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Oral Pathology Exam 1 > 5 Pulpal and Periapical Diseases > Flashcards

5 Pulpal and Periapical Diseases Flashcards

1
Q

3 signs of pulpal injury:

A
  • external stimuli reaches a noxious level
  • degranulation of mast cells
  • inflammatory mediators are released
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2
Q

Inflammatory mediators released with pulpal injury:

They cause (3):

A
  • histamine, bradykinin, prostaglandins

- cause vasodilation, increased blood flow, vascular leakage with edema

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3
Q

describe normal pulp tissue and how pulpal injury occurs

A
  • increased blood flow promotes healing through removal of inflammatory mediators and swelling of the injured tissue usually occurs
  • dental pulp is a confined area
  • activate dilation of the arterioles leads to increased pulpal pressure
  • secondary compression of the venous return can lead to strangulation
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4
Q

What causes pulpal injury?

A

increased pulpal pressure + accumulation of mediators = vessel damage, pulpal inflammation, and tissue necrosis

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5
Q

4 causes of pulpal inflammation (pulpitis):

A

1) Mechanical damage- traumatic accidents, iatrogenic damage from dental procedures, attrition, abrasion
2) Thermal injury- severe thermal stimuli can be transmitted through large uninsulated metal restorations , dental procedures (cavity preps, polishing, chemical rxns of dental materials)
3) Chemical irritation- from erosion, acidic dental materials (unsafe use of them)
4) Bacterial effects- toxins, extension from caries

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6
Q

reversible vs irreversible pulpitis

A

Reversible

  • tissue is capable of returning to a normal state
  • pain does not occur without stimulation
  • stops within seconds if stimulus is removed (more dramatic response to cold)
  • electric pulp testing (EPT) response at lower levels of current than control tooth
  • no mobility
  • no sensitivity to percussion
  • tx: removal of local irritant
  • if untreated, duration of the pain upon stimulation can become longer –> can become irreversible

Irreversible

  • higher level of inflammation has developed
  • pulp is damaged beyond the point of recovery
  • invasion by bacteria is often the transition between the two
  • pain may be spontaneous, continuous, or worse when the pt lies down
  • initially the tooth responds to EPT at lower levels
  • thermal stimulus = sharp, severe pain that continues after the stimulus is removed (cold is worse, sweet and acidic foods also cause pain) ​nd
  • mobility and sensitivity to percussion are usually absent
  • if pulpal drainage occurs, the symptoms may resolve (crown fracture, fistula, pain can return if drainage is blocked)
  • tx: endo or extraction
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7
Q

early vs later signs of irreversible pulpitis

A

Early

  • pain can usually be localized to the specific tooth
  • as it worsens, harder to identify exact tooth

Later

  • pain increases in intensity
  • throbbing pressure, keeps awake at night
  • heat increases pain, cold may produce relief
  • tooth responds to EPT at higher levels of current or demonstrates no response
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8
Q
  • affects children and young adults
  • large pulpal exposures (entire dentinal roof is gone),
  • tooth is asymptomatic
  • irritation and bacteria lead to chronic inflammation
  • hyperplastic granulation tissue comes out of the pulpal chamber
A

pulp polyp (chronic hyperplastic pulpitis)

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9
Q

most common teeth affected by pulp polyp

A

primary molars

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10
Q

primary vs secondary vs tertiary dentin

A

Primary- formed before completion of the crown

Secondary- odontoblasts continue to deposit dentin slow and gradual, leads to smaller pulp chambers and canal systems, deposition increases after age 35-40, deposition begins in the coronal portions of the tooth and proceeds apically, believed to be result of aging

Tertiary- new dentin laid down in areas of injury, laid down in areas of injury to peripheral odontoblastic processes, reactionary or reparative

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11
Q

significant traumatic injury can lead to early obliteration of the pulp chamber and canal, may be noticed clinically by a yellow discoloration of the crown

A

calcific metamorphosis

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12
Q

radiographic appearance: premature closing of the pulp chamber and canal (compared to adjacent or contralateral teeth), pulpal space is obliterated or reduced dramatically

A

calcific metamorphosis

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13
Q

tx for calcific metamorphosis: primary vs permanent teeth (vital and non-vital)

A

Primary teeth

  • asymptomatic: monitor, wait for them to exfoliate
  • symptomatic: extract and space maintain

Permanent teeth

  • non-vital: endo therapy
  • vital: periodic reevaluation
  • esthetics: bleaching or full coverage
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14
Q

occurs in about 20% of all people, characterized by an increased # of calcifications in older teeth or teeth with a history of trauma or caries

A

pulp calcifications

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15
Q

Where are pulp calcifications usually formed?

A

within the coronal portions of the pulp

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16
Q

90-95% of periapical lesions are ?

5-10% of periapical lesions are?

A

90-95% of periapical lesions are inflammatory, tooth-related lesions (cyst, granuloma, abscess),

5-10% are something else (other odontogenic cysts, non-odontogenic cysts, dysplastic bone disease, benign neoplasms, malignant neoplasms)

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17
Q

Radiographic features: periapical cyst vs granuloma

A

Periapical cysts and granulomas are more likely to be: slow growing, well-defined, corticated

Larger lesions = more likely to be cyst than granuloma

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18
Q

3 periapical inflammatory lesions:

A

periapical granuloma
periapical cyst
periapical abscess

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19
Q

Name the periapical inflammatory lesion: aka apical periodontitis

A

periapical granuloma

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20
Q

Name the periapical inflammatory lesion: collection of chronically inflamed granulation tissue at the apex of a nonvital tooth

A

periapical granuloma

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21
Q

Most apical inflammatory lesions are ______.

A

periapical granulomas

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22
Q

Name the periapical inflammatory lesion: defensive reaction secondary to the presence of bacteria in the root canal, spread of related toxic products into the apical zone

A

periapical granuloma

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23
Q

Name the periapical inflammatory lesion:

  • asymptomatic or painful
  • soft tissue overlying the apex may be tender
  • usually no mobility or significant sensitivity to percussion
  • thermal or EPT: no response or may see some response if pulpal necrosis is limited to a single canal in a multi-rooted tooth
A

periapical granuloma clinical findings

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24
Q

radiographic findings: radiolucent lesion of variable size, loss of apical lamina dura, circumscribed or ill-defined, root resorption can be seen (not uncommon)

A

periapical granuloma

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25
Q

histopathology: inflamed granulation tissue and fibrous CT, cells seen: lymphocytes, neutrophils, plasma cells, macrophages

A

periapical granuloma

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26
Q

tx of periapical granuloma in restorable vs non-restorable teeth

A

Restorable
- endo therapy (should be evaluated at 1 and 2 year intervals to rule out possible lesional enlargement and ensure proper healing, strong emphasis should be placed on the importance of recall visits)

Non-restorable

  • extraction
  • curettage of all apical soft tissue
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27
Q

Name the periapical inflammatory lesion: use of systemic antibiotics NOT recommended unless associated swelling or systemic changes are present

A

periapical granulomas

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28
Q

Tx of periapical granuloma may fail to heal for several reasons (6)

A

1) Cyst formation
2) Persistent pulpal infection- poor access design, missed or perforated canals, vertical root fractures, inadequate technique or instrumentation, leaking restorations
3) Periapical foreign material
4) Associated periodontal disease
5) Penetration into maxillary sinus
6) Fibrous scar formation (“periapical scar”)

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29
Q

defect created by peripheral inflammatory lesions may fill with dense collagenous tissue rather than normal bone

A

“periapical scar” (associated with failure of periapical granulomas)

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30
Q

Name the periapical inflammatory lesion: arises from epithelial rests of Malassez most commonly, may be traced to crevicular epithelium or sinus lining

A

periapical cyst / lateral radicular cyst

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31
Q

Name the periapical inflammatory lesion: stimulus is inflammation (epithelium at the apex of a nonvital tooth is stimulated by inflammation to form a true epithelium-lined cyst)

A

periapical cyst / lateral radicular cyst

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32
Q

Name the periapical inflammatory lesion:

  • non-vital tooth
  • radiolucent lesion of varying size
  • may be corticated
  • loss of apical lamina dura
  • can see root resorption
  • recurrence is rare
A

periapical cyst / lateral radicular cyst

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33
Q

Name the periapical inflammatory lesion: site is root apex or lateral root surface

A

periapical cyst / lateral radicular cyst

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34
Q

Name the periapical inflammatory lesion: dx by pulp testing or biopsy

A

periapical cyst / lateral radicular cyst

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35
Q

tx for periapical cyst / lateral radicular cyst

A

extraction, endo therapy

36
Q

histopathology: fibrovascular CT and granulation tissue supporting a mixed infiltrate of chronic and acute inflammatory cells, nonkeratinized stratified squamous epithelial lining, may see foreign material

A

periapical/lateral cyst

37
Q

tx of periapical/lateral radicular cyst

A
  • extraction or endo therapy (some believe large cystic lesions cannot be resolved with conventional endo)
  • follow up at 1 and 2 years is advised (at minimum)
  • biopsy required for nonresolving cases
38
Q

tool for the resolution of periapical inflammatory disease, lesions that fail to respond to proper therapy

A

Periapical surgery (apicoectomy)- curetage of all periradicular tissue and submission for histopathologic examination, amputation of the apical portion of the root, seal the foramen of the canal

39
Q

Why submit tissue removed from a periapical disease for microscopic exam?

Things to consider carefully in patient history:

A

possibility of more serious process unrelated to periapical inflammatory disease

Consider:

  • does the patient have previous tx for a jaw lesion
  • previous malignancy
  • metastatic tumor history (breast, lung, colon, prostate)
40
Q

can develop in any edentulous space that at one point was dentulous, periapical cyst that did not resolve following extraction of the affected tooth

A

residual cyst

41
Q

radiographic appearance: unilocular RL of varying size, corticated or non-corticated

A

residual cyst

42
Q

dx: biopsy + extraction history

A

residual cyst

43
Q

tx for residual cyst

A

surgical removal (recurrence unlikely)

44
Q

Name the periapical inflammatory lesion: accumulation of acute inflammatory cells at the apex of a non-vital tooth

A

periapical abscess

45
Q

Name the periapical inflammatory lesion: may be the initial periapical pathology OR a secondary flare up of a chronic periapical inflammatory lesion

A

periapical abscess

46
Q

Name the periapical inflammatory lesion: source of the infection is usually obvious, pulpal death may be trauma-related (tooth doesn’t have a cavity or restoration)

A

periapical abscess

47
Q

Name the periapical inflammatory lesion: becomes symptomatic as purulent material accumulates within the alveolus (tenderness of affected tooth)

A

periapical abscess

48
Q

Progression of a periapical abscess:

A

pain becomes more intense –> extreme sensitivity to percussion –> extrusion of tooth may occur –> swelling of tissues

49
Q

Name the periapical inflammatory lesion:

  • tooth does not respond to cold or EPT
  • headache, malaise, fever, and chills may be present
A

periapical abscess

50
Q

How does a periapical abscess spread?

A

along the path of least resistance

51
Q

Radiographic findings—widening of apical PDL space, ill-defined radiolucency, sometimes no changes can be detected if not enough time has passed for detectable bone destruction

A

periapical abscess

52
Q

when purulence of a periapical abscess spreads through medullary spaces in bone

A

osteomyelitis

53
Q

How does a periapical abscess perforate the cortex?

A
  • spread diffusely through the overlying soft tissues as cellulitis
  • channel through overlying soft tissue and perforate the oral epithelium creating an intraoral sinus tract (drainage)
54
Q

accumulation of inflamed granulation tissue located at the opening of the sinus tract

A

parulis

*associated with periapical abscess

55
Q

If an abscess is not able to establish drainage through the skin or into the oral cavity, what happens?

A

may spread through fascial planes of soft tissue (cellulitis)

56
Q

2 dangerous forms of cellulitis

A

Ludwig’s angina

cavernous sinus thrombosis

57
Q

cellulitis of the submandibular region, aggressive and rapidly spreading

A

Ludwig’s angina

58
Q

angina comes from the Latin word _____ meaning to strangle

A

angere

59
Q

70% of cases develop from spread of an acute infection from mandibular molars

A

Ludwig’s angina

60
Q

causes: acute infection from mandibular molars, peritonsillar or parapharyngeal abscesses, oral lacerations, fractures of the mandible, submandibular sialadenitis

A

Ludwig’s angina

61
Q

Ludwig’s angina has an increased prevalence in people who are ?

A

immunocompromised

62
Q

spaces involved in Ludwig’s angina

A
  • sublingual, submandibular, and submental spaces
  • once it enters the submandibular space, may extend to lateral pharyngeal (parapharyngeal) space and then to retropharyngeal space
  • may result in spread to the mediastinum
63
Q

tx of Ludwig’s angina

A
  • maintenance of the airway
  • elimination of original focus of infection
  • IV antibiotic therapy
  • incision and drainage
64
Q

mortality rate of Ludwig’s angina

A

10% (pericarditis, pneumonia, mediastinitis, sepsis, empyema, respiratory obstruction)

65
Q

a major dural sinus encased between the meningeal and periosteal layers of the dura, receives venous drainge from the orbit via the superior and inferior ophthalmic veins

A

cavernous sinus

66
Q

___% of cases of cavernous sinus thrombosis are the result of dental infections.

Other causes:

A

10%

Other: sinusitis, conditions prone to blood clotting, lupus, an infection in the ears or eyes

67
Q

Cavernous sinus thrombosis: developing from anterior vs posterior pathway

A

Anterior pathway: infection in maxillary anterior teeth perforate the facial maxillary bone and spread to the canine space

Posterior pathway: infections in maxillary premolar or molar teeth spreads to buccal or infratemporal space

68
Q
  • swollen eyelids and conjunctiva with cavernous sinus thrombosis
  • protrusion around eye, forehead, and nose
  • pupil dilation and loss of vision
A

periorbital edema

69
Q
  • induration and swelling of forehead and nose
  • fever, chills, tachycardia
  • nausea and vomiting
  • mental state changes
A

cavernous sinus thrombosis

70
Q

tx for cavernous sinus thrombosis

A
  • aggressive IV antibiotics (3-4 weeks)
  • removal of source of infection if identifiable (draining an infected sinus, extract a tooth and drainage)
  • anticoagulation therapy
71
Q

mortality rate of cavernous sinus thrombosis

A

~30%

72
Q
  • purulence from a periapical abscess can spread through medullary spaces in the bone
  • majority of cases caused by bacterial infections
  • expanding lytic destruction of involved bone that extends away from the initial site involvement
  • suppuration and sequestra formation
A

osteomyelitis

73
Q

3 classifications of osteomyelitis:

A
  • acute suppurative osteomyelitis
  • chronic suppurative osteomyelitis
  • diffuse sclerosing osteomyelitis
74
Q

Name the osteomyelitis: acute inflammatory process spreads through the medullary spaces of the bone, < 1 month duration

A

acute suppurative osteomyelitis

75
Q

Name the osteomyelitis: signs and symptoms include fever, leukocytosis, lymphadenopathy, significant sensitivity, soft tissue swelling, paresthesia of the lower lip may occur, drainage or necrotic bone spicule exfoliation

A

acute suppurative osteomyelitis

76
Q

tx for acute suppurative osteomyelitis

A

Surgical intervention

  • resolve infection
  • establish drainage
  • remove infected bone
  • culture the bacteria

Antibiotics are key!!
- penicillin, clindamycin, metronidazole

77
Q

Name the osteomyelitis: if left untreated, acute suppurative osteomyelitis progress to this

A

chronic suppurative osteomyelitis

78
Q

Name the osteomyelitis: signs and symptoms include swelling, pain, sinus formation, purulent discharge, sequestrum formation, tooth loss, or pathologic fracture

A

chronic suppurative osteomyelitis

79
Q

radiographic appearance: patchy, ragged, and ill-defined radiolucent, often contains central radiopaque sequestra

A

chronic suppurative osteomyelitis

80
Q

Name the osteomyelitis: surgical intervention is mandatory, removal of all infected material down to bleeding bone is mandatory in all cases

A

chronic suppurative osteomyelitis

81
Q

localized areas of bone sclerosis, associated with the apices of traumatized teeth (caries, excessive occlusal forces)

A

condensing osteitis

82
Q

radiographic appearance: uniform zone of radiopaque change directly associated with root surfaces, widened PDL space may be seen

A

condensing osteitis

83
Q

most common locations of condensing osteitis

A

most commonly mandible, premolar and molar

84
Q

tx for condensing osteitis

A
  • resolution of the odontogenic infection

- extraction or endo tx of the involved tooth

85
Q

about 85% of cases regress, partially or totally

A

condensing osteitis

86
Q

residual area of condensing osteitis remaining after resolution of the inflammatory focus

A

bone scar

Oral Pathology Exam 1 (16 decks)

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