Pulpal and jaw infections Flashcards

1
Q

Discuss the two causes of pulpitis

A
  1. Inflammatory challenge
    • The pulp is surrounded by dentine which limits the ability of the pulp to tolerate oedema
    • Thus the pressure rises in the pulp and this may cause local collapse of the venous part of the microcirculation
    • This leads to local tissue hypoxia and anoxia, which in turn may lead to localized necrosis
    • Chemical mediators released from the necrotic tissue lead to further inflammation and oedema, and total necrosis of the pulp may follow
  2. Bacterial challenge/ pus
    • Collection of pus at the root of a tooth
    • Caused by bacterial infection which causes neutrophil chemotaxis
    • Neutrophils recruit a lot of free oxygen radicals, and release a lot of enzymes
    • The FOR kill/damage bacteria, but also important tissues
    • Pus is just dead neutrophils and inflammatory exudate
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2
Q

List the histopathological features of pulpitis (7)

A
  • Pulp hyperaemia (dilation of blood vessels)
  • Inflammatory cell infiltrate (neutrophils)
  • Granulation tissue
  • Exudate
  • Reactionary dentine
  • Tubules may be purple -> signifies bacterial invasion
  • Local ischaemia may lead to local necrosis and pulp abscess formation
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3
Q

For reversible- irreversible pulpitis, explain the significance of these terms.

A
  • Not Pathological Terms
  • Not Absolutely Correlated with Pulpal Histo-Pathology
  • Always Intensely Painful
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4
Q

Describe what happens in irreversible pulpitis

A
  • Pulp starts to die once it loses its blood supply due to swelling
  • The dead tissue is broken down by the body’s immune system, but if there is too much infection and dead tissue, then an abscess can form
  • Inflammation and other symptoms, such as pain, are severe, and the pulp cannot be saved
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5
Q

For reversible- irreversible pulpitis, state their clinical features:

  • Pain duration
  • Sensitising stimuli
  • Electric testing
A

Irreversible pulpitis:
Pain duration:
• Prolonged, Delayed

Sensitising stimuli:
• Only to hot, cold
• Irresponsive to sweet/sour

Electric testing:
• Irresponsive to electric pulp testing

Reversible pulpitis:
Pain duration:
• Short, immediate

Sensitising stimuli:
• Hot, cold, sweet and sour

Electric testing:
• Responsive to electric pulp testing

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6
Q

Explain how a clinical diagnosis is made for acute and chronic pulpitis

A

Acute pulpitis:
Clinical diagnosis is usually made:
• Patient complains of a severe throbbing pain, at times lancinating in type
• Pain is precipitated by hot or cold stimuli or on lying down, and which often keeps the patient awake

Chronic pulpitis:
Clinical diagnosis is usually made:
• Spontaneous attacks of dull aching pain that can last for an hour or more

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7
Q

For chronic hyperplastic pulpitis, explain how it occurs

A

Cause:
• Deciduous or recently erupted permanent teeth with wide-open carious cavities
• The wide-open pulpitis prevents build-up of tissue pressure compromising pulpal blood flow, and the good apical blood supply facilitates pulpal defence and repair = granulation tissue forms, creating a hyperplastic response

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8
Q

For chronic hyperplastic pulpitis, explain its histological features by stating:

  • The origin of the epithelial border
  • General histological features
A

Origin of epithelial border:
• Epithelial cells present in the saliva may make the polyp epithelialized
• However, it is truly unknown where these epithelial cells originate from
• It is hypothesised that the cells come from the region of the basal cell layer and might be released from trauma to the oral mucosa or from the gingival sulcus

General histology signs:
• Blob of granulation tissue on top of the pulp
• Chronic, inflammatory cell infiltrate

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9
Q

For chronic hyperplastic pulpitis, list the differences between the clinical features of an ulcerated polyp and an epithelialized polyp.

A

Ulcerated polyp:
• Dark red, yellow-flecked (because of the fibrinous exudate) mass protruding from the pulp chamber
• Bleeds readily on probing

Epithelialized polyp:
• Firmer
• Pinkish-white in colour
• Does not bleed readily
• No feeling on gentle probing
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10
Q

Define acute periapical periodontitis and state its histopathological features

A

Definition:
• Apicalportion of a tooth’s root becomes inflamed, following trauma or infection

Histopathological features:
• Acute inflammatory exudate in the periodontal ligament within the confined space between the root apex and the alveolar bone

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11
Q

Describe what happens in chronic periapical periodontitis, and state why granulation tissue is usually present

A

Cause:
• Persistent irritation from bacteria and their products in the pulp leads to chronic periapical periodontitis
• This is characterized by resorption of the periapical alveolar bone and its replacement by chronically Inflamed granulation tissue to form a periapical granuloma

Cause of granulation tissue:
• The periapical vascular network is very rich, greatly enhancing the ability of the tissue to heal if the cause of the inflammation is removed (hence the granulation tissue

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12
Q

State the histopathological features of chronic apical periodontitis

A
  • Granulation tissue infiltrated by lymphocytes, plasma cells, and macrophages
  • Dense bundles of collagen fibres that separate the chronically inflamed granulation tissue from the surrounding bone
  • These collagen fibres, forming a sort of capsule around the lesion
  • Deposits of cholesterol and haemosiderin are often present in a periapical granuloma. These are derived from the breakdown of red blood cells
  • Cholesterol crystals in the granulation tissue appears as clefts
  • Multinucleate foreign-body giant cells are grouped around the cholesterol clefts
  • There may be foam cells as well
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13
Q

Explain how recrudescence occurs (apical lesions form in chronic periodontitis - why it goes from asymptomatic to symptomatic)

A
  • Host response may be in equilibrium with level of irritation
  • Then, there is imbalance in factors and this may cause recurrence of apical lesions in a chronic setting
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14
Q

List the clinical and radiographic features of acute apical periodontitis

A

Clinical features acute apical periodontitis:
• Pain occurs due to external pressure (on the tooth) because the pressure is transmitted through the fluid exudate to the sensory nerve endings (tender to percussion)
• As the fluid is not compressible, the tooth feels elevated in its socket
• Hot or cold stimulation of the tooth does NOT cause pain

Radiographic features of acute apical periodontitis:
• NO bone resorption
• Slight widening of the periodontal ligament
• Lamina dura around the apex may be less well defined than normal

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15
Q

List the clinical and radiographic features of chronic apical periodontitis:

A

Clinical features of chronic apical periodontitis:
• Usually asymptomatic
• Occasional tenderness of the tooth to palpation and percussion
• Percussion may produce a dull note because of the lack of resonance caused by the granulation tissue around the apex
• Elevated tooth

Radiographic features of chronic apical periodontitis:
• Bone resorption is seen
• Radiolucency around non- vital tooth
• May have sclerotic margins

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16
Q

Discuss the causes of abscesses, and mention which microorganism is responsible for their formation

A
  • May develop either directly from acute periapical periodontitis or more usually from a chronic periapical granuloma
  • Is the result of a mixed bacterial infection. Strict anaerobes are usually the predominant organism
17
Q

List the difference between an acute abscess and a chronic abscess.

A

Acute abscess
• Not draining
• Only has granulation tissue wall if recrudescence

Chronic abscess
• Draining through the sinus wall of chronic inflammatory granulation tissue

18
Q

Explain what actinomycosis is by stating:

  • Which bacteria is responsible
  • Sources of entry
  • Age and gender of affected patients
A

Which bacteria is responsible:
• Chronic, suppurative, polymicrobial infection
• Endogenous gram positive anaerobic bacteria
• Actinomyces israelii predominate

Sources of entry:
• Infection is endogenous, and either a tooth socket, most commonly a lower third molar, or an infected root canal are thought to be the portals of entry.

Age and gender of affected patients:
• Younger subjects
• M > F

19
Q

List the histological features of actinomycosis

A
  • Abundant granulation tissue and fibrous tissue
  • A central area of suppurative necrosis
  • Granules consisting of tangled meshes of Gram-positive, radiating filaments ofactinomyces = “sulphur granules” in pus from actinomycotic lesions
  • Gram stain: gram positive so it shows up as dark blue masses
20
Q

State the clinical features of actinomycosis by stating:

  • What is most affected
  • Characteristics
  • Pain levels
A

What is most affected:
• The soft tissues of the submandibular area and neck are most commonly involved

Characteristics:
• Characterized by multiple foci of chronic suppuration
• Firm swellings which eventually soften
• Pus which discharges through multiple sinuses

Pain levels:
• Pain is variable and the swellings are often painless.

21
Q

Briefly explain the treatment for actinomycosis

A
  • Penicillin - starting with high dose parenteral therapy for at least 6 weeks
  • In chronic infection with a lot of fibrosis = incision and drainage, together with antibiotics
22
Q

Explain what alveolar osteitis is and state its risk factors

A

Explanation:
• This unpredictable complication in the healing of extraction wounds
• A dry socket is a localized inflammation of the bone following either the failure of a blood clot to form in the socket, or the premature loss or disintegration of the clot

Risk factors:
• Failure of a clot to form may be due to a relatively poor blood supply to the bone due to diseases or from the excessive use of vasoconstrictors in local anaesthetics
• In cases where the blood clot is lost it may be due to it being washed away by excessive mouth rinsing
• The clot may disintegrate prematurely due to fibrinolysis of the clot due to infection by proteolytic bacteria

23
Q

State the histopathological characteristics of alveolar osteitis

A
  • Healing is extremely slow and follows the proliferation of granulation tissue from the surrounding vital bone.
  • The dead bone is gradually separated by osteoclasts and a number of tiny sequestra may be formed
24
Q

State the clinical features of alveolar osteitis

A
  • Highest incidence of dry socket follows the extraction of impacted lower third molars.
  • Food debris, saliva, and bacteria collect in the empty socket, the bone of which becomes infected and necrotic.
  • Associated with severe pain developing a few days after the extraction
  • The socket often contains foul tasting and smelling decomposing food debris (can be washed away to reveal the denuded bone lining the cavity)