epithelial-mesenchymal signaling
Dental papilla:
Undifferentiated ectomesenchymal cells
HERS induces dental papilla cells to
differentiate to pre-odontoblasts, then odontoblasts
Root dentin forms in step with
HERS proliferation
HERS is a
transient structure
HERS disintegrates shortly after
inducing root odontoblast differentiation
Some HERS cells become
epithelial rests of Malassez (ERM)
Epithelial rests of Malassez (ERM)
ERM appear as clumps, strands, or networks of cells in the PDL
Surrounded by basement membrane
Sometimes close to root, sometimes several cell layers away
Function(s)? Can cause cysts. Also speculated to be involved with periodontal homeostasis or regeneration, but not proven…
Root dentin
continuous with
crown dentin
Dentinogenesis largely the same as crown
(exception: Interacting with IEE of HERS instead of IEE of enamel organ)
Cells:
Ectomesenchyme»_space; Dental papilla»_space; Pre-odontoblasts»_space; Odontoblasts
Types: Mantle dentin, circumpulpal dentin, predentin, primary/secondary/tertiary dentin, etc.
Epithelial-mesenchymal signaling in root
HERS
Smad4 transcription factor (TF) Sonic hedgehog (SHH) secreted signal → papilla cells
Dental papilla
Induces Gli1 TF
Downstream Nfic TF
Odontoblast differentiation
Without Nfic, dental papilla cannot respond to
HERS signaling and cells do not differentiate into odontoblasts
Result: Rootless teeth!
Developmental root defects
Defects of HERS growth and/or root dentin formation
Can make teeth prone to breakage, exfoliation, ankylosis, or cause difficult extraction and other issues
Dilaceration: deformity in shape/direction
“Rootless teeth”
Taurodontism: large pulp chamber at expense of root/furcation
Cementum comes in two main types
Defined by:
Presence/absence of cells within its matrix
Origin of collagen fibers of the matrix
Major types you need to be familiar with:
Acellular cementum = Acellular extrinsic fiber cementum (AEFC) = Primary cementum
Cellular cementum = Cellular intrinsic fiber cementum (CIFC) = Secondary cementum
Acellular cementum =
Acellular extrinsic fiber cementum (AEFC) = Primary cementum
Cellular cementum =
Cellular intrinsic fiber cementum (CIFC) = Secondary cementum
Cellular mixed stratified cementum (CMSC): A mix of =
alternating acellular and cellular layers
2 major types of cementum:
primary accellular cementum (covers 2/3rds of root).
Secondary Acellular cementum (covers apical 1/3rd of root)
Acellular afibrillar cementum
at CEJ
Acellular cementum
Cervical 2/3 of root
Primary cementum = formed first
Acellular extrinsic fiber cementum (AEFC)
No cells included
Cellular cementum
Apical 1/3 of root
Secondary cementum = second formed
Cellular intrinsic fiber cementum (CIFC)
Cementocytes included
Cementum: Attachment: Cementum important for
strong periodontal structure; “cementing” the tooth in the socket (acellular cementum primarily)
Cementum: Protecting root from
resorption and repairing resorption pits
Cementum: Adjusting
tooth position (Cellular cementum only)
Cementum: Sealing
dentin tubules – hydrodynamic theory of dental sensitivity, inhibiting bacterial invasion
Cementum composition and properties
Composition (similar to bone, dentin) ~50% inorganic: Mineral (hydroxyapatite) 35% organic: Collagen type I (90%), other non-collagenous proteins and glycosaminoglycans (10%) 15% water Physiology (different from bone) Avascular Non-innervated No turnover – growth by apposition
Classic hypothesis for cementum origins:
Ectomesenchyme > dental follicle > cementoblast
Fenestration of HERS allows follicle cells (pre-cementoblasts) to access root surface
Alternative hypothesis for cementum origins:
Dental epithelium > HERS > Epithelial-mesenchymal transformation to cementoblast
Cementoblasts
Origin: (Thought to be derived) from dental follicle (ectomesenchyme)
Function: Make acellular and cellular cementum
Products: Collagens, extracellular matrix (ECM) proteins, enzymes that promote cementum mineralization
Fate: Remain in PDL close to cementum surface, regulate slow cementum growth throughout life; direct cementum repair
Cementocytes
Origin: A subset of cementoblasts becomes embedded in cellular cementum matrix (i.e. from dental follicle, ectomesenchyme)
Function: ????????
Products: Much less than cementoblasts
Features: Reside in lacuna (small space in the matrix), extend dendrites (cell processes) through canaliculi (small tunnels) to communicate and receive nutrients
Fate:
Some remain in lacunae for life
Some deep lacunae appear empty- cementocyte death?
Dental follicle (dental sac)
Ectomesenchymal origin
Precursors to: Cementoblasts, PDL fibroblasts, osteoblasts
We don’t know exactly how specific follicle cells become specific differentiated cells, but location is part of it
Root dentin –
the “scaffold” for cementum formation
HERS disintegrates, exposing
root dentin surface
Cementoblast differentiation
From
dental follicle
Remain on/near root surface
Initial collagen fibers
Cementoblasts secrete these
Intermingle with dentin at the CDJ
These short fibers are intrinsic, not yet connected with PDL
Dentin-cementum junction (DCJ)
Cementum initial collagen fiber bundles intermingle with dentin collagen fibers
Dentin completes mineralization
DCJ remains a less hard “cushion” interface between cementum and dentin
PDL Fibroblasts
Produce primary collagen fiber bundles of PDL space
Stitched to first cementum intrinsic fibers
Extrinsic fibers
Continuity of extrinsic fibers and initial intrinsic fibers
These will become mineralized Sharpey’s fibers within cementum
Extrinsic fibers are the
MAJOR fiber group for acellular cementum
Extrinsic fibers enter
acellular cementum at HIGH DENSITY
Extrinsic fibers are critical to the
FUNCTION of acellular cementum
Dense, highly organized Sharpey’s fibers (in red) inserting into both the
acellular cementum and alveolar bone
These are mineralized collagen fiber bundles providing strong anchorage of tooth-PDL-bone
Additional views of acellular cementum and Sharpey’s fibers
Note lines perpendicular to root surface– mineralized collagen (Sharpey’s) fibers
Continuation of cementogenesis
Mineralization of fibers
Cementoblasts promote hydroxyapatite deposition between and within collagen fibers
Sharpey’s fibers are mineralized collagen fibers continuous with PDL, also found in alveolar bone
Collagen substrate (type I and others) -
the scaffold
Cells secrete non-collagenous extracellular matrix (ECM) proteins that participate in
mineral precipitation
Cells direct mineralization in and between
collagen fibers, e.g. by ECM proteins and enzymes
Progressive mineralization of
extrinsic collagen fibers
Progressive mineralization of
extrinsic collagen fibers
Mechanism of acellular cementum mineralization
Fiber fringe (FF) before cementum initiation FF becomes engulfed and mineralized = Sharpey’s fibers Mineralization continues slowly over time (~3 mm/yr)
(Secondary) Cementoblasts
Produce
cementum matrix rapidly – cementoid
Produce many intrinsic collagen fibers, deposit the cellular cementum ECM
Cellular cementum: Often minimal or absent in
incisors and canines = little role in tooth attachment
Cellular cementum: “Adaptive cementum” maintains
tooth in proper occlusal position by compensating for enamel attrition throughout life
Cellular cementum can repair
cementum resorption anywhere on root
Mechanism of cellular cementum mineralization
A clear unmineralized cementoid
Equivalent to predentin or osteoid
Cementoblast secretes collagen and other proteins»_space; Time lag»_space; Matrix mineralizes
Conditions that delay/inhibit mineralization may affect cementoid similarly to osteoid
Cementocytes
Embedded in
cellular cementum matrix
Connected to one another and surface (PDL)
Equivalent to osteocytes in bone?
Both acellular and cellular cementum continue
growing SLOWLY throughout life
No remodeling/turnover– cementum
appositional growth (adding to the existing layer)
Longitudinal lines/striations/appositional growth lines indicate
successive layers
BUT resorption does sometimes occur…
Reparative cementum
Following root cementum resorption by osteoclasts/odontoclasts
Repair cementum fills resorption pit (Howship’s lacuna)
Reparative cementum is often cellular, regardless of location (i.e. even on cervical root)
Concerns:
Is new cementum well bonded with dentin (i.e. quality of CDJ)?
Is new cementum well attached to PDL (i.e. density of extrinsic fibers?)
What can go wrong with cementum?
too little
Too little: cementum aplasia or hypoplasia
What can go wrong with cementum?
too much
Too much: hypercementosis, possibly leading to ankylosis
What can go wrong with cementum? Loss of cementum
Loss of cementum: External root resorption
Hypophosphatasia
Rare skeletal disease
Mutations in ALPL, gene for tissue-nonspecific alkaline phosphatase (TNAP protein)
TNAP breaks down pyrophosphate (PPi), an inhibitor of mineralization
HPP: High PPi
Acellular cementum aplasia or hypoplasia
HPP affects
bone (skeletal and craniofacial), dentin, and enamel
Acellular cementum most dramatically
HPP
affected tissue in terms of severity and prevalence
HPP
Defective/absent cementum →
Loose teeth, premature loss of primary and/or secondary teeth
Hypercementosis
Excessive cementum growth
Trauma, genetic disease, idiopathic
Generally asymptomatic, may cause ankylosis and difficulty in extraction
Unusual example of genetic hypercementosis that is opposite of HPP
What factors are important in mineralization?
acellular cementum
Bone sialoprotein (BSP)
First discovered in bone, but also present in dentin and cementum
Promotes hydroxyapatite mineral formation
Critical role in acellular cementum formation
BSP knock-out mouse has cementum hypoplasia, PDL detachment, periodontal breakdown
No known human equivalent, though phenotype consistent with some aspects of aggressive periodontitis
Root resorption (external)
Odontoclasts (osteoclast-like cells)
Very common to have “mild” resorption in 1 or more teeth
Excessive orthodontic force (usually apical effect)
Related to trauma, severe periodontitis, genetic factors
“Idiopathic”
Multiple idiopathic cervical root resorption
very aggressive, no treatment
Root (surface) caries
Bacteria/plaque initiated
Exposed root surface
Soft, progressive lesion – distinct from clastic resorption
Alveolar bone structure
Alveolar process/alveolar bone forms the socket that holds the tooth
Tooth-associated bone
Cortical plates (buccal/lingual)
Trabecular bone (spongiosa)
Alveolar plate is the focus for today’s lecture- the most involved with periodontal function
More in lecture 11 by Dr. Sun…
Alveolar bone:
The partner of cementum
Includes extrinsic collagen fiber bundles, mineralized Sharpey’s fibers (similar to acellular cementum)
Primary fibers entering bundle bone are larger in diameter and less dense (vs. cementum)
Bundle bone,
Bundle bone =
Bundle bone = Bone lining the socket, inner aspect facing tooth root
Lamina dura=
Radiographic feature of alveolar bone
Radiopaque layer lining the socket
Increased radiopacity from thick bone without trabeculation, NOT because of increased mineral content
Lamina dura is
Lamina dura is opaque (radiopaque)
PDL is
radiolucent
Cribriform plate = structure pierced by
many small holes
Bone remodeling in
response to function – osteoclasts and osteoblasts work in tandem
“Clasts” and their role in resorption
Normal remodeling of alveolar bone- FASTEST remodeling bone in the body
Normal bone resorption allowing tooth eruption
Normal tooth resorption when deciduous teeth are exfoliated
Abnormal when clasts resorb the roots of permanent teeth
Alveolar bone – tooth interactions
Alveolar bone distributes
occlusal loads
Existence of alveolar bone depends on
this interaction with dentition
“Mechanostat” theory of bone loading
Bone loading causes growth (e.g. tennis player effect)
Bone unloading causes loss (e.g. astronaut effect)
Edentulous mandible gradually loses alveolar bone
The periodontal ligament (PDL)
Soft fibrous connective tissue between tooth and alveolar bone (i.e. occupies the periodontal space)
Ligament =
Fibrous connective tissue connecting bone to bone
Periodontal ligament connects bone to tooth in a unique joint called a
gomphosis, or tooth socket
Normal width ~ 0.1 - 0.4 mm (BUT varies by person and tooth) is tightly regulated in health
Functions of PDL
Supportive:
Primary collagen fibers attach tooth to bone
Functions of PDL
Nutritive:
Blood supply to cells of the region, including cementoblasts and cementocytes
Functions of PDL
Sensory:
Innervated for sensing position and pain
Functions of PDL
Defensive:
Delivers immune cells including macrophages and neutrophils
Functions of PDL
Maintenance/Reparative:
Contains stem and progenitor cells that can repair or regenerate PDL, bone, cementum
Functions of PDL
Adaptive:
Based on mechanical loading (functional input), adapts fiber orientations and influences neighboring alveolar bone remodeling
Optimal arrangement to accept and distribute tensile forces from mastication
Even after orthodontic tooth movement, PDL returns to same width
Composition of PDL
Ground substance”
Amorphous background material
Proteins, proteoglycans, water
Composition of PDL
Collagen fibers
Collagen types I, III, XII major types
Fiber bundles – “spliced rope”
97% of fibers
Composition of PDL
Oxytalan fibers
Small elastic fibers, support collagen fibers and blood vessel walls
3% of fibers
NO elastic fiber bundles = PDL is more stiff for withstanding forces
PDL principal fiber groups
Collagen fiber bundles spanning PDL from mature tooth to bone (*except transseptal group is tooth-tooth)
Function:
Resist intrusive and extrusive forces, tipping and lateral movements
Defined by location or orientation
6 groups: TAHOAI
Oblique group is predominant- main group resisting occlusal loads (intrusive force)
Transseptal fibers travel from
tooth to tooth
Fibroblasts
Majority of cells in PDL
Secrete and remodel matrix
Intimately associated with collagen fibers- cells may act as mechanotransducers
Other PDL cells
Cementoblasts Osteoblasts, Osteoclasts Epithelial rests of Malassez (ERM) Stem/progenitor cells: Ability to differentiate and regenerate Immune cells
PDL is
well vascularized
Superior and inferior alveolar arteries
Perforating vessels, sometimes called alveolar or intra-alveolar – MAJOR route
Apical routes and gingival vessel routes also
Venous drainage in - PDL
axial direction
Gingival crevicular fluid (GCF)
Found in the sulcus/gingival margin
Transudate from vasculature
Diagnostic value
(1) Free endings, tree-like
Most common, found along the length of the root
Nociceptors and mechanoreceptors
(2) Ruffini endings
(slowly adapting, found in skin)
Found near apex
Mechanoreceptors
(3) Coiled endings
Mid-region of PDL
Function unknown
(4) Encapsulated endings
Found near apex
Function unknown
Cementicle
Ectopic cementum in PDL, attached or unattached
Ankylosis
Cementum-bone fusion
Loss of PDL space
Gingival epithelium
Oral epithelium
Sulcus epithelium
Junctional epithelium
Junctional epithelium
Enamel and cementum
Barrier to microbial invasion
Fast turnover
(Recall, this is derived from leftover enamel organ/reduced enamel epithelium)
Gingival ligament groups
Not PDL, but collagen fiber bundles spanning from tooth/bone to gingiva/connective tissue
In lamina propria (underlying connective tissue) of the gingiva
Function: Resist gingival displacement
4 groups: CDDA (transseptal group sometimes included, but we are grouping with PDL)
