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OMOPOR > Bony Inflammatory Lesions > Flashcards

Bony Inflammatory Lesions Flashcards

1
Q

What are the major factors for cyst expansion?

A
  1. Proliferation of epithelial lining and fibrous capsule
  2. Hydrostatic pressure of cyst fluid
  3. Resorption of surrounding bone
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2
Q

What is the most common investigation for a cyst?

A

Fine needle aspiration cytology

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3
Q

What are the sources of odontogenic epithelium?

A
  1. Dental lamina
  2. Rests of Dental lamina (Rests of Serres
  3. Enamel organ
  4. REE
  5. Rests of Hertwig’s epithelial root sheath
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4
Q

Etiology of a Periapical Granuloma

A

Arise as an initial periapical pathosis or after quiescence of a Periapical abscess

Defensive reactive due to microbial infection in the root canal, with spread of related toxic products into apical zone

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5
Q

Definition of a Periapical Granuloma

A

A mass of chronically or subacutely inflamed granulation tissue at the apex of a non-vital tooth

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6
Q

What is a Phoenix Abscess?

A

A secondary acute inflammatory change within a periapical granuloma due to worsening pulpal infection

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7
Q

Clinical Findings of a Periapical Granuloma

A
  • Asymptomatic Pulp Necrosis
  • Pain and sensitivity in acute condition
  • Associated with large restoration and caries
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8
Q

Radiographic Findings of a Periapical Granuloma

A

L: Periapical region
E: Well-circumscribed, well-defined
S:
I: Radiolucent with or without radiopaque rim
O: Sometimes surrounded by dense sclerotic bone

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9
Q

Histopathologic Findings of a Periapical Granuloma

A

Chronic inflammatory infiltrate: Lymphocytes, histiocytes and plasma cells

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10
Q

How do you confirm the diagnosis of a periapical granuloma?

A

Histology
Radiographic features are not diagnostic because PA inflammatory disease is not static and granuloma can turn into cysts or abscess without significant radiographic change

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11
Q

Management of a Periapical Granuloma

A
  1. RCT
  2. Extract followed by curettage of all apical soft tissues
  3. NSAIDs for symptomatic cases
  4. For larger lesions >2cm and teeth not suitable for RCT, consider periapical surgery
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12
Q

Definition of an Abscess

A

Accumulation of acute inflammatory cells at the apex of a non-vital tooth

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13
Q

Etiology of an Abscess

A

Arise as an initial periapical pathosis or from an acute exacerbation of a chronic periapical inflammatory lesion (Phoenix abscess)

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14
Q

Where does an abscess spread?

A

Along the path of least resistance
Extend through medullary spaces away from the apical area -> osteomyelitis
Perforate the cortex and spread diffusely through overlying soft tissue -> Cellulitis

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15
Q

Clinical Findings of an Abscess

A
  • Pulp necrosis
  • Purulent material within alveolus
  • TTP and TTPp
  • Severe pain, swelling and mobility
  • Elevation of involved tooth
  • Facial swelling, lymphadenopathy possible
  • Sinus tract (Asymptomatic)
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16
Q

Radiographic Findings of an Abscess

A

L: Periapical region of a non-vital tooth
E: Diffused, ill-defined
S:
I: Radiolucent
O: Loss of apical lamina dura or thickening of apical PDL. Resorption of apical bone

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17
Q

Histopathological Findings of an Abscess

A
  • Inflammatory infiltrate: Polymorphonuclear leukocytes, lymphocytes and neutrophils intermixed with inflammatory exudate, cellular debris, necrotic material
  • Pus formation
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18
Q

Differential Diagnosis of an Abscess

A
  • Acute apical periodontitis: May be found in vital teeth secondary to trauma
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19
Q

Management of an Abscess

A
  • Drainage and elimination of the focus of infection
  • Clinical expansion of bone or soft tissue => Incisional drainage
  • Extruded tooth -> Occlusal reduction
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20
Q

Definition of Condensing Osteitis

A
  • Localised areas of bone sclerosis associated with apices of teeth with pulpitis/pulp necrosis
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21
Q

Clinical Findings of Condensing Osteitis

A
  • Occurs with pulpitis or pulp necrosis
  • Variable responses to sensibility testing
22
Q

Radiographic Findings of Condensing Osteitis

A

L: Apices of teeth
E: Diffused
S:
I: Localised uniform zone of radiopacity
O: Thickened PDL or apical inflammatory lesion. Dense sclerotic bone around root

23
Q

Histopathological Findings of Condensing Osteitis

A

Increase in trabecular bone in response to persistent irritation

24
Q

Differential Diagnosis of Condensing Osteitis

A
  • Periapical/Focal cement-osseous dysplasia: Exhibits a radiolucent border, vital teeth
  • Enostosis: Vital teeth
25
Q

Management of Condensing Osteitis

A
  • Extraction or RCT
  • 85% will regress
26
Q

What medications are related to Medication related osteonecrosis of jaw?

A

Anti-resorptive medications used for treating multiple myeloma, osteoporosis and metastasis

IV bisphosphonates: Zolendronate (Zometa)
Oral bisphosphonates: Alendronate (Fosamax)
Rank L inhibitor: Denosumab

27
Q

Possible precipitating events causing MRONJ?

A
  1. Dentoalveolar surgery and extractions
  2. Concomitant oral disease e.g. periodontitis
  3. Denture usage
  4. Spontaneous development
28
Q

Pathophysiology of MRONJ

A
  1. Inhibition of osteoclastic bone resorption and remodeling, causing delayed healing
  2. Infection and inflammation
  3. Inhibition of angiogenesis, causing disruption to blood supply
29
Q

AAOMS 2014 Staging of MRONJ: Stage 0

A

No clinical evidence of necrotic bone. Non-specific symptoms or clinical and radiographic findings

30
Q

AAOMS 2014 Staging of MRONJ: Stage 1

A

Exposed and necrotic bone or fistulae that probes to bone AND
Have no evidence of infection

31
Q

AAOMS 2014 Staging of MRONJ: Stage 2

A

Exposed and necrotic bone or fistulae that probes to bone AND
With evidence of infection, symptomatic

32
Q

AAOMS 2014 Staging of MRONJ: Stage 3

A

Exposed and necrotic bone or fistulae that probes to bone AND
With evidence of infection + Extend past alveolar bone/ pathologic fracture/ extra-oral fistula/ Oro-antral communication, osteolysis extending to inferior border of mandible or sinus floor

33
Q

What is the AAOMS 2014 Criteria for MRONJ?

A
  1. Exposed bone or bone that can be probed through an intramural or extraoral fistula in the maxillofacial region that has persisted for more than 8 weeks
  2. Current or previous treatment with AR or anti-angiogenic agents
  3. No history of radiation therapy to jaws or obvious metastatic disease to the jaws
34
Q

Possible symptoms of MRONJ

A
  1. Odontalgia not an odontogenic cause
  2. Dull,aching bone pain, in the body of mandible which may radiate to the TMJ region
  3. Sinus pain
  4. Altered neurosensory function
35
Q

Clinical Features of MRONJ

A
  • Posterior mandible
  • Exposed bone after invasive dental procedure
  • Pain and swelling or asymptomatic
  • Loosening of teeth
  • Fistula not associated with pulpal necrosis
36
Q

Radiographic Findings of MRONJ

A

Indistinguishable from osteomyelitis and ORN
L:
E: Ill-defined
S:
I: Mixed RL and sclerosis with sequestration: Moth-eaten appearance
O: Alveolar bone loss, increased density, persistent unremodelled bone in extraction socket. Lamina dura thickening, decrease in PDL space

37
Q

Histopathological Findings of MRONJ

A
  • Irregular bone trabeculae of pagetoid bone, with adjacent enlarged and irregular osteoclasts
  • Sclerotic lamellar bone
  • Loss of osteocytes from lacunae
38
Q

Differential Diagnosis of MRONJ

A
  • Always consider malignancy: Osteosarcoma, SCC
39
Q

Investigation of MRONJ

A
  • Biopsy of vital bone altered by aminobishosphonates
40
Q

Management of MRONJ

A
  • Dental clearance prior to IV Bisphosphonates
  • Surgical intervention with or without hyperbaric oxygen
  • Stop BP for a period of time
  • For bone exposure, use mouth rinses with or without systemic antibiotics
41
Q

Definition of Osteoradionecrosis

A

Presence of exposed bone for > 3 months following radiation therapy.

42
Q

Disease mechanism of ORN

A

Bone necrosis from high doses of radiation, exacerbated by infections, extraction, trauma

43
Q

Pathophysiology of ORN - Bone

A
  • Low doses stimulate osteoblasts
  • Intermediate doses causes osteoblast cell death
  • High doses damage intact and mature bone (necrosis)
44
Q

Pathophysiology of ORN - Bone vasculature

A
  • Damage to endothelial cells in smaller vessels, leading to bone hypoxia and infarction, hypocellular and hypovascular bone
45
Q

What is Stage I of ORN? (Marx 1983)

A

Exposed alveolar bone without pathological fracture, which responds to HBO therapy

46
Q

What is Stage II of ORN? (Marx 1983)

A

Disease does not respond to HBO therapy, requires sequestrectomy and saucerisation

47
Q

What is Stage III of ORN? (Marx 1983)

A

Full thickness bone damage or pathologic fracture, usually complete resection and reconstruction with free tissue

48
Q

Clinical Findings of ORN

A
  • Exposed bone with or without sequestration
  • With or without pain
  • Intermittent swelling
  • Extra-oral drainage
49
Q

Radiographic Findings

A

Similar to osteomyelitis but periosteal reaction is rare
L: Posterior mandible
E:
S:
I: Mixed, surrounding more RO sclerotic bone
O: Pathological fracture, extensive bone loss

50
Q

Management of ORN

A
  1. Appropriate clearance (removal of hopeless teeth) prior to RT
  2. Current management is unfavourable due to poor healing
  3. Preventive dental treatment to maintain OH

OMOPOR (7 decks)

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