Bone Inflammation Flashcards

1
Q

What is the strict definition of osteomyelitis?

A

Bone marrow inflammation

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2
Q

What are the different types of osteomyelitis?

A
  1. Acute osteomyelitis
  2. Chronic osteomyelitis
  3. Focal sclerosing osteomyelitis - Consensing osteomyelitis
  4. Diffuse sclerosing osteomyelitis
  5. Osteomyelitis with proliferative periostitis (Garre’s Osteomyelitis)
  6. Alveolar Osteitis (dry socket)
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3
Q

What are the clinical presentations along with the systemic symptoms of Acute Osteomyelitis?

A
  • Clinical Presentations:
    • Short duration <1 month
    • Significant pain
  • Systemic Symptoms
    • Fever
    • Lymph node swelling
    • Elevated white blood cell count
    • Swelling of overlying soft tissue
    • Purulent drainage may be seen
    • Necrotic bone sequestra may be exfoliated
    • May cause paresthesia in the distribution of nerves passing through the involved area
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4
Q

What are the radiographic findings with Acute Osteomyelitis?

A
  • Earliest stages - no changes
  • Infection progresses - ill-defined, often asymmetric radiolucency is seen
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5
Q

What is the treatment for Acute Osteomyelitis?

A
  • Antibiotics!!
  • Surgical drainage may be necessary if it does not occur spontaneously
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6
Q

What are the clinical presentations of Chronic Osteomyelitis?

A
  • Long duration with variable pain
  • Usually not sharp and consistent pain
  • Swelling of overlaying tissues
  • Purulent drainage
  • Bone sequestration
  • Sinus tract formation
  • Tooth loss in area of involvement may be seen
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7
Q

What are the radiographic features of Chronic Osteomyelitis?

A
  • Ill-defined, often asymmetric radiolucency
  • Radiopaque internal sequestrum may be seen
  • Increased density of surrounding bone as a reactive response may be seen
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8
Q

What are the treatments for Chronic Osteomyelitis?

A
  • Surgical debridement is often necessary
  • Antibiotics
    • Often requires long duration therapy
    • Often must be given intravenously
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9
Q

Describe Chronic Focal Osteomyelitis.

A
  • Generally considered to be a reaction of periapical bone to low-grade odontogenic infection.
  • Low grade inflammation in an immune competent host can result in increased density (sclerosis) of the bone as the body tries to wall off the infection.
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10
Q

Will the tooth be vital with Chronic Focal Osteomyelitis?

A

No - tooth non vital!!!

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11
Q

What are the radiographic features of Chronic Focal Sclerosing Osteomyelitis?

A
  • Irregular area of opacity, may be asymmetric and often blends with surrounding bone
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12
Q

What are the treatments for Chronic Focal Osteomyelitis?

A
  • Address the odontogenic infection
  • RCT or extraction
  • Area may (85%) or may not remodel
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13
Q

Describe Chronic Diffuse Sclerosing Osteomyelitis.

A
  • Controversial bony condition that is often confused with other pathologic conditions, particularly cemento-osseous dysplasia which frequently becomes secondarily infected.
  • Considered to be a reaction to low grade odontogenic infection, often following trauma or surgery.
  • Equivalent of focal sclerosing osteomyelitis but affects a large area of bone in one quadrant
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14
Q

Where does Chronic Diffuse Sclerosing Osteomyelitis characteristically affect?

A

The posterior mandible

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15
Q

How does a Chronic Diffuse Sclerosing Osteomyelitis look radiographically and what are the treatment options?

A
  • Radiograph - Diffuse radiopacity of varying density
  • Tx:
    • Eliminate sources of infection
    • Antibiotics often not effective as sclerotic bone is hypovascularized
    • Monitor
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16
Q

What is the synonym for Garre’s Osteomyelitis?

A
  • Chronic Osteomyelitis with Proliferative Periostitis
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17
Q

What’s the unique characteristics of Chronic Osteomyelitis with Proliferative Periostitis?

A
  • Specific form of osteomyelitis
  • Low grade osteomyelitis
  • Immune competent host
    • Usually younger patients therefore
  • Inflammation involves periosteum
  • On or near the cortical surface
  • Draining sinus tract from an infected tooth most often
  • Periosteal infalmmation stimulates bone production
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18
Q

What is the clinical presentation of Chronic Osteomyelitis with Proliferative Periostitis, and what are the radiographic findings?

A
  • Clinical presentation - bony hard swelling (mandible most often affected)
  • Radiographic - Immature bone is laid down outside cortex but under periosteum
  • Thin layering of cortical bone produces expansion “onion skin” pattern
  • May have lucency under cortex
  • Layered bone is weakly opaque, usually less dense than cortical bone
  • May need occlusal films to see layering
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19
Q

What are the treatments for Chronic Osteomyelitis with Proliferative Periostitis?

A
  • Eliminate source of infection
  • Endo therapy
  • Extraction
  • Antibiotics do not usually alter process
  • Physiologic remodeling occurs over time
  • Surgical recontouring is not necessary
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20
Q

What is the synonym for Alveolar Osteitis?

A

Dry Socket

21
Q

What are the clinical presentations of Alveolar Osteitits?

A
  • Post extraction complication
    • Often associated with complicated/traumatic extraction (mandibular 3rd molars usually)
    • More likely in sites of infection
    • Women more common - associated with birth control pills
22
Q

What exactly causes Alveolar Osteitis, and what are some of the characteristics?

A
  • Loss/breakdown of the blood clot in the socket
  • Exposed bone visible without soft tissue covering
  • Typically occurs 3-4 days following extraction
  • Produces severe pain and a foul odor
23
Q

What is the treatments for Alveolar Osteitis?

A
  • Packing the socket with protective dressing
24
Q

What is the cause of Bisphosphonate-induced osteonecrosis?

A
  • Bisphosphonates - drugs that inhibit action of osteoclasts (also affects angiogenesis and osteoblasts)
25
Q

What are the therapeutic indications of bisphosphonates?

A
  • To attempt to control malignant disease in bone or hypercalcemia of malignancy
  • Multiple myeloma
  • Metastatic disease (breast & prostate carcinoma)
  • To increase bone density in older individuals suffering from osteoporosis
  • Treatment of Paget’s disease and other metabolic bone diseases
26
Q

What are the common important implications of bisphosphonates with it’s users?

A
  • Dose dependent,
  • 6-10% of cancer patients on IV tx
  • lower for patients with osteoporosis on oral tx
  • 85% of cases in patients with myeloma or metastatic breast cancer
  • 4% of cases in patients on oral tx
  • Nitrogen containing compounds produce greater risk**
27
Q

What are the common bisphosphonates?

A
  • Aredia (IV - nitrogen containing)
  • Zometa (IV - nitrogen containing)
  • Boniva (IV - nitrogen containing)
  • Bonefos
  • Fossamax (PO - nitrogen containing)
  • Actonel - (PO - nitrogen containing)
  • Didronel
  • Skelid
28
Q

What are the clinical presentation of BRONJ?

A
  • Bone necrosis
  • Often follows surgical procedures (60%)
  • May follow simple, dental tx
  • May be spontaneous
  • May be progressive
  • Difficult to control
  • Often will not heal or resolve
29
Q

What is the treatment of BRONJ?

A
  • Prevention & informed consent
  • Attain maximal oral health prior to initiation of bisphosphonate therapy
  • Good oral hygiene
  • Control of pain
  • Control of infection
  • Antibiotic mouth rinse may be helpful
  • Local debridement of dead bone
  • Wide excision, as in osteoradionecrosis, not advocated
  • Hyperbaric oxygen shows variable efficacy
30
Q

What type of osseous dysplasia does not easily fit into a specific etiologic category?

A

The Cemento-Osseous Dysplasias

31
Q

What are some characteristics of Cemento-Osseous Dysplasias?

A
  • Not inflammatory in origin
  • Not neoplastic
  • No genetic pattern
  • May be from a defect in progenitor cells in the PDL which affects their ability to remodel bone and cementum
32
Q

What’s the demographic pattern of Periapical Cemento-osseous dysplasia?

A
  • Middle age, 30-45 years
  • 70% blacks
  • 90% females
33
Q

What’s the clinical presentation of Periapical cemento-osseous dysplasia?

A
  • Anetior mandible affected
  • Painless, often discovered on routine radiographic study
  • TEETH ARE VITAL
  • No appreciable expansion
34
Q

What are the radiographic findings of Periapical cemento-osseous dysplasia?

A
  • Anterior mandibular teeth affected, one or more often multiple
  • Lesions found at apex of teeth
  • Root tip visible despite presence of lesions
  • Variable presentation depending on duration
    • Earliest lesions are radiolucent
    • Progress to lucency with central opacification
    • Late stage lesions are opaque with a thin lucent rim
    • Sclerotic lesions can fuse to tooth roots
35
Q

What are the treatments for periapical cemento-osseous dysplasia?

A
  • None required - recognition
  • DO NOT DO RCT
36
Q

How do Florid Cemento-osseous Dysplasias compare to Periapcial ones?

A
  • Same demographic pattern (middle age, blacks, females)
  • Multiple posterior quads affected, can affect anterior mandible as well
  • Tx: guard against infection
37
Q

How do Focal Cemento-osseous dysplasias differ from Periapical and Florid?

A
  • Does not affect “classic” population (wider age range from old to young, females still predominate, whites more than blacks)
  • Mandibular body primary site (premolar/1st molar most common & edentulous areas)
  • Rounded or lobular architecture (generally smaller than florid, rarely larger than 1.5cm)
  • Opaque lesions with lucen halo
  • Tx: none - monitor for change
38
Q

What are the other names for Langerhan’s Cell Histiocytosis?

A
  • Langerhan’s Cell Disease
  • Histiocytosis X
39
Q

What are the common characteristics of Lanerhan’s Cell Histiocytosis?

A
  • Younger patients (50% under 10)
  • Classic radiograph - teeth floating in air
  • Spectrum type disease
40
Q

What are the 3 types of Langerhan’s Cell Histiocytosis spectrum diseases?

A
  • Letterer-Siwe Disease
  • Hand-Schuler-Christian Disease
  • Eosinophilic Granuloma
41
Q

Of the spectrum of Langerhan’s Cell Histiocytosis, which one affects teenagers and young adults primarily, and prognosis is generally good?

A

Eosinophilic Granuloma

42
Q

Of the spectrum of Langerhan’s Cell Histiocytosis, which one affects children aged 3-10 years and multiple sites are involved, with a slower progression and a better prognosis?

A

Hand-Schuler-Christian Disease

43
Q

Of the spectrum of Langerhan’s Cell Histiocytosis, which one affects infants under 2, involves multiple organs and sites and is aggressive that is invariably fatal?

A

Letterer-Siwe Disease

44
Q

What is the treatment of Langerhan’s Cell Histiocytosis?

A
  • Curretage
  • Low-dose radiation therapy
  • A combination
45
Q

What are the clinical features of osteoradionecrosis?

A
  • Always seen in an area of radiation therapy
  • Pt will give a history of prior cancer, usually squamous cell carcinoma
  • Radiation permanently destroys blood vessels in area
  • Will not heal without surgical intervention
46
Q

What is the treatment for osteoradionecrosis?

A
  • Prevention!!
  • Dental eval before radiation
    • Caries, perio disease, extractions
    • Good oral hygeine
  • Once it’s present
    • Hyperbaric oxygen
    • Resect dead bone to viable bleeding bone
    • Soft tissue closure over surgical site
47
Q

What are the clinical features of a Traumatic Bone Cyst?

A
  • Radiolucen lesion, scallops up between tooth roots
  • Young patients, asymptomatic
  • Mandible most exclusively
48
Q

Which lesion produces scalloping up between tooth roots?

A

Traumatic Bone Cysts

49
Q

What are the surgical findings and treatments for Traumatic bone cysts?

A
  • Empty “hole” in bone, little/no tissue recovered, or contains blood, tinged fluid
  • Entry into lesion stimulates bleeding or walls are curetted to produce bleeding which ordinarily results in healing