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DMD2 > The Pulpodentine Complex 3 > Flashcards

The Pulpodentine Complex 3 Flashcards

1
Q

What are the types of pulpodentine insults that can affect the pulp?

A

Microbial

Traumatic

Iatrogenic

Chemical

Others

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2
Q

What determines the destruction or healing of exposed pulp?

A

Bacteria are the major determinant for destruction or healing of exposed rodent pulps

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3
Q

What are the routes of bacterial infection of pulp?

A

Caries (most common route for bacteria and their by-products affecting the pulp)

Dental anomalies

Cracks (tooth, restoration)

Marginal breakdown of restorations

Fractures (tooth, restorations)

Trauma

Periodontal diseases (exposed lateral canals, damaged cementum)

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4
Q

How do caries progress?

A

Intermittently: Periods with rapid activity alternating with periods of quiescence, they progress quickly through demineralised enamel but more slowly in dentine.

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5
Q

What affects pulp response to dental caries?

A

Thickness of remaining dentine

Degree of calcification of remaining dentine

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6
Q

Do bacteria that cause dental caries create pulp inflammation?

A

Cariogenic bacteria do not cause significant pulp inflammation

Anaerobic bacteria that occur as a sequelae causes inflammatory changes to the pulp

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7
Q

How do bacteria cause damage to the pulp?

A

Bacterial toxins released or formed when bacteria die.

These toxins include: Acids, proteinases (dissolve and digest enamel and dentine) , LPS, Lipotechoic acid (breakdown the walls of gram +ve bacteria), these toxins diffuse along the dentinal tubules (can reach pulp at a very early stage relative to the surface changes. Rate determined by variation in composition and thickness of enamel and dentine.

Bacteria can also travel within dentinal tubules themselves, however, the pulp inflammatory response is to their toxins rather than the bacteria themselves.

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8
Q

What are the types of trauma based injures that can occur to teeth?

A

Accidental:

Cracks / Fractures

Concussion

Luxation

Avulsion

Traumatic occlusion

Physiological:

Attrition

Abrasion

Traumatic occlusion

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9
Q

What are some iatrogenic causes of injury to the pulp?

A

Cavity preparation (heat, dehydration, deep cavity, pulp exposure)

Restoration procedures (Insertion, cementing, polishing)

Accumulative (area of dentine cut)

Prosthetic manipulation (Fixed and removable prosthodontics)

Orthodontics (Tooth movement)

Periodontics (Treatment of deep pockets)

Radiation (Radiotherapy for carcinoma)

General anaesthesia (Trauma during intubation procedures)

Surgery (Dento-alveolar surgery, oral surgery)

Electrical (Galvanic reaction)

Local analgesia (reduced blood flow due to vasoconstrictors)

Smoking (reduced blood flow)

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10
Q

What kind of chemical insults can cause damage to teeth?

A

Restorative materials and toxic materials

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11
Q

What happens to dentition during ageing?

A

Pulp vasculature is reduced (reduced arterioles, venules, and terminal capillary network is less pronounced)

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12
Q

What happens to tooth in response to sickle cell anaemia?

A

Persistent hypoxia of the pulp results in pulp necrosis, toothaches, and dental abscesses.

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13
Q

What is hereditary hypophoosphataemia?

A

Metabolic disturbance of calcium and phosphate that leads to poor mineralisation of calcified structures (poorly mineralised dentine, high pulp horns enlarged pulp chambers, and dental abscesses)

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14
Q

How does pulp respond to injury?

A

In the same way as other connective tissues: 2 phase immune response:

Innate immunity (Non-specific, rapid occurence, reaction to new antigens)

Acquired immunity (Specific, occurs several days after innate)

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15
Q

What are the types of protection that the pulp innate immunity uses?

A

Natural barriers (intact enamel, cementum, dentine, and dentinal fluid, junctional complexes between odontoblasts)

Ag Recognition (odontoblasts have TLRs, dendritic cells, macrophages)

Chemical barrier (Cytokines, chemokines, complements)

Phagocytosis (Neutrophils and macrophages)

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16
Q

What local modifying factors affect the response to caries?

A

Bacteria enter the pulp at a very late stage in carious process. (pulp dentine complex acts like a molecular sieve to insults)

Low compliance of tissue (Oedema formation must be restricted from formation and expansion due to being a hard tissue.)

Lack of collateral blood supply (Limits the supply and drainage of blood)

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17
Q

How does dentine respond to insults?

A

Dentine deposits a calcified barrier

Dentine sclerosis takes place which occludes tubules and icnreases collagen deposition by odontoblast process

Tertiary dentine formation (reactionary if odontoblast survives and reparative if odontoblast dies) Dentine bridge forms at the site of exposure

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18
Q

What factors affect the dentine responses to insults?

A

Extent and duration of the stimulus

Dentine permeability

Age of the tooth

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19
Q

What factors affect the dentine immune response to insults?

A

Vascular:

Low-compliance system theory (build up of pressure in the pulp compresses blood vessels at apical foramen resulting in necrosis of tissue)

vs. Transcapillary fluid theory

Compartmentalised inflammation

Neural:

Neurogenic inflammation

Neuroimmune modulation

Nociception

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20
Q

How is the inflammation distributed in the dental pulp?

A

It is compartmentalized so necrosis is separated in different parts of the pulp

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21
Q

What do firm resilient pulp ground substances do to the pulp tissue?

A

They limit the spread of pulp tissue and prevent the pressure increase

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22
Q

How do bacterial toxins kill the pulp?

A

Pulp necrosis occurs when toxin is in direct contact with the pulp. It exerts its effects by contacting the tissue directly.

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23
Q

What neuropeptides are released by sensory nerves?

A

Substance P

Calcitonin gene-related peptide

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24
Q

Which neuropeptides are important for vasodilation?

A

CGRP

Substance P

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25
Q

What triggers neurogenic inflammation?

A

Unmyelinated C fibers are activated

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26
Q

What is the purpose of neurogenic inflammation?

A

It supports the tissue in overcoming potential threats. It does this by:

Providing optimal nutrition for cells

Augmenting clearance of harmful products from the affected tissue compartment

Increasing outward flow of noxious elements along patent dentinal tubules by moderate increase in tissue pressure

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27
Q

What happens to dendritic cells and nerve fibers in response to neuroimmune modulation?

A

They are in close anatomic relationship and increase in parallel in pulp inflammation.

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28
Q

What changes are associated with neuroimmune modulation during pulp inflammation?

A

Anatomical changes:

Include sensory nerve sprouting (occurs as early as 1 day after exposure and decreases 3 - 4 weeks later) and sympathetic nerve sproutings (occurs about 3 - 4 weeks later)

Cytochemical changes:

Upregulation of sensory (Substance P and CGRP) and sympathetic neural peptides (NPY)

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29
Q

What do sympathetic nerves do during neuroimmune modulation?

A

They control pulp blood flow (constrict pre-capillary sphincters)

Modulate pulp inflammation (Inhibit pro-inflammatory cytokines, stimulate the production of anti-inflammatory cytokines, recruit immune cells, stimulate tertiary dentine formation, and reduce release of NPs from sensory nerve)

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30
Q

What chemicals are released during pulp inflammation to interact with nociceptors?

A

Protons (lowering pH)

Arachidonic acid and its metabolites (prostaglandins)

Bradykinin

Histamine

Substance P and CGRP

Serotonin

Nerve growth factor

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31
Q

Which neural pathway (tract) is responsible for pain sensation in the pulp?

A

Paleospinothalamic tract

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32
Q

How is nociception through the C fiber localised?

A

Nociception C fibre arising from a molar - slow pain - poorly localised:

Carried by the first order neurons in the trigeminal ganglion

Via trigeminal tract into the trigeminal spintal tract nucleus: Synapses at the subnucleus caudalis region, with a wide dynamic range
neuron (WDR, the second order neurons)

Via the paleospinothalamic tract - modulated - into the thalamus

Passing through the reticular formation and many modulating interneurons

Onto the cortex for interpretation

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33
Q

What are the types of projection neurons?

A

3 types:

Low-threshold mechanoreceptive types (activated only by light tactile stimulation)

Nociceptive specific type (Activated by supra-threshold nociceptive stimuli)

Wide dynamic range type (Input from a wide range of tactile and noxious/non-noxious stimuli from larger areas outside the pulp)

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34
Q

How is nociception modulated?

A

Local circuit interneurons

Projection neurons

Terminal endings of descending neurons

Glial cells

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35
Q

What terminal ending of descending neurons modulate nociception?

A

The ones originating in the periaqueductal gray matter

Endogenous opioid peptides (Beta-endorphin)

Endogenous cannabinoid system (inhibit central terminals of C fibers and are 10x more than opioid receptors in the CNS)

36
Q

What do glial cells do to modulate nociception?

A

They release proinflammatory cytokines (IL-1, TNF2, glutamate, NO, and prostaglandins)

37
Q

What are tge features of fast pain?

A

No inflammation

Stimulus-induced pain

Mediated by Aδ fibres

Rapid transient sharp pain

Source of pain easily localized (Fast pain pathway which ascends directly to the thalamus)

It is protective

38
Q

What are the features of slow pain?

A

Active inflammation

Stimulus induced or spanteous pain

Mediated by C fibers

Deep dull aching pain

Source of pain is poorly localized

Slow pain pathway (Paleospinothalamic tract)

Protective: Producing pain/hypersensitivity after injury and during healing

39
Q

What kind of pathway is inflammatory pain?

A

A positive feedback loop allowing inflammation to persist far beyond cessation of noxious stimuli

40
Q

What is peripheral sensitisation?

A

A pain state characterized by increased excitability of pulp nociceptors due to morphological and phenotypical changes

41
Q

What causes increased peripheral sensitization?

A

Increased expression of NeuroPeptides and membrane protein channels.

Sensory nerve sprouting and increased receptive field

Awakening the silent nociceptors

42
Q

What drugs are used to reduce inflammation and sensitization?

A

NSAIDs

43
Q

What is pulp disease?

A

Pulp disease is an inflammatory condition.

It is progression of pulp inflammation.

44
Q

What are the short term insults that lead to acute inflammation?

A

Cavity preparation

Trauma without irritation

45
Q

What does acute inflammation lead to in the pulp if not treated?

A

Healing with or without fibrosis

46
Q

What insults lead to chronic inflammation?

A

Loss of coronal tooth integrity:

Caries, restoration breakdown

Attrition, erosion

47
Q

What does chronic inflammation lead to in the pulp if not treated?

A

Necrosis then infection then pulpless apical periodontitis

48
Q

How does pulp disease progress?

A

Normal pulp gets inflamed

Inflammation can be reversible or irreversible.

Irreversible inflammation can lead to partial necrosis which leads to total necrosis which can lead to infection which leads to loss of pulp tissue

Apical periodontitis can arise at any stage of this progression

49
Q

What is necrobiosis?

A

Partial necrosis with pulpitis

Pulp chamber vs root canals

50
Q

What causes pulp disease and necrosis?

A

Persistent irritants

Only when bacterial toxin spreading throughout the pulp

51
Q

What happens when pulp is necrotic?

A

It gets digested by bacteria which start to migrate to the apex

Degeneration follows and calcification affects the pulp.

52
Q

What is pulp calcification?

A

Discrete pulp stones are formed and there is diffuse mineralization after trauma (thrombi in pulp b.v. sheaths around vessel walls.

Pulp calcification is a protective mechanism to trauma or other continual stimuli. It is a normal physiological response to ageing

53
Q

What happens to the pulp when it undergoes pulpitis that leads to necrosis?

A

Pulp becomes highly vascularised inflammatory tissue.

Stem cells form the pulp proper which form multinucleated elastic cells which leadds to resorption of dentine canal wall.

54
Q

What protective structure forms between the sterile alveolar bone and the microbe rich oral cavity?

A

A bridge.

55
Q

What life threatening condition can arise from pulp diseases?

A

Oral sepsis can arise which is life threatening

56
Q

What are the potential complications of pulp infections spreading into surrounding tissue?

A

Infection in the root canal space may spread into periradicular tissues (acute apical abscess) and fascial spaces (cellulitis)

Oral sepsis can arise which is life threatening

57
Q

What are fascial spaces?

A

Potential anatomic areas

Exist between the fascia and the underlying organs/other tissues

Form during infection as a result of spread of purulent exudate

58
Q

What complications can arise from pulp infection of maxillary teeth?

A

Purulent sinusitis

Meningitis

Brain abscess

Orbital cellulitis

Cavernous sinus thrombosis

59
Q

What complications can arise from pulp infection of mandibular teeth?

A

Ludwig’s angina

Parapharyngeal abscess

Mediastinitis

Pericarditis

Emphysema

Jugular thrombophlebitis

60
Q

What happens during ludwig’s angina?

A

Infection of the lower molar when the root apices lie below attachment of the mylohyoid muscle.

Purulent exudate break through the lingual cortical plate involves sublingual space, submandibular space, and submental space at the same time.

Theres a chance it can advance to the pharyngeal and cervical spaces resulting in airway obstruction which is life threatening.

61
Q

What do symptoms tell us about the severity of pulpitis?

A

No correlation between clinical symptoms and histologic status of the pulp.

Incidence of painless pulpitis to pulp necrosis is 40 - 60%

62
Q

Is a sensibility test a good indication of the health of a tooth?

A

Not necessarily:

Test is for nerve supply but doesn’t indicate blood supple and so a positive response isn’t necessarily indicative of a healthy pulp

63
Q

How do we diagnose pulp disease?

A

Identification of diseased tissues

Identification of healthy tissues

Identification of any other problems

64
Q

What is the purpose of diagnosis?

A

It will:

Indicate management options

Determine the treatment details

65
Q

What are the characters of acute and chronic disease?

A

Acute is characterised by moderate to severe pain, recent onset, patient seeks relief.

Chronic is characterised by very mild or no pain, present for a long time with no urgency.

66
Q

How are pulp and root canal conditions classified?

A

Clinically normal pulp (based on clinical findings)

Reversible pulpitis (acute/chronic)

Irreversible pulpitis (acute/chronic)

Necrobiosis (part infected part inflamed)

Pulp necrosis (No sign of infection / infected)

Pulpless root canal system (infected)

Pulp degeneration (atrophy, pulp canal calcification, hyperplasia, internal resorption)

Previous endodontic treatment (No sign of infection, infected, Technical standard which can be adequate or inadequate based on radiographs)

Other problems

67
Q

What are the steps of the diagnostic process?

A

History (medical dental presenting complaint)

Clinical examination (Clinical tests including pulp sensibility tests, percussion, palpation mobility, periodontal probing, transillumination, biting tests, radiographic examination, and identifying the cause)

Diagnosis (Tooth, pulp, periapical, and cause)

Management plan

Discussion with pt

Tooth investigation (suitability to restore, case selection)

Written records.

68
Q

What does pulp sensibility testing tell us?

A

Indicates pulp / root canal status.

Normal response is not pronounced pain that doesn’t linger

Exaggerated response that produces pain suggests pulpitis that can or can be not reversible.

No response suggests pulp necrosis, pulpless tooth or RCF (it can also be a calcified or false response)

Needs to be assessed along with periapical radiographs

69
Q

What does percussion and palpation tell us?

A

Current periapical status

70
Q

What does mobility and periodontal probing tell us?

A

Indicate periodontal status

71
Q

What does transillumination and biting tests tell us?

A

Indicates possible cause or causes of pain

72
Q

what does radiographic examination tell us?

A

Indicates periapical and periodontal status and possible causes

73
Q

What are the symptoms of dentine hypersensitivity?

A

Short, sharp, shooting pain

Can be intense

No spontaneous pain

Triggered by cold foods and drinks, tooth cleaning, a light touch of the exposed dentine surfaces

Can continue for years

74
Q

What are the signs of dentine hypersensitivity?

A

Exposed dentine surfaces typically cervically

Exaggerated response to the pulp sensibility tests with no lingering pain

*this is caused by hydrodynamic movement of the fluid within the patent dentinal tubules.

75
Q

How is pulp status diagnosed (inflammation)?

A

Severity and duration of symptoms change with temperature changes

Pulp sensibility tests

76
Q

How is an infected canal diagnosed?

A

Infected Canal
Necrosis, Pulpless or RFed

Based on:
Periapical status: symptoms

Pulp sensibility tests

Radiographs (based on periapical radiolucency)

77
Q

How is pulp status diagnosed (reversible or irreversible)?

A

It is a provisional diagnosis that asseses the true status of pulp. It is impossible to assess clinically.

Should be treated CONSERVATIVELY

78
Q

What kind of process is pulp disease typically?

A

Usually a dynamic process that lies on a continuum

79
Q

How does pulp disease progress?

A

Clinical normal pulp -> chronic and acute reversible pulpitis -> Chronic and acute irreversible pulpitis -> Pulp necrobiosis -> Pulp necrosis with infection -> Pulpless infected RCS -> Acute apical periodontitis

80
Q

What needs to be recorded and assessed for endodontic diagnosis?

A

The tooth

State of the pulp or RCS

State of the periapical tissues

Cause of the disease

Always include an assessment and identification of the cause of the disease (bacteria are often the main cause)

81
Q

What happens if endodontic treatment is not undergone?

A

It will eventually manifest in the periapical tissues resulting in inflammation, cyst formation, and abscesses/cellulitis

82
Q

What causes the periapical radiolucency seen during endodontic disease?

A

Loss of alveolar bone around the apex which is an indication of an inflammatory response

83
Q

How is pulp disease managed conservatively?

A

Nil

Desensitisation

Caries control

Restoration

Pulp capping (direct or indirect)

Pulpotomy

84
Q

How is pulp disease managed if it can’t be managed conservatively?

A

Pulpectomy

Orthograde endodontic tx

Retrograde endodontic tx

Periapical surgery

Extraction

85
Q

What is the main purpose of treatment?

A

To remove the source of irritation

To remove the diseased tissue

To provide a suitable environment for the pulp to heal itself

86
Q

What factors affect the ability of the pulp to repair surrounding tissues?

A

Reduced cell numbers

Reduced innervation

Reduced vascularity

The immune response remains active

87
Q

3 / 2

A

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DMD2 (89 decks)

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