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BDS 2 BAMS > Oral Biology > Flashcards

Oral Biology Flashcards

1
Q

what is the role of periodontium

A

retain tooth in socket, resist masticatory forces, provide a barrier for underlying tissue

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2
Q

what is the structure of cementum

A

similar to bone, lamellae arrangement but in a linear structure as opposed to radial like bone

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3
Q

what are the types of cementum and where can they be found

A

acellular extrinsic fibre cementum - found cervically, has no cementocytes so gets fibres from other sources - sharpey fibres
cellular intrinsic fibre cementum - found apically, contains cementocytes to produce it’s own fibres, formed secondary

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4
Q

what is the structure of alveolar bone

A

outer layer of cortical bone - dense in lamellae arrangement, lamina dura - PDL attaches here
inner traberculae layer - woven bone with marrow, makes for a lighter structure and contains Volkmann’s canals

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5
Q

what makes up the periodontal ligament

A

cells - fibroblasts, immune cells, cemetoblasts, cementoclasts, osteoblasts and osteoclasts
fibres - collagen type 1 and 3
ground substance - glycoproteins and proteoglycans
nerves and blood vessels

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6
Q

what structures give the PDL it’s properties

A

strong and resist forces, load bearing - fibres

elastic - ground substance

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7
Q

what nerve fibres are present in PDL

A

Abeta - fast responding, for jaw jerk reflex
A delta - slower responding for changing mastication, also pain and temperature
C fibres - pain and temperature
autonomic - controlling blood flow

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8
Q

where can true periodontal fibres be found

A

connecting tooth to bone, cervically on cementum - sharpey’s fibres. oblique, horizontal, alveolar crest

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9
Q

where can trans-septal fibres be found

A

connecting two teeth together - inter-dental

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10
Q

describe the change of PDL displacement when a load is applied

A

load applied e.g. mastication - initially rapid displacement of PDL, but as load persists, displacement is reduced
when load removed - initially rapid change back, but reduced as time goes on
adaptation due to visco-elastic properties

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11
Q

where does enamel and gingiva meet

A

junctional epithelium

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12
Q

what does bacteria attack in gingivitis/ perio

A

hemidesosomes at the basal lamina in junctional epithelium

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13
Q

where can crevicular epithelium be found

A

at the sulcus of the gingiva, before junctional epithelium

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14
Q

what is the mucogingival line

A

when the gingiva becomes attached to the mucosa, no longer free

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15
Q

what areas are para-keratinised

A

anterior dorsum of tongue, hard palate, attached gingiva, alveolar mucosa, vermilion of lip

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16
Q

what is the function of the pulp

A

provide nutrients to dentine, produce secondary and tertiary dentine, neuronal activation

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17
Q

what ways are pulp and dentine linked

A

developmental, functionally, structurally

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18
Q

how are pulp and dentine linked developmentally

A

both develop from dental papilla

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19
Q

how are pulp and dentine linked functionally

A

pulp stimulates secondary dentine production when sufficient primary dentine has been produced.
pulp stimulates tertiarty dentine production after tooth wear and dentine is exposed. exchange of materials between structures. pulp sends nutrients, nerves and dentine to dentine. chemicals and bacteria can travel from dentine to pulp

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20
Q

how are pulp and dentine linked structurally

A

the odontoblast layer separates the pulp and dentine. some nerves and immune cells (dendritic cells) can get through this layer to enter dental tubules

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21
Q

what types of dentine are produced in tertiary dentine

A

reactionary - produced by primary odontoblast when injury is mild
reparative - severe damage, primary odontoblasts are damaged, produced by secondary odontoblasts

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22
Q

how is dentinal fluid produced

A

blood vessels enter the pulp through apical foramen, leave in venules at a lower pressure, therefore fluid moves out of the capillaries and into the pulp chamber. as the pulp is enclosed, the fluid has nowhere to go so it travels through the dentinal tubules

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23
Q

how is the dentinal fluid described as protective

A

it has an outward pressure, prevents bacteria travelling inwards toward the pulp

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24
Q

what is rachow’s plexus

A

nerve fibres as the branch out in the pulp chamber, sub-odontoblast layer

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25
Q

where are terminal nerve branches more commonly found in dentinal tubules

A

at cusps - 40%, cervical dentine has much less innervation

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26
Q

what is the hydrodynamic mechanism

A

when dentine is exposed due to tooth wear, the dentinal fluid can move around more freely. this activates nerve fibres, which reach AP and travel to the brain to stimulate perception of pain

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27
Q

what activates different nerve fibres

A

a delta - hydrodynamic mechanism

c fibres - direct activation via chemicals, electrical current or intense temperatures, more intense pain

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28
Q

how can different stimuli alter the hydrodynamic mechanism

A

different stimuli changes the direction of movement of dentinal fluid. when the fluid moves outwards - more likely to cause pain as nerve fibres are stretched more.
outward flow - cold, drying, decrease hydrostatic press
inward flow - heat, increase hydrostatic pressure

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29
Q

what controls blood flow to the pulp

A

autonomic neurones, metabolites, chemicals, drugs

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30
Q

how does inflammation occur in the pulp

A

exposing dentine, increasing dentinal fluid flow and activating nerve receptors, generates AP but also stimulates inflammation. kinins are produced - vasodilators which increase blood flow. in doing so - increases flow of dentinal fluid

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31
Q

what is the result of increasing flow of dentinal fluid in pulpitis

A

increase in flow - increase in nerve fibre activation. increased sensitisation. only requires small stimulus to stimulate AP - sensitive to cold air or to bite down

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32
Q

what can happen if inflammation and nerve activation is mild

A

can get regeneration of dentine

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33
Q

what are some variations of enamel thickness

A

thicker at cuspal regions, and incisal edges, thinner cervically

34
Q

what is the main component of enamel

A

enamel rods - contain crystals of hydroxyapatite

35
Q

what is the relationship of enamel rods to ADJ

A

perpendicular to ADJ

36
Q

what other lines can be see in enamel

A

striae of retzius - incremental growth lines

37
Q

describe the development of crystals in enamel

A

tomes process releases calcium phosphate encapsulated in protein capsule. this cocoon protein is broken down to allow calcium phosphate to become super saturated. crystal forms. as it is in the mouth, phosphate replaced with fluoride or hydroxyl

38
Q

what is gnarled enamel

A

enamel with a higher concentration of rods - in cuspal and incisal regions

39
Q

what are enamel tufts and lamellae

A

hypomineralised enamel. tufts project slightly, lamellae run the whole way

40
Q

what are enamel spindles

A

odonotblasts that project on to enamel

41
Q

what is hypersensitivity

A

when tooth wear results in exposed dentine which can cause nerve activation. results in short sharp pain in response to thermal stimuli, biting or touching

42
Q

what are some causes of tooth wear

A

attritition, erosion, abrasion, periodontal disease resulting in gum recession

43
Q

how do sensitive toothpastes work

A

contain potassium - moves membrane potential further from threshold - requires a stronger stimulus to generate nerve activation and pain perception
blocking tubules - contains novamin

44
Q

how does novamin work

A

enters tubules, reacts with saliva to allow it to bind with collagen fibres to block tubules. release calcium phosphate - strong and acid resistant, layer over tubule. prevents stimulus entering tubule

45
Q

what are the two types of bone and how do they differ

A

cortical - lamellae arranged in osteon, very dense, haversian canal through the middle
trabercluae - lamellae arranged in rods, with bone marrow between, much lighter

46
Q

what is the difference between lamellae bone and woven bone

A

lamellae is laid down slower, has collagen in parallel arrangement and few osteocytes
woven is laid down rapidly in response to injury or in fetus, has many osteocytes, collagen in any direction

47
Q

what are the different types of cartilage

A

elastic - external ear, epiglottis
fibrocartilage - pubic symphsis, vertebral discs
hyaline - end of growing bones, trachea, embryonic skeleton

48
Q

what is the process of mineralisation of cartilage to bone

A

ossification

49
Q

what are the two types of ossification and give examples

A

intramembranous - between bones in skull

endochondral - long bones

50
Q

what are the stages of endochondral ossification

A

primary - as the embryonic skeleton is laid in hyaline cartilage, this is mineralised at diaphsial ossification centre
secondary - as the long bones continue growing, chondroblasts proliferate to produce cartilage, this is then mineralised at epiphyseal ossification centre

51
Q

what is achondroplasia

A

genetic defect in which cartilage is not produced, lack of endochondral ossification. results in dwarfism with normal size skull as intramembranous ossification is fine

52
Q

what is the resting membrane potential

A

-70 or -90, ICF negative to ECF due to arrangement of ions

53
Q

what maintains the resting membrane potential

A

potassium ion channels constantly opening, continuous leak of potassium. active transport of Na/K pump - 3Na out, 2K in

54
Q

describe the AP

A

ligand binds to receptor, generates opening of Na channels, as Na moves in, threshold of -55mV is reached, voltage gated Na channels activated, influx of Na. As voltage over shoots 0 and reaches +35mV, H gate closes, and voltage gated K channels are opened. Efflux of K causes membrane potential to return to normal. Refractory period of inactivation, before restored

55
Q

what causes the refractory period

A

H gate of Na channel remains closed, despite the voltage returning, it is still unable to be activated as this gate is not voltage gated. As this gate opens, M gate closes ready for activation

56
Q

describe the gates of the Na channel

A

2 gate - H and M. H is more commonly open, does not required to be activated. M gate requires a voltage to be opened. However, H gate becomes inactivated and closed at voltage above +35mV

57
Q

what is saltatory conduction

A

direction of movement of AP, cannot go backwards due to refractory period. also, due to myelination, AP jumps from node to node of ranvier

58
Q

what embryology does tooth structures develop from

A

ectoderm - enamel

ectomesenchymal (neural crest cells) - dentine, cementum, pulp

59
Q

what are the stages of tooth development

A

initiation, bud stage, cap stage, early & late bell stage,

60
Q

what happens at the initiation stage of tooth development

A

ectoderm, forming epithelium, invaginates into ectomesenchymal cells, forming dental lamina and vestibublar lamina

61
Q

what happens at the bud stage of tooth development

A

EM cells become dense around dental lamina - form dental papilla. dental lamina also condenses to form enamel organ

62
Q

what happens at the cap stage of tooth development

A

Enamel organ divides into 2 layers - internal and external enamel epithelium which meet at the cervical loop, dental lamina continues to develop

63
Q

what happens at the early bell stage of tooth development

A

a further 2 layers of enamel organ develop. stellate reticulum - provides structure, support and nutrients to the enamel organ. stratum intermedium - between the IEE and EEE

64
Q

what happens at the late bell stage of tooth development

A

the dental papilla differentiates into odontoblasts. this results in pre-dentine formation, as it is not mineralised, this stimulates IEE cells to differentiate into ameloblasts to begin enamel formation

65
Q

describe dentinogenesis

A

dental papilla cells differentiate into odontoblasts, at each division, one odonotblast is produced and one cell remains EM. odonotoblasts allow for primary and secondary dentine formation. however, if injury results in damage to these odonotoblasts, EM cells remain to produce more and produce tertiary dentine.

66
Q

describe the stages of amelogenesis

A

differentiation - odonotblast and dentine formation stimulate IEE cells to elongate and differentiate - columnar cells with nuclei at basal end
secretory - once differentiated, secrete organic proteins (amelogins) to produce the shape desired for enamel, only 30% mineralised at this point
maturation - once shape laid out, proteins are then broken down - matrix metallopeptidase - enamelysin - mineralisation of matrix
protective - ameloblasts regress, layer over top of enamel for protection

67
Q

describe root formation

A

migration of cervical loop, IEE and EEE migrate (herte’s epithelial root sheath) , in doing so, stimulate dental papilla to produce odontoblasts, once reached length, epithelium regresses (may have some left over debris of malassez). dental follicle then contacts the root dentine - stimulates formation of cementoblasts to produce cementum

68
Q

what causes amelogenesis imperfecta and how can it be seen

A

lack of protein matrix metallopeptidase due to genetic defect. means proteins cannot be removed and mineralisation cannot occur. lack of maturation.
mineral content of enamel and dentine is not different - no ADJ seen in radiograph. teeth will be more prone to tooth wear, yellow and rough surface

69
Q

what is dentinogenesis imperfecta and how can it be seen

A

dentine is undermineralised. enamel relies on this for support so this is weakened. dentine moving more than it should - tooth wear. can be seen in radiograph - ADJ is apparent but cannot differentiate between dentine and pulp

70
Q

what is the difference between gemination and fusion

A

gemination - one tooth (root) split into 2 crowns

fusion - 2 roots but crowns fused to 1

71
Q

how does LA prevent sensation of pain

A

blocks Na channels, cannot reach threshold for AP, so not generated, no neuronal pathway to brain, no perception of pain

72
Q

how does the structure of the nerve effect how the LA effects the nerve

A

LA has diffuse through connective tissue to reach nerve, will act on those closest to the membrane first. Also contains a lot of fat which will retain the LA for longer

73
Q

what factors affect the sensitivity of a nerve to LA

A

diameter - wider diameter, more Na channels therefore more need to be blocked to prevent AP propagation. Larger axons will take longer to be anaesthetised.
Myelination - LA only has to work at nodes of ranvier, but there is a high concentration of channels here so high number must be blocked

74
Q

what is the order in which nerves are blocked, from fastest to slowest

A

A delta, c, a beta, a alpha

75
Q

what are the components of LA

A

aromatic ring - lipophilic for diffusion through membrane
amide or ester bond
amine with hydrochloride - hydrophilic, better water solubility

76
Q

how does the amine group and hydrochloride work with LA

A

when together, ionised, active form but lipophobic so cannot cross membrane. must be in unionised, dis-associate inactive form to cross the cell membrane. once in, can ionise, re-associate and become active

77
Q

give examples of an ester and amide bond

A

ester - benzocaine, topical

amide - lidocaine, prilocaine

78
Q

why is a vasoconstrictor required in a local anaesthetic

A

LA is normally a vasodilator, increases blood flow so increases clearance and more is required. vasoconstrictor reduces the flow so it lasts for longer and less is required

79
Q

what vasoconstrictors are used

A

adrenaline - used with lidocaine

felypressin - synthetic adrenaline, used with prilocaine

80
Q

what is the difference between adrenaline and noradrenaline

A

adrenaline - systemically, no preference for alpha or beta receptors, so increases HR on beta 1 but also causes vasodilation on beta 2, no no overall increase in MAP
noradrenaline - higher affinity for alpha to beta, beta still increases HR but also causes vasoconstriction through alpha, increases MAP, causes the body to reduce BP to counteract this, might be light headed

BDS 2 BAMS (12 decks)

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