OR signs of inflammation Flashcards
what is periosteal reaction
§ Periosteum lifted by inflammatory exudate
§ Stimulates osteoblasts to form new bone
§ Usually parallel layers- onion skin appearance
§ More typical in the mandible
what are the inflammatory lesions that can take place at the PA and the jaw
§ Periapical
□ Apical rarefying osteitis (ARO)
□ Condensing osteitis( apical sclerosing osteitis)
□ Mixed of ARO and Condensing osteitis
§ Jaw
□ Osteomyelitis
□ ORN
□ MRONJ
what are the hall mark features of PA lesion
associated with NV teeth
disruption of lamina dura, widening of PDL spaces
what could widening PDL space be due to
§ Pulpal insult, TFO/attrition, iatrogenic, malignancy
○ Inflammatory exudate accumulates in PDL space
○ Clinical features
§ Can be asymptomatic or ttp
what is the radiographic description of periapical granuloma
§ Circumscribe, well defined radiolucent area of bone loss at apex ( apical rarefying osteitis)
what is the clinical symptoms of PA granuloma
○ Pulp necrosis, but usually asymptomatic
○ Little or no pain to percussion and palpation
what is PA granuloma comprise of
○ Chronic inflammatory infiltrate of lymphocytes, histiocytes and plasma cells
what is the radiographic features of PA cyst
similar to PA granuloma, but larger in size >1cm
What is the hiisto of PA cyst
○ Central cavity lined by stratified squamous epithelium, origin from the cell rests of Malassez
what is the clinical features of acute apical abscess
§ 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
what is the radiographic description of acute apical absces
§ Loss of apical lamina dura
§ Resorption of apical bone
§ Appearance may vary
§ Could have diffused, ill defined radiolucency for more destructive inflammation
what is the radiographic description of condensing osteitis
§ Diffuse radiopaque dense sclerotic bone around root of tooth
what are the clinical features of condensing osteitis
§ Occurs with pulpitis or pulp necrosis
§ Variable responses to vitality tests or percussion/palpation
what is osteomyelitis
inflammation of the bone marrow not confined to localised area typically results in necrosis
how does osteomyelities typically occur
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
where is the more common site for osteomyelitis
mandible» maxilla due to better blood vascularity for maxilla
What type of pt would be at greater risk for osteomyelitis
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
what is the hallmark of osteomyelitis
sequestra
what is the radiographic description of osteomyelitis
Subtle decrease in bone trabeculation, increase in radiolucency, ill corticated
how does chronic osteomyelitis appear radiographically
□ Sequestrum, ranges in size
Starts to appear sclerotic, moth eaten appearance, often mixed radiolucent and radiopaque internally
what is the histopathology of osteomyelitis
§ Necrotic bone, loss of osteocytes from lacunae
§ Inflammatory infiltrate/soft tissue component
§ Predominantly neutrophils> mononuclear cells
what is the management of osteomyelitis
§ 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
what is osteoradionecrosis
presence of exposed bone for 3 months or more following radiotherapy
what is the disease mechanism for ORN
○ Disease mechanism
§ Bone necrosis from high doses of radiation
§ Exaerbated by infections, dental extractions, dental trauma
§ Mandible» maxila due to blood supply difference
pathophysiology of ORN
§ 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
what is marx staging for ORN based on? how many stages are there
based on response to Hyperbaric oxygen therapy, 3 stages
what is the clinical features of ORN
§ 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
what is the radiographic features of ORN
§ Similar to osteomyelitis but periosteal reaction is rare, because radiotherapy has killed off osteoblasts
§ Ill defined non corticated moth eaten, mixed. Sequestrum present
what is the management of ORN
□ Dental clearance prior to radiation therapy is crucial
□ Preventive dental treatment ( maintaining OH, denture hygiene)
□ Surgical intervention (curettage, decortication, sequestrectomy)
Hyperbaric oxygen with antibiotics
what is MRONJ
○ 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
what is aaoms criteria for MRONJ
§ 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
what is stage 2 of MROnJ
□ 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
what is stage 3 of mronj
□ 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
what is the pathophysiology of MRONJ
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
what are the risk factors for MRONJ
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
management strategies for MRONJ
§ 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)
what are the risk of MRONJ pt
® Osteoporotic pt on BP –> 0-0.15%
® Osteoporotic pt on DMB–> 1%
Cancer pt on BP–> 1.6-14.8%
