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STAGE 2 > CTB > Flashcards

CTB Flashcards

1
Q
  1. What is coordinated with the development of the periodontium?
A

Tooth root formation

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2
Q
  1. Where does the PDL attach the tooth?
A

To the alveolar bone

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3
Q
  1. Describe the coordinated root and periodontal tissue formation
A
  1. Odontoblast induction and dentine formation
  2. Stretching and disintegration of HERS
  3. differentiation of dental follicle cells:
    - Cementoblasts = cementum
    - Fibroblasts = PDL
    - osteoblasts = alveolar bone
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4
Q
  1. Which genetic factors regulate the differential formation of periodontal tissue?
A
  1. Insufficiency investigated:
    - FGF’s (fibroblast growth factor) = cell proliferation and migration
    - BMP’s (bone morphogenic proteins) = cell diff and bone formation
  2. Use of growth factors:
    - e.g. FGF2, BMP2 to stimulatre periodontal regeneration
  3. Stem cells in PDL
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5
Q
  1. Functions of PDL
A
  1. Tooth attachment:
    PDL fibres insert into cementum and alveolar bone to form a fibrous joint (v. little/ no movement)
  2. Withstand forces of mastication/ shock absorber
  3. Sensory receptor:
    - Sensation of pain and tension/compression
    - Repositioning of teeth to achieve occlusion
  4. Remodelling function (tooth movement):
    - High turnover of ECM and collagen
    fibres. Source of progenitor/stem cells.
  5. Nutritive function:
    Highly vascularised tissue
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6
Q
  1. Fibrous joint with very little or no movement
A

→ gomphosis, synarthrosis

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7
Q
  1. Timing of PDL development and differentiation varies btn….
A

Species, tooth types and pirm/perm teeth

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8
Q
  1. Stage 1 of PDL development
A

Initiation stage:
The ligament space between cementum and bone consists of an unorganised connective tissue.
(→ fibroblasts and extracellular matrix).
Short fibre bundles (FB) formed near cementum/ bone extend only a short distance into the ligament space.

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9
Q
  1. Stage 2 of PDL development
A
  1. Fine brush-like fibres emerge from cementum (C) and only a few fibres project from alveolar bone
    (B) into the ligament space.
  2. Fibroblasts produce more collagen fibrils that assemble as fibre bundles and gradually extend from bone to cementum to establish a continuous attachment.
    Bone side: Thick AND widely spaced fibre bundles
    Cementum side: Thin and closely spaced
    Fine intermediate meshwork
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10
Q
  1. Stage 3 of PDL development
A

Alveolar crest fibres formed first at cemento-enamel junction
- As the root forms, fibre formation then proceeds apically.
Orientation is initially oblique, then horizontal and then oblique again
- PDL is continuously modified by eruptive tooth movements and occlusion.
- Thick fibre bundles only form when teeth occlude and function.

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11
Q
  1. What are the Principle fibre groups of the PDL?
A
  1. Alveolar crest group
  2. Oblique group
  3. Horizontal group
  4. Apical group
  5. Interradicular group
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12
Q
  1. What is the Alveolar crest group
A
  • Type of principle fibre group of the PDL
  • Below CEJ → rim of alveolus
  • resists extrusive forces
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13
Q
  1. What is the horizontal group?
A
  • Type of principle fibre group of the PDL
  • Below alveolar crest group;
  • at right angle to tooth axis
  • resists horizontal forces (‘tipping’)
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14
Q
  1. What is the oblique group
A
  • Type of principle fibre group of the PDL
  • Most abundant fibre group
  • resists intrusive forces (→ mastication)
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15
Q
  1. What is the apical group?
A
  • Type of principle fibre group of the PDL
  • Radiates around root apex
  • forms base of the socket
  • resists extrusive forces
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16
Q
  1. What is the interradicular group?
A
  • Type of principle fibre group of the PDL
  • Only multi-rooted teeth
  • connects to crest of interradicular septum
  • resists extrusive forces
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17
Q
  1. Types of PDL
A
  • Each collagen fibre bundle resembles a spliced rope and individual fibrils can be continuously remodelled whereas the overall fibre maintains its architecture and function. => Possibility to adapt to mechanical/masticatory forces.
  • Elastic fibres: Oxytalan fibre; fibrillin (no elastin);
    run perpendicular to collagen fibres in cervical region associated with neurovascular bundles;
    form 3D meshwork surrounding root;
    Function: regulation of vascular flow?
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18
Q
  1. What are Sharpey’s fibres?
A

Mineralised PDL fibres in alveolar bone and cementum

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19
Q
  1. What are the cell types in the PDL?
A
  • Fibroblasts
  • Osteoblasts and osteoclasts
  • Cementoblasts and Cementoclasts
  • Rests of Malassez
  • Undifferentiated messenchymal stem cells
  • Immune cells
  • Blood vessels
  • Nerve fibres
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20
Q
  1. What do fibroblasts produce/secrete?
A
  • ECM (ground substance)
  • Collagen fibrils (fibre bundles)
  • Growth factors/ cytokines
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21
Q
  1. what are the progenitors of PDL cells?
A
  • perivascular fibroblasts

- endosteal fibroblasts

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22
Q
  1. Fibroblasts
A
  • rich in organelles
  • form cell-to-cell contacts (adherens and gap junctions)
  • well developed cytoskeleton allows shape change and migration
  • align along the direction of fibre bundles
  • activity induced by mechanical/masticatory forces
  • involved in functional tooth movements
  • dual function in remodelling - synthesis and degradation of ecm and collagen
  • matrix metalloproteases MMP’s - therapeutic target in perio disease
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23
Q
  1. What is the composition of PDL
A
  • 60% ground substance

- fibres: 90% collagen, 10% oxytalan (fibrilling microfibrils w/o elastin)

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24
Q
  1. Does collagen composition of PDL change with age?
A

No

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25
Q
  1. Types of collagen in PDL
A
  • 80% = type 1
  • 15% = type 3 - reticular fibres; meshwork
  • the remainder = 4, 5, 6, 7, 12
  • 12 = links other collagens, only present after eruption and expresed on pressure side following mechanical loading
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26
Q
  1. what is the composition of ECM?
A
  • glycosaminoglycans (GAGs: hyaluronic acid, dermatan sulfate; also chondroitin and heparin sulfate)
  • proteoglycans
  • glycoproteins
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27
Q
  1. function of ecm
A
  • Ion and water binding
  • 70% water (“shock absorber”)
  • orientation of collagen fibres
  • ECM binds growth factors and cytokines: FGF, TGF-beta (BMP), IGF, PDGF, VEGF, Interleukins, Prostaglandins.
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28
Q
  1. what does ecm control
A

hydration of the tissue

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29
Q
  1. how does ecm affect collagen fibrils
A

increases strength of collagen fibrils

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30
Q
  1. how does composition of ecm vary according to developmental state
A
  • Hyaluronan decreases during development of PDL from dental follicle.
  • Proteoglycans increase during tooth eruption.
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31
Q
  1. what is the role of fibronectin?
A
  • found in ecm
  • mediates attachment of cells to collagen fibrils => influence on cell migration and differentiation.
  • Clinically used to promote wound healing
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32
Q
  1. What are osteoblasts and osteoclasts associated with?
A

Bone remodelling

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33
Q
  1. What are cementoblasts and cementoclasts associated with?
A

Cementum remodelling

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34
Q
  1. what are Rests of Malassez?
A

Remnants of HERS (source of epithelial stem cells?)

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35
Q
  1. what are Undifferentiated mesenchymal stem cells a source of
A

all mesenchymal cell types (e.g. fibroblasts, osteoblasts, cementoblasts)

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36
Q
  1. what are the immune cells of the PDL
A

Macrophages
Mast cells
Eosinophils

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37
Q
  1. why is PDL highly vascularised?
A

due to its high turnover rate of pdl components requiring a constant nutrient supply

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38
Q
  1. what innervates the PDL?
A
  1. Branches of the superior and inferior alveolar arteries

2. Branches of the lingual and palatine arteries

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39
Q
  1. where do branches of the lingual and palatine arteries enter the PDL?
A

through ginigiva

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40
Q
  1. describe the route the superior and inferior alveolar arteries takes to innervate the PDL
A
  1. Enter the pulp at the apex (A).
  2. Interalveolar vessels pass through the alveolar process to form perforating arteries
    - more abundant in posterior and mandibular teeth.
    - enables PDL function after endodontic treatment.
    - extractions wounds: formation of blood clot and invasion of cells involved in healing
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41
Q
  1. what forms ‘interstitial areas’ within PDL?
A 
perforating arteries 
(Interalveolar vessels pass through the alveolar  process)
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42
Q
  1. where do neurovascular bundles pass through?
A

perforations in the alveolar bone and form the interstitial areas in the PDL

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43
Q
  1. where are interstitial areas usually located in the PDL?
A
  • closer to the alveolar bone
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44
Q
  1. what do interstitial areas contain?
A

neurovascular bundle

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45
Q
  1. describe the vasculature of the PDL
A

Blood vessels form a capillary plexus near the root surface and a postcapillary plexus from which venules pass into the alveolar bone.

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46
Q
  1. what directions do blood vessels of the PDL run in?
A

apical-occlusal direction

and form arteriovenous anastomoses

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47
Q
  1. vasculature of PDL - where is the venous drainage
A

at the apex

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48
Q
  1. vasculature of PDL - where are the lymphatic vessels
A

follow the venules

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49
Q
  1. What is the diff between the circular plexus and the crevicular plexus?
A
  • Circular plexus surrounds the root surface
  • Crevicular plexus surrounds the tooth in the region beneath the gingival crevice
  • Function: defence at DGJ?
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50
Q
  1. what is a special feature of the PDL?
A

Fenestrated capillaries

usually not found in other connective tissues

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51
Q
  1. what is the function of fenestrated capillaries in PDL?
A

Generates increased diffusion capacity consistent with the high metabolic rate in the PDL (especially during tooth eruption!)

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52
Q
  1. What pattern does the nerve fibre generally follow in the PDL?
A
  • follows the pattern of the vasculature. (From apex to gingival margin and through lateral perforations of the alveolar bone)
  • Perforating nerve fibres divide into an apical and a gingival branch.
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53
Q
  1. what type of variation is there in innervation of PDL?
A

Regional variation:

  • More nerve endings at the tooth apex
  • Upper incisors: denser innervation throughout the PDL compared to molars.

Could be related to masticatory response?
Initial contact with food could specify the level of force required to process the food.

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54
Q
  1. Types of nerve fibres in the PDL?
A
  1. Sensory:
    - Nociception: pain
    - Proprioception (mechanoreception): pressure
    → Food sensing; position of tongue & neck musculature; salivary reflexes
  2. Autonomic:
    - Regulation of blood flow (constriction and dilation of blood vessels)
  3. Myelinated fibres:
    - Sensory only

Myelinated and unmyelinated fibres:

  • Sensory
  • Autonomic
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55
Q
  1. Types of nerve endings in the PDL
A
  1. Free-ending
  2. Ruffini’s corpuscles
  3. Coiled type
  4. Encapsulated spindle type
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56
Q
  1. Free nerve ending in PDL
A
  • treelike type
  • Evenly distributed across the PDL
  • Unmyelinated fibres (enveloped by one Schwann cell; inset)
  • Extend up to the cementoblast layer
  • Sense pain and pressure
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57
Q
  1. Ruffinis corpuscle in PDL
A
  • Found in PDL at root apex
  • Myelinated fibres with dendritic endings
  • Associate with collagen fibres (inset)
  • Sense pressure
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58
Q
  1. Coiled type nerve ending in PDL
A
  • Found in middle region of the PDL

- Unknown function

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59
Q
  1. Encapsulated spindle type nerve ending in PDL
A
  • Found in PDL at root apex (infrequent)

- Surrounded by fibrous capsule

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60
Q
  1. where is the PDL the thinnest?
A

thinnest in middle third of the root

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61
Q
  1. how is PDL thickness affected with age
A

as age increases, PDL thickness decreases

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62
Q
  1. How does mastication affect PDL thickness?
A
  • Mastication induces periodontal remodelling resulting in increased PDL width and in increased alveolar bone size.
  • PDL is thicker in areas of tension than in areas of compression.
  • Decreased function results in reduction/loss of periodontal tissues
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63
Q
  1. what forms the tooth sockets
A

alveolar process of the mandible

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64
Q
  1. what is the mechanism of bone formation
A
  1. Endochondral ossification
  2. Intramembranous ossification
  3. Sutural ossification
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65
Q
  1. what is endochondral ossification?
A

Bones made from a cartilage model
(Chondrocytes produce cartilage that is replaced by osteoid/bone produced by osteoblasts)
e.g. Long bones (epiphyseal growth plate), base of skull (synchondrosis), mandibular condyle (secondary cartilage)

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66
Q
  1. what is Intramembranous ossification?
A

Intramembranous ossification
Bones made by osteoblasts that have differentiated from mesenchymal stem cells
e.g. Flat skull bones; Facial bones: mandible, maxilla, alveolar bone

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67
Q
  1. what is sutural ossification?
A

Similar to intramembranous ossification but with fibrous connection
Providing stability during growth
e.g. Postnatal growth of flat skull bones

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68
Q
  1. bone composition:
A
  • Mineralised, living connective tissue
  • Organic matrix is permeated by hydroxyapatite (deposited between Type I collagen fibrils)

Non-collagenous proteins: Bone sialoprotein, osteocalcin, osteonectin, osteopontin
(all of these bind to calcium or HA
=> control of mineralisation), proteoglycans, cytokines, growth factors, serum proteins

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69
Q
  1. Composition of bone varies…
A

from different sites and developmental stages

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70
Q
  1. what are the functions of bone
A
  • locomotion
  • support
  • protection
  • mineral reservoir (calcium and phosphate)
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71
Q
  1. what is bone physiology controlled by?
A

hormones

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72
Q
  1. what hormones INCREASE bone mass/formation?
A
  • calcitonin
  • vitamin d
  • leptin
  • estrogen
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73
Q
  1. what hormones DECREASE bone mass/formation?
A
  • PTH

- glucocorticoids

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74
Q
  1. how are menopausal women affected in terms of bone

hint: reduced levels of estrogen during menopause

A
  • estrogen supports bone formation

- osteoporisis

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75
Q
  1. what growth factors are involves in bone homeoestasis?
A
  • BMP

- TGF-B

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76
Q
  1. What is the role of cytokines in bone formation?
A

involved in the communication between osteoblasts (make bone) & osteoclasts (reabsorb bone)

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77
Q
  1. what is a woven bone?
A
  • Bone formed during development characterised by randomly oriented collagen fibrils.
  • Becomes replaced by lamellar bone.
  • forms rapidly as part of the wound healing response
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78
Q
  1. what is the first bone to form during development?
A

woven bone

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79
Q
  1. why is bone softer than dentine?
A

because it is less mineralised

80
Q
  1. what is compact bone?
A

dense outer area of the bone

81
Q
  1. what is a Trabecular bone?
A
  • cancellous, spongy
  • cavity filled with bone marrow interrupted by a network of bone plates (trabeculae)
  • Network of little boney plates, leaving spaces in between – where the bone marrow sits
82
Q
  1. what are the 3 types of bone lamellae?
A
  1. Circumferrential
  2. Concentric (Haversian)
  3. Interstitial
83
Q
  1. What is Circumferrential lamellae?
A

It encloses the entire inner and outer perimeter of the bone

84
Q
  1. What is Concentric (Haversian) lamellae?
A

form the basic unit of bone (osteon) and make up the bulk of the compact bone

85
Q
  1. What is Interstitial lamellae?
A
  • interspersed btn adjacent osteons.

- remnants of remodelled osteons

86
Q
  1. what is an osteon
A
  • concentric ring of bone with a blood vessel in the middle

- generally orientated parallel to the long axis of the bone

87
Q
  1. central (Haversian) canal consists of…
A
  • blood capillary lined by a layer of osteoblasts
88
Q
  1. how are adjacent haversian canals interconnected?
A
  • volkmann’s canals (osteons from lateral canals between each other)
89
Q
  1. what is the periosteum in bone?
A
  • external surface
  • connective tissue membrane, consisting of 2 layers:
    1. Outer (fibrous) layer: Dense collagen fibres
    2. Inner (cellular) layer: Osteoblasts and their precursors, highly vascularised
90
Q
  1. what is the endosteum in bone?
A
  • internal surface
  • Not well demarcated
  • loose connective tissue including osteoblasts
  • separates bone surface from marrow
  • less active in bone formation than periosteum
91
Q
  1. what are osteoblasts derived from?
A

mesenchymal stem cells.

92
Q
  1. describe Active osteoblasts cell shape
A

cuboidal

93
Q
  1. describe Inctive osteoblasts cell shape
A
  • flat

- bone lining cells

94
Q
  1. what do osteoblasts synthesise?
A
  • organic bone matrix (osteoid; mainly collagen type 1)
95
Q
  1. what do osteoblasts produce?
A

alkaline phosphotase

96
Q
  1. what is the role of alkaline phosphotase?
A
  • cleaves inorganic phosphate to initiate and promote mineralisation
  • regulates mineralization
97
Q
  1. what growth factors do osteoblasts produce and what is their role?
A
  • IGF1, TGF-beta, PDGF
  • Increase bone repair
  • considered for dental therapy; perio disease, dental implants
98
Q
  1. what is an osteocyte?
A

Once osteoblasts mature and become trapped inside the bone matrix they produce osteoblasts that become trapped in unmineralised or mineralised matrix

99
Q
  1. how do osteocytes appear different to osteoblasts?
A
  • smaller

- produce a white space in the matrix (lacunae)

100
Q
  1. how are adjacent osteocytes connected
A
  • network of cellular processes that connect adjacent osteocytes
    (resulting in canaliculi in the future bone)
101
Q
  1. functions of osteocytes?
A
  • sensors of changes in the bone environment

- signalling centres to maintain bone integrity (e.g. induce bone remodelling)

102
Q
  1. what are osteoclasts?
A

Bone resorbing cells

103
Q
  1. what are osteoclasts derived from?
A

haematopoietic cells (blood making cells)

104
Q
  1. describe the cell structure of osteoclasts?
A
  • large

- multinucleated

105
Q
  1. what do osteoclasts produce during bone resorption?
A

Howship’s lacunae - holes left in the bone

106
Q
  1. what enzymes do osteoclasts produce?
A
  • acid phosphatase
  • lysosomal enzymes - Create an acidic environment, which activates these enzymes – degrading the bone – swallow up degradation products by endocytosis
107
Q
  1. what is the resorption sequence of bone?
A
  • Attachment of osteoclast to bone
  • Creation of acidic microenvironment
    for demineralisation
  • Degradation of exposed matrix by
    enzymes
  • Endocytosis of degradation products
108
Q
  1. describe the mechanism for intramembranous ossification
A
  1. Mesenchymal cells in the cellular periosteum differentiate to become osteoblasts which produce an irregular bone type (woven bone).
  2. Gradual turnover of woven bone to lamellar bone.
    Formation of primary osteons by osteoblasts surrounding a blood capillary.
  3. Continued bone replacement produces highly organised, mature bone.
    - fewer cells, secondary & tertiary osteons, circumferential lamellae.
109
Q
  1. describe the mechanism for the development of the alveolar process.
A
  • Mandible takes the shape of a trough underneath the inf. alv. nerve.
  • alveolar process grows towards the tooth germ
  • Alveolar process almost surrounds incisor tooth germ
  • IAN (incisive branch) enclosed in bony canal.
  • To accommodate the growing tooth germ (stellate reticulum), alveolar bone must be resorbed on the inner wall of the alveolus (osteoclast) and new bone must be deposited on the outer wall (osteoblasts).
110
Q
  1. what shape are bone lining cells(inactive osteoblasts)?
A

Flat

111
Q
  1. what is the function of bone lining cells?
A

Area of bone inactivity:

  • protection from resorption
  • initiating bone remodelling
  • mineral metabolism
  • source of progenitor cells?
112
Q
  1. what are the stages of bone remodelling?
A
  1. Resorption:
    - Recruitment, migration and activation of osteoclasts
    - bone resorption
  2. Reversal:
    - Cessation of resorption, disappearance of osteoclasts (apoptosis or migration)
  3. Formation:
    - Recruitment, migration and differentiation of osteoblasts
    - bone formation
  4. Resting:
    - Cessation of bone formation
    - Surface covered by flat bone-lining cells
113
Q
  1. why do resting (parallel) lines form in histological bone pictures?
A
  • pause in bone deposition

- when the osteoclasts have stopped producing bone

114
Q

why do reversal (scalloped) lines form in histological bone pictures?

A

Change from bone resorption to deposition (position of Howship’s lacunae)

115
Q
  1. terminology of a tooth socket (look at diagram)
A

A: Buccal cortical plate - thicker
B: Lingual cortical plate
C: Alveolar (“cribiform”) plate: perforations in bone for blood vessels and nerves
D: Interdental septum: alveolar bone between two teeth
E: Interradicular septum: alveolar bone between two roots

116
Q
  1. what contains the tooth socket?
A

alveolar process

117
Q
  1. Alveolar bone - outer compact layer?
A

cortical plate

118
Q
  1. Alveolar bone - central trabecular layer?
A

spongiosa

119
Q
  1. Alveolar bone - inner compact layer?
A

alveolar plate/ cribriform plate

- perforations for nerves and vessels connecting to PDL

120
Q
  1. why is there a outer compact, trabecular and then inner compact structure of bones instead of them all being compact?
A
  • to have light bones

- all compact would limit movement

121
Q
  1. Cortical plate of alveolar bone
A
  • Surface layer of lamellar bone supported by osteons (Haversian systems)
  • Thinner in maxilla than mandible
  • Thickest on buccal aspect of mandibular premolars and molars
122
Q
  1. Spongiosa of alveolar bone
A
  • Trabecular (cancellous) bone
  • Bone marrow spaces rich in adipose tissue (→ “yellow bone marrow”)
  • Absent in anterior teeth; cortical and alveolar plate are fused
123
Q
  1. Alveolar plate of alveolar bone
A
  • Lamellar bone and bundle bone

- Contains Sharpey’s fibres

124
Q
  1. what is the bundle bone?
A
  • The innermost layer of the alveolar plate (directly lining the socket)
  • called this because the collagen fibre bundles of the PDL are embedded
  • Provides the attachment for PDL fibres
  • Bundle bone is apposed to lamellar bone (Haversian systems)
125
Q
  1. describe how orthodontic tx/ tooth drift use bone remodelling?
A
  1. resorption of the right side of the alveolar plate creates space that the tooth can move into
  2. to compensate for this bone loss, new bone must be formed onto the cortical plate on the opposite side (to keep alveolar thickness consistent)
  3. b/c the tooth moves to the right, the space in the socket must be filled by bone deposition onto the alveolar plate
  4. the excess bone must be resorbed from the cortical plate on the opposite side.
  5. alveolar bone remodelling proceeds through the same stages (resorption, formation, resting) but occurs at the same site resulting in no bone displacement
126
Q
  1. what type of teeth have few interproximal contact points?
A

unworn teeth

127
Q
  1. what cause hard tissue loss on occlusal and interproximal surfaces
A

attrition

128
Q
  1. what is an increase in interproximal distance compensated by?
A

mesial (forward) drift

129
Q
  1. what is tooth ankylosis and what is it caused by?
A
  • Dental trauma or infection
  • fusion of tooth root to alveolar bone
     Prevents exfoliation; leads to impaction of successor tooth
130
Q
  1. in what tooth is tooth ankylosis most common and what does it prevent?
A
  • primary molars (e.g. partial root resorption)

- Prevents exfoliation - leads to impaction of successor tooth

131
Q
  1. what is infraocclusion?
A

teeth found with their occlusal surface below the adjacent teeth, long after they should have reached occlusion

  • Further growth of alveolar bone results in “submergence” of ankylosed tooth; clinical term: ‘Infraocclusion’
  • Extraction to prevent malocclusion or periodontal problems
132
Q
  1. on radiographs what is the alveolar plate referred to?
A

lamina dura

- has increased radiopacity due to thick cortical bone

133
Q
  1. what does an interrupted lamina dura in the apical region indicate?
A
  • periapical abscess

- appears as dark shadow

134
Q
  1. maxillary sinus
A
  • Close proximity of premolar/molar roots and alveolar bone

- During tooth extraction, bone can fracture (oro-antral connection/fistula; infection!)

135
Q
  1. Following tooth extraction or chronic periodontitis, the alveolar process can resorb. What are the implications?
A
  • Placement of dental implants will be difficult.
  • Implanting soon after tooth loss decreases the rate of alveolar ridge resorption.
  • Bone loss impacts on construction of removable prostheses.
136
Q
  1. what happens after tooth extraction ?

re wound healing

A

After tooth extraction, socket fills with blood and forms blood clot

137
Q
  1. what is a dry socket?
A
  • Detachment of blood clot
  • Leads to painful bone inflammation
  • bad odour
  • mainly affects mandibular teeth
138
Q
  1. what is the definition of gingiva?
A

part of the oral mucosa that surrounds and is attached to teeth and the alveolar bone
`

139
Q
  1. what is the gingiva in contiuum with?
A
  • oral mucosa

- pdl

140
Q
  1. what created the Dentogingival junction?
A

tooth eruption

141
Q
  1. how does tooth eruption for the DGJ?
A

During tooth eruption, the REE fuses with the oral epithelium (OE) to establish the DGJ
A: Tooth approaches oral epithelium; only thin layer of connective tissue separates REE (similar to simple epithelium) from the OE (stratified squamous epithelium).
B: Fusion of REE with OE and degeneration of central epithelial cells.
- Epithelial continuity at all times (no connective tissue exposure → no bleeding!)
Tooth erupted and DGJ formed: Junctional epithelium → Tooth attachment

142
Q
  1. stage 1 of DGJ formation
A

Immediately after tooth eruption, the junctional epithelium consists entirely of REE.

  • not keratinised
  • attaches firmly to the enamel
143
Q
  1. stage 2 of DGJ formation
A

Some time after tooth eruption
- gingival epithelium (stratified, keratinised) appears to “overgrow” and replace the REE.
–> Sulcular epithelium (stratified, not keratinised)
Mechanism?
- Switch from gingival to sulcular keratinocyte identity
- Stratification of REE cells and rete peg formation

  • Junctional epithelium (simple, not keratinised) still appears like reduced enamel epithelium.
144
Q
  1. what is the development of (e.g. depth) of gingival sulcus induced by?
A

masticatory forces

145
Q
  1. stage 3 of DGJ formation
A
  • 2-3 years after tooth eruption
  • gingival epithelium appears to have completely replaced the REE
  • Small epithelial tag from REE remains:
    –> Cell remnants and primary enamel cuticle (= Nasmyth’s membrane)
    BUT, despite similar histology, molecular markers indicate that junctional epithelial cells are diff from gingival epithelial cells.
    Mechanism?:
  • REE (similar to simple epithelium) could become stratified and develop rete pegs.
146
Q
  1. what evidence suggests that stem cells can reform the JE?
A
  • tooth attachment is restored after gingivectomy

- gingival tissue grafting is possible

147
Q
  1. what are the 2 enamel matrix proteins that are immunohistolgically stained in mouse teeth?
A

Amelotin and odontogenic ameloblast-associated (ODAM):

  • Normally expressed by maturation stage ameloblasts (→ forming the REE)
  • Expression in internal basal lamina and junctional epithelial cells suggests junctional epithelium is derived from REE.
148
Q
  1. what do (gingival) epithelial cells secrete onto the enamel surface?
A

primary enamel cuticle (internal basal lamina)
External basal lamina (typical composition) attaches to lamina propria.
 Very strong ‘epithelial attachment’ to tooth
 Once lost in periodontal disease it is difficult to regenerate!

149
Q
  1. what does the primary enamel cuticle bond with and how?
A
  • enamel proteins

- attach via hemidesmosomes

150
Q
  1. where does external basal lamina attach?
A
  • lamina propria
  • Very strong ‘epithelial attachment’ to tooth
  • Once lost in periodontal disease it is difficult to regenerate!
151
Q
  1. why is junctional epithelium permeable?
A
  • reduced number of desmosomes

- larger intercellular spaces.

152
Q
  1. what does the permeability of the junctional epithelium allow?
A

passage of gingival crevicular fluid (GCF) and defence cells into the sulcus.

153
Q
  1. what does GCF contain?
A
  • Immunoglobulin molecules
  • Complement factors
  • Macrophages
  • Desquamated sulcular and junctional epithelial cells
  • Cytokines and metalloproteases (during infection)
154
Q
  1. what is the function of GCF?
A

1st line of defence against bacteria

155
Q
  1. what if GCF is overproduced?
A

Tissue destruction caused by inflammation

156
Q
  1. what are the ginigval landmarks?

look at diagram slide 12

A 
A: Attached gingiva
Tigthly attached to tooth and alveolar bone
B: Alveolar mucosa
Loosely attached to alveolar bone
C: Submucosa (of alveolar mucosa)
D: Free gingiva
not bound to other tissue  E: Free gingival groove  F: Gingival margin
G: Gingival sulcus
H: Junctional epithelium
I: Sulcular (crevicular) epithelium
157
Q
  1. what is Mucogingival junction (MGJ)?
A
  • Boundary between alveolar mucosa (lining mucosa; non-keratinised
  • dark pink; translucent and superficial blood vessels
    and attached gingiva
158
Q
  1. describe the attached gingiva?
A
  • masticatory mucosa
  • parakeratinised and partially orthokeratinised)
  • light pink
  • ‘surface stipples’
159
Q
  1. Histology of attached gingiva
A

Attached gingiva:

  1. Epithelium
    - thick
    - parakeratinised + orthokeratinised
  2. Lamina propria
    - long, narrow papillae
    - dense collagen fibres
  • submucosa is absent
160
Q
  1. what is the role of the submucosa
A
  • provides mobility
  • acts as a cushion
    e. g. in lining mucosa
161
Q
  1. what is a mucoperiosteum
A
  • Lamina propria is more fibrous and directly joined with the periosteum of bone: e.g. masticatory mucosa (middle of hard palate, gingiva
162
Q
  1. what gingival privipal fibre group is seen in the buccal view
A

Transseptal fibre group

  • Run interdentally from CEJ over the alveolar crest to CEJ of neighbouring tooth.
  • Fiber system that connects all teeth of the jaw.
  • controls mesio-distal spacing
163
Q
  1. what is the clinical relevance of transseptal fibre group?
A

The slow pace of remodelling of this fibre system even under mechanical stress can cause post-retention relapse of orthodontically repositioned teeth.

164
Q
  1. what gingival privipal fibre groups are seen in the buccal view
A
  • Dentogingival group
  • alveogingival group
  • dentoperiosteal group
  • circular group
165
Q
  1. describe the dentogingival group
A
  • largest group

- Connects cervical cementum to lamina propria of free and attached gingiva

166
Q
  1. describe alveogingival the group
A

Connects bone of alveolar crest to lamina propria of free and attached gingiva.

167
Q
  1. describe dentoperiosteal the group
A
  • Running from the cementum over outer surface of the alveolar process
  • insert either into the alveolar process or the vestibular muscle and floor of mouth
168
Q
  1. describe the circular group
A
  • smallest group
  • Forms band around the neck of teeth
  • interlaces with other fibres in the free gingiva
  • Binds free gingiva to the tooth
169
Q
  1. what does dental plaque accumulation cause?
A

an inflammtory response

- tx stops spreading of inflammation into PDL and alveolar bone

170
Q
  1. what does persistent inflammation result in?
A
  • Further destruction of connective tissue by inflammatory cells causes apical migration of junctional epithelium
  • Formation of gingival pocket
  • Advanced: Loss of PDL and alveolar bone
171
Q
  1. what is the mechanism of epithelial down growth?
A
  • Growth until intact connective tissue is reached
  • Compensation for loss of mechanical stability.

Prevention (periodontal surgery):

  1. Insertion of membrane (physical barrier)
    - Formation of fibrin clot against root surface
172
Q
  1. how can we measure perio health?
A
  • composition of GCF

- depth of gingival sulcus

173
Q
  1. healthy and unhealthy depths of gingival sulcus
A 
healthy = 0.5-2mm 
unhealthy = >3mm
174
Q
  1. why does probing generally overestimate the pocket depth?
A

because the probe actually penetrates into inflamed tissue

175
Q
  1. what does the oral mucosa form a contiuum with?
A
  • gingiva

- tooth attachment tissues

176
Q
  1. what does regional variation in oral mucosa reflect?
A

functional adaptation

177
Q
  1. where is the oral epithelium & the external lining of the body derived from (epidermis)
A

embryonic ectoderm

- form a conituum

178
Q
  1. the oral epithelium and epidermis are similar, but what is one difference?
A
  • morphological features -> ectodermal appendages

- similarities and differences in GENETIC REGULATION (of development, differentiation and maintenance)

179
Q
  1. what is the buccopharyngeal memebrane?
A

early structure where epithelia from ectoderm meets epithelia from endoderm

180
Q
  1. what specifies the appearance of the oral cavity?
A

buccopharyngeal membrane

181
Q
  1. what is oral vestibule
A

slit like space btn lips and cheeks and alveolar bone and teeth

182
Q
  1. landmarks in the oral VESTIBULE
A
  • vestibular fornix
  • upper labial frenum (TSS)
  • frenum near maxillary molars
183
Q
  1. what can a large labial frenum with attachment near alveolar crest cause?
A

midline diastema btn maxillary central incisors

184
Q
  1. implications of prominent frena
A

impacts stability of dentures

185
Q
  1. what is the oral cavity proper?
A

separated from vestibule by alveolar bone/ teeth

186
Q
  1. landmarks in oral cavity PROPER
A
  • palatoglossal fold (formed by glossopalatine m.)
  • palatopharyngeal fold (pharyngopalatine m.)
  • palatine tonsil
  • uvula (breathing, sleep apnoea, gag reflex… projected from soft palate)
  • soft palate - mobile, muscular, not attached to bone, (swallowing, speech, taste)
  • hard palate - immobile, attached to bone (feeding, speech)
187
Q
  1. functions of the oral mucosa
A
  • mechanical protection (masticatory forces)
  • barrier to mogs and toxins
  • immuno defence (immediate and adaptive)
  • lubrication and buffering (saliva from minor glands)
  • sensation (touch, pain, taste, proprioception)
188
Q
  1. what are the regional variations of the oral mucosa
A
  • degree of keratinisation
  • epithelial thickness
  • interface w/ connective tissue
  • composition of connective tissue
  • presence or absence of submucosa
189
Q
  1. oral mucosa vs skin - oral epithelium
A

EPIDERMIS in skin
Stratified squamous epithelium:
- Epithelial ridges (rete or pegs)
- Keratinocytes (→ cell layers; express keratin proteins)

190
Q
  1. oral mucosa vs skin - lamina propria
A 
DERMIS in skin 
Connective tissue:
- Papillae
- Fibroblasts, macrophages, lymphocytes
Collagen (I, III) and elastic fibres
- Blood vessels and nerves
191
Q
  1. oral mucosa vs skin - submucosa
A 
HYPODERMIS in skin
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)
192
Q
  1. what is the major difference btn architecture of oral mucosa and skin?
A
  • no hair follicles

- no sweat glands

193
Q
  1. function of submucosa
A

provides mobility and acts as a ‘cushion’

e.g. lining mucosa

194
Q
  1. what is mucoperiosteum?
A
  • lamina propria is more fibrous
  • directly joined with periosteum of bone
  • e.g. masticatory mucosa (middle of hard palate, gingiva)
195
Q
  1. explain the process of regeneration of skin and oral mucosa
A
  1. basal layer of keritinocytes that divides. Cell differentiate along the axis and become flatter and flatter. Become exfoliated by the time the reach epidermis and are shed.
  2. stem cells in the layer below - maintain a pool of cells that can regenerate the area

STAGE 2 (2 decks)

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