OR signs of inflammation Flashcards

1
Q

what is periosteal reaction

A

§ Periosteum lifted by inflammatory exudate
§ Stimulates osteoblasts to form new bone
§ Usually parallel layers- onion skin appearance
§ More typical in the mandible

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2
Q

what are the inflammatory lesions that can take place at the PA and the jaw

A

§ Periapical
□ Apical rarefying osteitis (ARO)
□ Condensing osteitis( apical sclerosing osteitis)
□ Mixed of ARO and Condensing osteitis
§ Jaw
□ Osteomyelitis
□ ORN
□ MRONJ

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3
Q

what are the hall mark features of PA lesion

A

associated with NV teeth

disruption of lamina dura, widening of PDL spaces

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4
Q

what could widening PDL space be due to

A

§ Pulpal insult, TFO/attrition, iatrogenic, malignancy
○ Inflammatory exudate accumulates in PDL space
○ Clinical features
§ Can be asymptomatic or ttp

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5
Q

what is the radiographic description of periapical granuloma

A

§ Circumscribe, well defined radiolucent area of bone loss at apex ( apical rarefying osteitis)

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6
Q

what is the clinical symptoms of PA granuloma

A

○ Pulp necrosis, but usually asymptomatic
○ Little or no pain to percussion and palpation

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7
Q

what is PA granuloma comprise of

A

○ Chronic inflammatory infiltrate of lymphocytes, histiocytes and plasma cells

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8
Q

what is the radiographic features of PA cyst

A

similar to PA granuloma, but larger in size >1cm

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9
Q

What is the hiisto of PA cyst

A

○ Central cavity lined by stratified squamous epithelium, origin from the cell rests of Malassez

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10
Q

what is the clinical features of acute apical abscess

A

§ Pulp necrosis
§ Ttp, ttPp
§ Severe pain, swelling, mobility
§ Elevation of tooth involved
§ In severe cases can have systemic symptoms like fever, facial swelling, lyphadenopathy, esp when pt is immunocompromised

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11
Q

what is the radiographic description of acute apical absces

A

§ Loss of apical lamina dura
§ Resorption of apical bone
§ Appearance may vary
§ Could have diffused, ill defined radiolucency for more destructive inflammation

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12
Q

what is the radiographic description of condensing osteitis

A

§ Diffuse radiopaque dense sclerotic bone around root of tooth

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13
Q

what are the clinical features of condensing osteitis

A

§ Occurs with pulpitis or pulp necrosis
§ Variable responses to vitality tests or percussion/palpation

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14
Q

what is osteomyelitis

A

inflammation of the bone marrow not confined to localised area typically results in necrosis

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15
Q

how does osteomyelities typically occur

A

from pyogenic bacteria introduced via
§ Abscessed tooth
§ Surgery
§ Hematogenous spread

	○ Stimulates reaction involving cancellous and cortical bone and periosteum
	○ Can range from acute to chronic
		§ Acute
			□ Rapid onset, pain, swelling of adjacent soft tissues, fever, lymphadenopathy, leukocytosis
			□ Associated teeth mobile, ttP
			□ Can have purulent drainage
			□ Can have paresthesia of lower lip
		§ Chronic
			□ Sequalae of acute phase
				® Intermittent recurrent episodes of usually less severe swelling, pain, fever, lymphadenopathy, can have paresthesia and drainage with sinus formation
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16
Q

where is the more common site for osteomyelitis

A

mandible» maxilla due to better blood vascularity for maxilla

17
Q

What type of pt would be at greater risk for osteomyelitis

A

greater risk
§ Systemic factors
□ Malnutrition, DM, leukemia, alcoholism
§ Disorders of decreased vascularity
□ Sickle cell anemia
□ osteoporosis
§ Immunosuppression
□ aids
§ On medication
□ Steroids, chemo, bisphosphonates
○ Related conditions to osteomyelitis
§ Chronic recurrent multifocal osteomyelitis (CRMO)
§ Synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO)
§ Both occurs de novo without acute phase, without identifiable pathogenic microorganism

18
Q

what is the hallmark of osteomyelitis

A

sequestra

19
Q

what is the radiographic description of osteomyelitis

A

Subtle decrease in bone trabeculation, increase in radiolucency, ill corticated

20
Q

how does chronic osteomyelitis appear radiographically

A

□ Sequestrum, ranges in size
Starts to appear sclerotic, moth eaten appearance, often mixed radiolucent and radiopaque internally

21
Q

what is the histopathology of osteomyelitis

A

§ Necrotic bone, loss of osteocytes from lacunae
§ Inflammatory infiltrate/soft tissue component
§ Predominantly neutrophils> mononuclear cells

22
Q

what is the management of osteomyelitis

A

§ Must remove source of infection
□ Curettage, sequestrectomy, decortication( remove poorly vascularised bone and placing vascular periosteum next to bone marrow to induce healing), resection
□ Antibiotic therapy only effective if bacterial cultures are positive

23
Q

what is osteoradionecrosis

A

presence of exposed bone for 3 months or more following radiotherapy

24
Q

what is the disease mechanism for ORN

A

○ Disease mechanism
§ Bone necrosis from high doses of radiation
§ Exaerbated by infections, dental extractions, dental trauma
§ Mandible» maxila due to blood supply difference

25
Q

pathophysiology of ORN

A

§ Low doses stimulates osteoblasts, leading to bone formation
§ Intermediate doses causes osteoblast/chondroblast cell death
§ High doses damage mature intact bone
§ Radiotherapy also causes damage to endothelial cells in smaller vessels.
□ Leads to bone hypoxia–> hypocellular and hypovascular bone

26
Q

what is marx staging for ORN based on? how many stages are there

A

based on response to Hyperbaric oxygen therapy, 3 stages

27
Q

what is the clinical features of ORN

A

§ Most common in posterior mandible( direction of radiotherapy beam)
§ Exposed bone may or may not have sequestration
§ Intermittent swelling
§ Extra oral damage
May or may not have pain

28
Q

what is the radiographic features of ORN

A

§ Similar to osteomyelitis but periosteal reaction is rare, because radiotherapy has killed off osteoblasts
§ Ill defined non corticated moth eaten, mixed. Sequestrum present

29
Q

what is the management of ORN

A

□ Dental clearance prior to radiation therapy is crucial
□ Preventive dental treatment ( maintaining OH, denture hygiene)
□ Surgical intervention (curettage, decortication, sequestrectomy)
Hyperbaric oxygen with antibiotics

30
Q

what is MRONJ

A

○ Typically associated wiith anti resorptive medications used for
§ Cancer related conditions including hypercalcemia of malignancy
§ Complications from bone metasteses from breast, prostate and lung CA, such as spinal cord compression and pathologic fractures; bone pain
§ Multiple myeloma
§ Osteoporosis related fracture
§ Metabolic bone diseases like paget’s disease, osteogenesis imperfecta
§ Others like giant cell tumour of bone, fibrous dysplasia
§ DRUG FOR BISPHOSPHONATES:
□ ORAL: alendronate(fosamax), risedronate (actonel)
□ IV: ibandronate (boniva), zoledronic acid (reclast)/ zolendronate(zometa)
denosumab, romosozumab

31
Q

what is aaoms criteria for MRONJ

A

§ Current or previous tx with anti resorptive therapy alone or in combination with immune modulators or antiangiogenic agents
§ Exposed bone or bone that can be probed through an intraoral or extraoral fistula in the maxillofacial regions that has persisted for more than 8 weeks
No history of radiation therapy to jaws or metastatic disease to the jaws

32
Q

what is stage 2 of MROnJ

A

□ Exposed and necrotic bone or fistula that probes to the bone in pt who are
® Symptomatic
® Have evidence of infection/inflammation
May present with stage 0 radiographic findings localised to alveolar bone

33
Q

what is stage 3 of mronj

A

□ Exposed and necrotic bone or fistula that probes to the bone in pt with
® Evidence of infection
® And one of the following
◊ Extra oral fistua
◊ Pathologic fracture
◊ Extra oral fistula
◊ Oro antral/oral nasal communication
Osteoysis extending to inferior border of mandible or sinus floor

33
Q

what is the pathophysiology of MRONJ

A

nhibition of bone remodelling
□ Antiresorptive drugs inhibit osteoclast formation, differentiation and function–> decreased bone resorption and remodelling, causing delayed healing
§ Infection and inflammation
□ Presence of inflammatory cytokines at MRONJ sites, poor OH and biofilm presence associated with development of MRONJ
§ Inhibition of angiogenesis
□ Some bisphosphonates directly inhibit angiogenesis, decrease vascularity at MRONJ sites
□ Antiangiogenic drugs associated with MRONJ
§ Innate or acquired immune dysfunction
□ Patients with metastatic or primary bone CA, in immunocompromised states, or those on immune modulating drugs at higher risk for MRONJ

33
Q

what are the risk factors for MRONJ

A

malignnacy

those taking denosumba higher risk than bisphosphonate

the longer the duration on antiresorptive, increased risk of MRONJ

local factors like dentoalvelar ops

mandible»maxilla

female higher prevelance

33
Q

management strategies for MRONJ

A

§ Education about risks of MRONJ
§ Dental clearance prior to start of antiresorptive therapy especially when AR therapy indicated for malignant diseases
§ Identify sites of acute or potential infection
§ Remove teeth with poor prognosis
§ Continued preventive maintenance after start of AR therapy ( perio maintainence)

34
Q

what are the risk of MRONJ pt

A

® Osteoporotic pt on BP –> 0-0.15%
® Osteoporotic pt on DMB–> 1%
Cancer pt on BP–> 1.6-14.8%

35
Q
A