Theme II: Part 2 Flashcards

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1
Q

How does the PDL develop and form. Are there more fibers in cementum or bone

A
  • After induction of dentine formation, HERS stretches and disintegrates and dental follicle cells differentiate into cementoblasts, fibroblasts and osteoblasts.
  • cementum and bone form with a ligament space in between. Short fibre bundles emerge from these tissues and form a continuous attachment to each other.
  • Cementum: there are more fibres and closely spaced. Thinner.
  • Bone: fewer, thicker and spaced wider
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2
Q

Functions of the PDL

A
  • Tooth attachment: Mineralised sharpey’s fibres from cementum and bone insert here
  • Withstands forces of mastication acting as a shock absorber
  • Remodels to reposition teeth to achieve occlusion
  • Nutritive: highly vascular
  • Senses pain and tension
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3
Q

Which type of PDL fibers develop first. Where do they insert

A

-Alveolar crest fibres form first. From CEJ to rim of alveolus
-Develop obliquely then horizontal then oblique again
[- As the root forms, fibre formation proceeds apically.]

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4
Q

Describe the 5 PDL fibre groups and their functions. Which is most abundant

A
  • Alveolar crest fibres: resist extrusive forces
  • Horizontal fibres: resist horizontal tipping forces
  • Oblique fibres: Resist intrusive compressive forces
  • Apical fibres: resists extrusive forces
  • Interradicular fibres: (only when multiple roots) Resist extrusive forces

-Oblique are most abundant

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5
Q

What is the PDL composed of. Cell types and ECM

A

-Fibroblasts, osteoclasts, osteoblasts, cementoblasts, cementoclasts, Rests of Malassez, mesenchymal stem cells, immune cells

  • 60% ground substance (ECM): glycosaminoglycans (hyaluronic acid) proteoglycans and glycoproteins that bind water and ions for shock absorption.
  • Collagen fibres (I & III). Fibronectin attaches cells to collagen fibrils for migration and wound healing
  • Elastic fibres (oxytalan) containing fibrillin but no elastin. Regulate blood flow. Perpendicular to collagen fibres
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6
Q

What do fibroblasts in the PDL do. What are perivascular and endosteal fibroblasts

A
  • Secrete collagen fibrils, growth factors and ground substance.
  • Remodel the PDL
  • Possible role in eruption: mechanical forces acting on the collagen mediate onto the fibroblasts which then contract.
  • Functional in tooth movements: mesial and vertical tooth drift
  • Perivascular: around vessels
  • Endosteal: align along the bone
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7
Q

What arteries supply the PDL. What unique capillaries are present and why

A
  • Branches of Superior and inferior alveolar arteries through apex
  • Interalveolar vessels through the alveolar process
  • Branches of the lingual and palatine arteries entering through the gingiva
  • Interstitial areas are usually located near the bone and contain neuromuscular bundles.

-Fenestrated capillaries are usually not in connective tissue but are in PDL to increase diffusion capacity. As high metabolic rate of PDL requires larger molecules.

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8
Q

How PDL changes with age. When remodelling occurs

A
  • Thickness decreases. More fibrotic, less cells
  • Loss of bone and decreased function decreases its thickness.
  • Hyaluronic acid decreases. Proteoglycan increases

-Remodelling is induced by mastication which increases thickness. Thickest in areas under tension, compared to compression

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9
Q

Innervation of the PDL. How it compares in incisor and molars

A
  • Myelinated sensory afferent fibers sense pain (free nerve endings) and pressure (Ruffini’s corpuscles)
  • Autonomic fibres regulate blood flow

-Denser innervation in upper incisors, as this is where initial contact with food is so requires more sensation as more force

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10
Q

Function of the 2 types of collagen in PDL

A
  • Type I (80%): forms the fibre bundles
  • Type III (15%): from reticular bundles that crosslink to form a collagen meshwork that supports vessels when PDL is compressed, and also interact with platelets to form clots
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11
Q

What is an osteon and its structure. What is an osteocyte

A
  • Osteon= cylinder units of bone. Consist of central Heversian canal with a capillary in it, surrounded by 3 layers of lamellar bone (circumferential, concentric, interstitial)
  • Adjacent canals connected by Volkmann’s canals.
  • osteoblasts align the canal. They enter the inside of the osteon through the blood vessel and produce bone matrix that is later mineralised to bone.

-When osteoblasts become trapped in the bone it is termed an osteocyte

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12
Q

What is Bundle bone and lamellar bone

A
  • Bundle bone is always found near the PDL, where sharpey’s fibers insert. Constantly remodelled in response to tooth movements.
  • Regions further away from the PDL consist of lamellar bone that forms the majority of the alveolar process.
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13
Q

Howship’s lacunae

A
  • Bone remodelling at the reversal stage.
  • Osteoclasts have stopped resorbing bone and have disappeared from the region, leaving behind resorption bays termed Howship’s lacunae.
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14
Q

What happens to the PDL and bone when you tap your tooth. What is the piezoelectric effect

A
  • The force lasts less than second
  • PDL incompressible
  • Alveolar bends due to the Piezoelectric signal: the force causes a movement of electrons causing a short flow of current. Bone bends to prevent atrophy.
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15
Q

What happens to blood flow in the PDL in areas under tension and in compression

A
  • Tension/ stretching= blood flow increases, vasodilation

- Compresssion/ under pressure= vessels occluded so decreases in blood flow. Cell death

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16
Q

Difference in response to heavy and light orthodontic forces

A
  • Light= slow continuous tooth movement by remodelling of bone so less destructive. Discourages resorption. Takes about 2 days.
  • Heavy= Movement occurs in steps, by undermining resorption. Takes 7-14 days.
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17
Q

What are the 5 types of tooth movements. What takes the most and least force. What are the forces required

A
  • Intrusion (force concentrated on apex) -15-25g
  • Tipping: 50-75
  • Rotation: 50-100
  • Extrusion: (pulling out, tension on PDL) 50-100
  • Translation: whole tooth moves side ways through the bone with PDL uniformly loaded 100- 150
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18
Q

Adverse effects of orthodontic forces

A
  • Compressed pulp causing transient inflammation leading to discomfort or even loss of vitality
  • Excessive root resorption causing thin and distorted roots
  • PDL can damage if existing periodontal disease
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19
Q

What are the main afferent nerve endings in the PDL

A
  • Free-ending: sense pain and pressure. Unmyelinated

- Ruffini’s corpuscles: sense pressure. Myelinated

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20
Q

What is endochondral and intramembranous bone. Which bone type is alveolar bone

A

1-Endochondral ossification occurs where chondrocytes make cartilage which is then replaced by bone. =in long bones

2-Intramembranous: Mesenchymal cells in the periosteum differentiate into osteoblasts which make bone = alveolar bone

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21
Q

What are the different bone types and layers in alveolar bone

A
  1. Dense outer layer= compact/ cortical bone:
    - 3 lamellae layers with Haversian canals in the centre, and numerous vascular Volkmann’s canals passing to PDL
  2. Cancellous/ trabecular bone (air filled)
  3. Alveolar/ cribriform plate: lining the socket (compact)
    4: alveolar crest: upper most outer portion
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22
Q

Composition of alveolar bone. Functions of some proteins

A
  • mineralised living connective tissue
  • type 1 collagen
  • Non-collagenous proteins:
    1. proteoglycans: bind to collagen, role in mineralisation.
    2. glycoproteins
    3. osteocalcins: bind to Ca and collagen so role in mineralisation
  • Inorganic = HA, deposited by collagen
  • Osteoblasts, osteoclasts, osteocytes
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23
Q

Function of alveolar bone

A
  • support teeth roots, protection, locomotion, mineral reservoir, attachment for muscles and tendons, remodelling
  • regulating metabolic processes, regulating Ca and PO4
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24
Q

What molecules control formation and resorption of bone

A
  • Formaiton = calcitonin, vit D, oestrogen

- Resorption= PTH, glucocorticoids

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25
Q

What is periosteum and endosteum

A
  • Periosteum: connective tissue membrane surrounding bone

- Endosteum= loose connective tissue lining the inside of medullary cavity, separating bone and marrow

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26
Q

What are osteoclasts, osteoblasts and osteocytes. [Where they are derived from, where they are found, what they make, and what they do]

A
  • Osteoblasts: from mesenchymal cells in follicle.
  • Active are cuboidal, inactive are flat.
  • Sit on bone surface producing bone matrix.
  • Make alkaline phosphatase which promotes mineralisation and produce growth factors for bone repair.
  • Osteoclasts: from monocytes. Produce howship’s lacunae during bone Resorption. Produce acid phosphatase to demineralise, and lysosomal enzymes to degrade.
  • osteocytes: osteoblasts trapped in bone matrix with a lacunae chamber and communicate via canaliculi processes. Detect load. 90% of bone cells.
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27
Q

Different stages of alveolar process development in utero

A
  • Mesenchymal cells make osteoblasts which secrete bone
  • Mandible initially makes a trough shape underneath the inferior alveolar nerve and tooth germ
  • Process grows upwards and almost surrounds the incisor germ. IAN is enclosed in bony canal
  • to make room for the growing germ and stellate reticulum, inner bone is resorbed and is deposited on the outside.
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28
Q

Describe some examples of bone defects. Perioapical abscess, infraocclusion, alveolar osteitis, ankylosis, sinus perforation

A
  • Bone resorption from chronic periodontal disease or extraction makes implants difficult as unsupported
  • Ankylosis: fusion of bone to root due to trauma or infection. No exfoliation
  • Infraocclusion: further growth of bone during ankylosis submerges the tooth causing malocclusion or PDL issues if not extracted
  • Periapical abscess: (pus at root apex) Noticed on Xray if lamina dura (alveolar plate) is interrupted
  • Alveolar osteitis: socket should fill with blood after extraction, however the clot can detach and expose the bone causing inflammation
  • Maxillary sinus perforation: during extraction roots can fracture the sinus floor causing a fistula between sinus and oral cavity and lead to infection.
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29
Q

What are the stages of bone remodelling. What happens during tooth drift

A
  • Occurs during mesial drift (inter proximal tooth wear) or orthodontic treatment resorption and deposition is needed
  • On Alveolar (inner) and cortical (outer) plates
  1. Resting stage: inactive osteoblasts are flat
  2. Resorption: migration and activation of osteoclasts to create space where tooth is moving to, to remove excess bone
  3. Formation: cuboidal active osteoblasts make bone to fill gaps and compensate loss
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30
Q

Difference between resting and reversal lines in bone

A
  • Resting line: Pauses in bone deposition. Straighter and less pronounced.
  • Reversal line: pronounced wavy lines in bone indicating increase in production of bone. A change from bone resorption to deposition has occurred here.
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31
Q

Where is the lamellar bone the thickest

A

Thickest on buccal aspect of mandibular premolars and molars

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32
Q

What are howship’s lacunae.

A

Once osteoclasts have stopped resorbing bone and have disappeared from the region, they leave behind resorption bays termed Howship’s lacunae.

33
Q

Different types of epithelia of dentogingival junction (keratinisation, function)

A

A: Gingival epithelium: Mainly parakeratinised and only partially orthokeratinised in areas of increased abrasion.
B: Sulcular epithelium: Nonkeratinised; bounds the gingival sulcus.
C: Nasmyth’s membrane is an epithelial tag between sulcular and junctional. composed of the primary enamel cuticle and cell remnants of the REE. The primary enamel cuticle is the (internal) basal lamina produced by REE cells and is attached to enamel.
D: Junctional epithelium: Nonkeratinised. Derived from REE. Attached to enamel.

34
Q

Why no bleeding during eruption

A

Fusion of the REE with the oral epithelium creates the dento-gingival junction resulting in an epithelial continuity. Connective tissue including blood vessels are never exposed to the oral cavity, therefore there is no bleeding. The junctional epithelium also remains tightly attached to the enamel surface.

35
Q

Effect of gingival inflammation on epithelia

A
  • Inflammation causes sulcular and junctional epithelium to form long, irregular rete processes that project into the lamina propria.
  • Intercellular spaces between epithelial cells become larger and the basal lamina may be damaged allowing for easier penetration by microbes and toxins.
  • Apical migration of junctional epithelium to compensate loss of tissue and for stability but suppresses wound healing and forms a pocket. -[Collagen membrane inserted to prevent over proliferation and down growth of junctional epithelium]
36
Q

Keratin function

A

-The keratinised layer of oral epithelia functions to resist abrasion caused by masticatory forces.
Thicker with tougher diets

37
Q

What is the functional significance of the folding of the epithelial-connective tissue interface. -Rete pegs

A
  • increases the surface area and the stability of the epithelium-connective tissue interface. This prevents separation of these two tissue layers, especially if exposed to masticatory forces.
38
Q

Oral Submucosa and mucoperiosteum. where they are found and differences in structure -( lamina propria)

A
  • Submucosa= in lining mucosa. It consists of loose connective tissue, adipose tissue, minor salivary glands, larger blood vessels and nerves.
  • It provides mobility and acts as a ‘cushion’ in mucosa not directly exposed to masticatory forces.
  • mucoperiosteum provides stability, withstands masticatory forces. More fibrous lamina propria which is directly attached to the periosteum of bone.
39
Q

collagen types in mucosa of gingiva and palate

A

Type I produces long, strong fibres that provide tensile strength to resist shearing forces.

40
Q

How is the dentogingival junction formed. During eruption and after eruption

A
  • The REE approaches the oral epithelium until they fuse. So there is epithelial continuity at all times so no bleeding.
  • Junctional epithelium has formed, consisting entirely of REE and connected to enamel.
  • After eruption, gingival epithelium overgrows down to replace the REE to become sulcular epithelium. Rete peg formation
  • Sulcus development induced by masticatory forces
  • Nasmyth’s membrane (an epithelial tag) develops from REE remnants and primary enamel cuticle.
41
Q

What is gingival cervical fluid. What it contains. Overproduction effect

A
  • defends against pathogens
  • contains immunoglobin, macrophages, cytokines, matrix metalloproteases etc.
  • overproduction causes tissue damage as MMPs degrade collagen
42
Q

How Junctional epithelium attaches to teeth

A
  • Junctional epithelial cells/ REE secrete a primary enamel cuticle (aka Nasmyth’s membrane) which is a basal lamina
  • the membrane bonds to enamel proteins, and to epithelial cells via hemidesmosomes
  • JE is non-keratinised as Keratinisation of the epithelium would prevent this interaction.
43
Q

What is the small epithelial tag and what does it demarcate

A
  • REE remnants

- Border between Sulcular and junctional epithelium

44
Q

What is the mucogingival junction

A
  • Boundary between alveolar muscoa and attached ginigiva

- Alveolar mucosa is darker and more translucent so can see superficial vessels

45
Q

What are the 5 main different gingival fibres. Where they connect and their function

A
  1. Transseptal: above the alveolar crest, connecting CEJ of adjacent teeth. Connects all teeth and controls mesial drift
  2. Dentogingival: from cementum to lamina propria of gingiva
  3. Alveogingival: alveolar crest to lamina propria of gingiva
  4. Dentoperiosteal: cementum to alveolar process
  5. Circular group: forms a band round the neck of teeth. Binds free gingiva to teeth.
46
Q

What is the normal depth of a gingival pocket

A

less than 3mm

47
Q

Repair and regeneration definitions. Examples of therapies for dental tissue repair. Where dental stem cells can be collected.

A
  • Repair: restoring tissue function but with impaired tissue architecture
  • Regeneration: complete restoration of tissue architecture and function
  • Stem cells can self renew or differentiate into other cell types for restoring damaged tissue.
  • Using primary teeth and 3rd molars is most accessible.
  • Using early epithelial and mesenchymal cells from a tooth germ.
  • Pulp and PDL stem cells, pulp for exfoliated teeth, dental follicle of unerupted teeth.
  • Tissue engineering using 3D printing or gene therapy.
48
Q

The 4 stages in wound healing of oral mucosa

A
  1. Haemostasis: fibrin and platelets make clot so no further blood loss and to protect exposed tissue.
  2. Immune response: toxins and microbes entering wound activate vasodilation, neutrophils, macrophages, cytokines, lymphocytes.
  3. Epithelial tissue repair: widening of intercellular spaces, increased proliferation of basal keratinocytes and epithelial cells. Epithelial cells migrate beneath the clot to re-establish epithelial sheet
  4. Connective tissue repair: new fibroblasts to make collagen
49
Q

Healing process after tooth extraction. How it differs to normal oral repair

A
  • Substantial tissue loss but same repair mechanism as in oral mucosa: haemostasis, inflammatory response, epithelial response.
  • However, instead of fibroblasts, osteoblasts are recruited to make bone to fill the extraction site.
  • Takes 10 days for repair rather than 5.
50
Q

The caries zones in enamel

A
  1. Translucent zone (inner): enamel demineralisation.
  2. Dark zone: undergoing remineralisation
  3. Body of lesion: enamel prism destruction
  4. Surface zone: intact enamel from remineralisation by saliva ions
51
Q

Regeneration of PDL. All the different cells needed and their sources

A
  • Co-ordinated response needed as fibres insert into bone and cementum.
  • Fibroblasts from mesenchymal cells, to remodel collagen
  • Cementoblasts from rest cells of Malassez (REE remnants)
  • Osteoblasts from mesenchymal cells in periosteum or endosteum
  • Growth factors and ECM molecules (EGF, FGF, BMP) initiate repair.
52
Q

List tooth features of ageing

A

1-Enamel: discolouration, thinner, surface more mineralised.
2-Dentine: secondary, reactionary, thicker, sclerotic, dead tracts
3-Cementum: thicker
4-PDL: thinner, less cells, more fibrous, decreased remodelling capacity, more mineralised fibres
5-Pulp: smaller, more fibrous, pulp stones, less cells, nerves & vessels.

53
Q

Causes of tooth wear

A
  • Mastication forces.
  • Attrition= tooth to tooth contact
  • Grinding
  • Jaw clenching/ grinding (bruxism)
  • Abrasion from foreign objects, excessive tooth brushing, abrasive tooth pastes.
  • Erosion from chemical dissolution from stomach acid, fizzy drinks, swirling wine, meds, low pH
54
Q

Features in teeth due to caries

A
  • Caries lesion, demineralisation, cavity
  • Reparative tertiary dentine
  • Sclerotic dentine with dead tracts
  • Inflammatory pulp cells
55
Q

Effect of vomitting on teeth. And why not to brush straight after

A

Stomach acid lowers weakens the enamel so brushing straight after is avoided to avoid erosion and allow saliva to buffer the acid and to remineralise the enamel.

56
Q

What are the 3 types of pulp stones

A
  1. True: made of dentine, lined by odontoblasts
  2. False: made from degenerating pulp cells that mineralise
    3: Diffuse: occur in close association with blood vessels or collagen
57
Q

What tissue is cementoblasts derived from. And what epithelial cells are postulated to have a role in cementum formation

A
  • Dental follicle

- rests of malassez

58
Q

What germ layer is the oral epithelium and oral cavity derived from. What membrane is between the ectoderm and endoderm

A
  • ectoderm
  • cavity formed when the infold of the ectoderm meets the endoderm - they meet at the buccopharyngeal/ oropharyngeal membrane which is the signalling centre for generating different regions of the oral cavity
59
Q

Function of the oral mucosa. What is functional adaption

A
  • mechanical protection against abrasion during mastication
  • barrier against microbes and toxins
  • immunological defense
  • lubrication and buffering from the saliva produced
  • touch, pain, taste

-functional adaption with different types of mucosa for specific functions: different epithelial thickness, keratinisation, connective tissue

60
Q

What is the oral vestibule and the oral cavity.

A
  • vestibule: space between lips/ cheeks and the teeth/ alveolar bone
  • oral cavity: separated from vestibule by teeth and bone.
61
Q

Give examples of lining, masticatory and specialised mucosa. What percentage they make up.

A
  • Lining (60%): lip, soft palate, alveolar, buccal. [submucosa]
  • Masticatory (25%): middle hard palate, gingiva. [periosteum]
  • Specialised (15%): dorsal tongue, taste buds
62
Q

The 3 main cell layers of oral mucosa

A

1-Oral epithelium: Stratified squamous epithelium, with epithelial ridges and keratinocytes
2-Lamina propria: connective tissue with fibroblasts and immune cells
3-Submucosa or mucoperiosteum.

63
Q

What is the difference between submucosa and periosteum and where they’re found

A
  • Submucosa: in lining mucosa. Provides mobility and cushioning. Contains vessels, nerves, glands.
  • Mucoperiostium: masticatory mucosa. Lamina propria is more fibrous and directly joined with the periosteum
64
Q

The 3 types of keratinisation and where they’re found in the different types of mucosa

A
  • Orthokeratinised: Resist abrasion, no nuclei. Hard palate, tongue, some gingiva
  • Parakeratanised: gingiva, lips.
  • Non-keratanised: live cells. Lining mucosa, junctional epithelium
65
Q

How regeneration of oral mucosa occurs, and how it compares to skin

A
  • Cuboidal keratinocytes divide and differentiate. They move upwards and become flatter with no cell organelle to produce a keratin layer. Eventually shed in the oral cavity
  • Keratinocytes are then regenerated by stem cells in the basal lamina layer

-Rapid regeneration of 9-14 days, unlike skin which is 27 days. So rapid healing and oral diseases are milder

66
Q

What are Fordyce’s spots

A
  • ectopic sebaceous glands, without hair follicle. In corner of mouth
  • produce sebum to lubricate, enable sliding of buccal mucosa against the teeth and to lubricate the lips
67
Q

What is the lip.

A
  • aka the vermillion zone.
  • Numerous capillaries giving red colour
  • Parakeratanised intermediate zone between lip and mucosa
68
Q

What germ layers is the post and ant tongue derived from. What is the tongue’s function

A
  • Anterior: ectoderm
  • Posterior: endoderm
  • Has implication for oral diseases (oral cavity v oropharyngeal cancer)

-Mastication, swallowing, speech, taste, immune function

69
Q

Types of papilla and tonsils on the tongue and their functions

A
  • Vallate papillae: before terminal sulcus. Taste
  • Foliate papillae: side of tongue. Taste
  • Fungiform papillae: anterior tongue. Taste
  • Filiform papillae: keratinised pikes on dorsum for mastication.
  • Lingual tonsils (behind vallate papillae) and palatine tonsils between the arches - lymph tissues for immune defence
70
Q

Age changes of the tongue and oral mucosa

A

1-Tongue: epithelial atrophy causing loss of spiky filiform papillae, causing smooth fissured surface. [From meds or iron deficiency]

  • Burning sensations
  • loss of taste
  • Varicose veins on underside of tongue: caviar tongue
  • Increased number of fordyce’s spots

2-Mucosa: degeneration, loss of tissue mass

  • Smoother, dryer surface
  • Thinner epithelium
  • Less cells, more fibrous
  • Less immune langerhans cells
  • Increased fordyce’s spots
  • Atrophy of minor salivary glands
71
Q

How oral cancer develops. Risk factors

A
  • Oral squamous carcinoma most common
  • overgrowth of epithelium (hyperplasia), thinning, dysplasia, cancerous epithelial layer which invades underlying connective tissue and then into blood.

-Tobacco, alcohol, paan, HPV, immunosupression, nutritional deficiency,

72
Q

White and red patches formation

A
  • Hyperkeratosis so thickening of outer epithelial layer
  • disturbances in proliferation and differentiation
  • Dysplasia: Drop shaped epithelium processes, enlarged nuclei, loss of cell polarity, becomes thin, increased inflammatory cells
73
Q

Which 3 PDL fibre types resist extrusive forces

A

-apical, alveolar crest and interradicular

74
Q

2 scenarios where bone resorption can occur

A
  • extraction

- chronic periodontitis

75
Q

What is the vestibular fornix

A

-trough formed by the alveolar mucosa and the lips/ cheeks

76
Q

Dentine hypersensitivity, reversible and irreversible pulpits. Pain sensations experienced

A
  • Hypersensitivity = short sharp pain from thermal, tactile, osmotic, chemical stimuli
  • Reversible pulpits = short, poorly localised, temporary pain
  • Irreversible = longer, persists, induced by cold
77
Q

Symptomatic and asymptomatic apical periodontitis. Acute and chronic apical abscess differences

A
  • Symptomatic = tender to touch, vital, responds to sensitivity to test
  • Asymptomatic = chronic, not tender, no response, apical translucency on X-ray
  • Acute = tender, non-responsive, swelling, fever
  • Chronic =draining sinus, mildly or not tender, non-responsive
78
Q

Light continuous force, intermittent and interrupted for orthodontics

A
  • continuous - encourages remodelling, not resorption
  • Intermitent = force decreases between adjustments
  • Interupted = force only present when appliance worn. Allows repair after tooth movement
79
Q

What submucosa contains. Its function

A
  • consists of loose connective tissue (fibroblasts), adipose tissue (adipocytes), minor salivary glands, and larger blood vessels and nerves.
  • provides mobility and acts as a ‘cushion’ in mucosae not directly exposed to masticatory forces