Bone infection and necrosis Flashcards

(39 cards)

1
Q

What is likely the cause of a acute periapical abscess?

A

Non-vital tooth. Source of infection is usually obvious! Pulp death could also be due to trauma where the tooth has no cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give me the clinical features of a periapical abscess

A
  • Symptomatic or asymptomatic
  • Becomes symptomatic as purulent material accumulates in the alveolus! Then it is percussion and mastication sensitive, does not respond to pulp test and swelling of the tissues occur.
  • progresses and spreads: either through medullary spaces (causes osteomyelitis) or perforates cortical bone which drains through intra oral sinus.
  • When draining, asymptomatic, but when drainage blocks it becomes symptomatic due to the pressure built up
  • GP can be used to determine origin of infection with radiograph.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give the radiological features of a periapical abscess

A
  • Widen PDL
  • Ill defined radiolucency!
  • Phoenix abscess: outline of original chronic lesion with associated ill-defined bone loss (rises from ashes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do we treat a periapical abscess?

A
  1. Drainage: -excision
    - root canal treatment
    - soft tissue drainage
  2. Eliminate focus of infection
  3. Use NSAIDS
    - pre-op
    - immediate post op
  4. Antibiotic cover:
    - not really needed as long as well localised or easily drained
    - Needed in immunocomp pts, if there is cellulitis, or dissemination.
  5. After RCT/extract!
    - sinus tract will resolve self and bone will take awhile to heal.
  6. If sinus tract persists then:
    - curettage tract
    - surgical removal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give the pathogenesis of a periapical granuloma

A

Mass of chronically or subacutely inflammed granulation tissue at apex of non-vital tooth.
Does not show true granulomatous inflammation!
Formation of apical inflammatory lesions represent a defensive reaction secondary to presence of microbial infection in root canal that spread to apical zone. NB CAN DEVELOP FROM PERAIPICAL ABSECESS OR AS INTIAL LESION AND CAN DEVELOP INTO A PERIAPICAL CYST!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give the clinical features of a periapical granuloma

A
  • acute lesions (acute apical periodontitis) are symptomatic, pain on biting with no obvious alterations
  • chronic lesions (chronic apical periodontitis) are asymptomatic!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give the radiographic features of a periapical granuloma

A
  • Early stages of infection see no radiographic alterations
  • loss of apical lamina dura
  • later detectable apical radiolucency which is small and barely predictable, can get greater than 2cm. Well circumscribed or ill defined.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give the treatment of a periapical granuloma

A
  1. endodontic treatment and then evauluate every 1,3, 6 months then 1 yr and 2yr
  2. extract badly damaged teeth.
  3. Use NSAIDS in symptomatic cases
  4. Periapical surgery for lesions larger than 2cm! will curettage all peri-radicular soft tissue, amputate apical portion of root (apicectomy), seal the canal foramen, all soft tissue removed submitted for histological exam.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a periapical fibrous scar?

A
  • sometimes periapical defects dont heal with normal bone but filled with fibrous tissue.
  • often occurs when both buccal and lingual cortical plates are lost
  • Often in areas with intact ortical plates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Supply the pathogenesis of condensing osteitis

A

Lesion is focal, periapical, hyperplastic bone reaction that results from chronic low grade pulpitis.
Excessive bone deposition without resorption results in increased bone density in periapical area of any tooth affected with either a chronic carious lesion or more commonly a leaking restoration. Its a localised area of bone sclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give the clinical features of condensing osteitis

A
  • Children and young adults in area of lower premolars and molars seen with pulpitis and pulpal necrosis.
  • Pain generally not a feature but mild sensitivity may be present
  • Most cases associated with md premolar and molars!
  • expansion of area should not be present clinically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give the radiological features of condensing osteitis

A
  • Well defined radiopaque lesion up to 2cm in diameter
  • At apical area
  • associated with root apex of carious or heavy restored teeth with pulpitis or non vital teeth
  • Lamina dura is intact!
  • Periodontal space may be widened!
  • NO radiolucent border (seen in focal or periapical osseous dysplasia)!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give a differential diagnosis for the radiographic findings of condensing osteitis

A
  1. Focal osseous dysplasia:
    - radiopacity with radiolucent rim
    - lower molars
    - middle age african females
  2. Idiopathic osteosclerosis:
    - radiopacity is separated from tooth apex
    - Teeth in area are sound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do we come up with a diagnosis of condensing osteitis?

A

Clinico-radiological features only

Biopsy not included

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of condensing osteitis?

A

Eliminate the odontogenic focus or source of infection. Extract or do root canal. 85% cases regress partially or totally. Lesions may also resolve with normalisation of PDL space.
If radiopacity persists and PDL space stays widen then re-evaluate endo treatment or is a bone scar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain what osteomyelitis is

A

Acute or chronic inflammatory process in medullary spaces or cortical surfaces of bone that extends away from site of involvement.

17
Q

Explain primary osteomyelitis

A
  • Ill defined group of inflammatory bone disorders.
  • Idiopathic
  • No obvious association with bacterial infection. Does not respond to antibacterial medications.
  • suppuration and sequestra formation absent
18
Q

Explain secondary (suppurative) osteomyelitis

A

Expanding lytic destruction of bone with suppuration and sequestra formation. Uncommon in developed countires but usually due to jaw fractures and immunosupression. Strong male predominance! Involves mandible more. In mx in children that arises from NOMA or NUG. Md is poorly vascularised compare to mx

19
Q

What is the aetiology of secondary osteomyelitis? Or what are the predisposing factors of secondary osteomyelitis?

A
  • After odontogenic infection
  • after jaw trauma fractures
  • gunshot wounds
  • spreads from periodonitis
  • spread from NUG
  • spread from NOMA
  • Chronic systemic diseases
  • immunosupression
  • decreased vascularity of bone leads to necrosis and inflammation.
  • radiation
  • osteopetrosis
  • pagets disease
  • end stage cemento-oeeous dysplasia
20
Q

How do we diagnose osteomyelitis?

A
  • Clinical and radiological features

- Bone biopsy for histology

21
Q

Give the pathogenesis of acute suppurative osteomyelitis

A

Acute inflammatory process
Spreads through the medullary spaces.
Mandible is less vascular than the maxilla, making it more prone to osteomyelitis.
The acute inflammatory process present in the medullary spaces leads to extravasation of fluids and proteins with resultant occlusion of the thin walled blood vessels. This leads to further bone necrosis!

22
Q

Give the clinical features of acute suppurative osteomyelitis

A
  • Signs and symptoms of acute inflammation as well as systemic signs of infection
  • Local sign and sympt include swelling due to oedema, pain and redness or draining fistula.
  • swelling fluctuant but reactive bone formation and fibrosis leads to a firm swelling!
  • affected bone becomes necrotic and separated from surrounding vital areas and eventually exfoliate through the overlying mucosa into oral cavity NB1
  • associated teeth may be tender and moobile
  • Paraesthesia of lower lip associated with mandible cases
  • sequestra exfoliation (gets pushed out through the oral mucosa)
  • Sytemically: fever, malaise, lymphadenopathy, leucocytosis
23
Q

Give the radiological features of acute suppurative osteomyelitis

A
  • Early in process no changes visible
  • patchy irregular radiolucencies visible with progression (moth eaten appearance)
  • widen PDL space loss of lamina dura
  • loss of circumscribed IAN canal or mental foramen.
  • sometimes central radiopaque masses representing the necrotic bone (sequestra) may be seen
24
Q

Give the treatment of acute supurrative osteomyelitis

A
  1. Antibiotics: penecillin with metronidazole (good bone penetration) or clindamycin (also good bone penetration)
  2. surgical intervention: resolve source of infection, Drainage, remove infected bone and get samples for culture and antibiotic sensitivity testing. Reconstruction of mandible. If untreated will lea to cellulitis and septicaemia!
25
Explain how we get chronic supurrative osteomyelitis
If acute osteomyelitis is not resolved then chronic osteomyelitis occurs but can also occur without acute phase.
26
Give the clinical picture of chronic suppurative osteomyelitis
- Swelling, pain, sinus formation, purulent discharge, sequestrum formation, tooth loss or pathological fracture. - Defensive response leads to granulation tissue production. - Dense scar tissue forms to wall off infected area.
27
Give the radiological features of chronic suppurative osteomyelitis
Patchy, ragged, ill-defined radiolucency that contains central radiopaque sequestra (mixed radiopaque radiolucent). Involucrum formation may have zones of radiodensity
28
Give the treatment of chronic suppurative osteomyelitis
Difficult to manage medically! Mainly because pockets of dead bone and organisms protected from antibiotic drugs by surrounding wall of fibrous connective tissue. 1. Surgicall intervention is a MUST! Antibiotic meds are similar to those used in acute form but must be given IV in high doses. Goal of surgery is to remove all infected tissues! Surgical intervention: remove all infected bone material down to good bleeding bone. Small lesion: curettage, remove necrotic bone, saucerisation. With extensive Osteomyelitis decortication or saucerisation. Combined with transplantation of cancellous bone chips. 2. persistant OM: due to incomplete removal of diseased tissue, resection the diseased bone and immediate reconstruction.
29
Give a brief description of diffuse sclerosing osteomyelitis
Ill-defined, highly controversial. Not fully known. Postulated that most cases are more likely to represent florid osseous dysplasia with superimposed secondary infection
30
Give the clinical features of diffuse sclerosing osteomyelitis
Diverse disease mostly characterised by intense pain in mandible, inflammation, trismus is often there, paraesthesia, sinus formation with purulent discharge, sequestra formation with tooth loss and eventually progessive mandible deformity. Exclusive to adults, no gender predilection and primarily mandible! Chonric intraosseous bacterial infection that leads to smouldering mass of chronically inflammed granulation tissue that induces sclerosis of surrounding bone.
31
Give the radiological features that will be seen with diffuse sclerosing osteomyelitis
Increased radiodensity around sites of chronic infection: periodontitis, pericornitis, apical inflammatory disease, secondary infected florid osseous dysplasia Progressive bone destruction is characterised by moth eaten mixed radiopaque radiolucent picture. Sometimes sequestra as well as sequestra surrounding vital bone (involucrum) may be present. Eventually diffuse radiopaque masses involving most of the affected quadrant will be seen
32
How do we diagnose Diffuse sclerosing osteomyelitis??
Clinico-radiological features | Bone biopsy done for histology.
33
What is the differential diagnosis of diffuse sclerosing osteomyelitis?
Fibro osseous lesion= have an initial radiolucent phase Florid osseous dysplasia = predilaection for middle aged african females
34
How do we treat diffuse sclerosing osteomyelitis?
Resolve adjacet foci of chronic infection. Sclerosis resolves in some, remains in others. Persistent sclerotic bone: hypovascular, no typical remodel, very sensitive to inflammation. Avoid future problems from periodonitis/apical inflamm disease. avoid tooth extract/surgical intervention in these areas. Also residual sclerotic bone and long term denture wear: sclerotic bone does not resorb like surrounding bone, may get bone expsure and get secondary suppurative osteomyelitis.
35
Give the pathogenesis of proliferative periostitis
A periosteal reaction secondary to chronic irrtation or inflammation of periosteum. Inner layer of periosteum, next the bone surface, consists of bone cells, their precursors and rich vascular suppply. When stimulated by the products of inflammation, reactive bone formation will occur. Several rows of bone formation occurs in the area and get expansion clinically. Bony hard swelling on lateral/lower border mandible most often in 1st molar area. May have mild pain. Occurs in all age groups and no gender predilection. AKA Garre osteomyelitis! but is actually not osteomyelitis.
36
Give the possible causes of periosteal new bone formation
- Dental caries and periapical inflammation - Periodontal infection - osteomyelitis - trauma and fracture - cysts like buccal bifurcaiton cyst - congenital syphilus - vit C def - Neoplasms
37
What radiographical features are seen with proflierative periostitis
- Often in lower molar or premolar areas - hyperplasia along lower border/buccal cortex of md - onion like duplication of cortical plate - radiolucent between separation layers between new bone.
38
How do we diagnose proliferative periostitis?
Clinico radiological!
39
Treatment of proflierative periostitis?
Aim to eliminate source of infection aided by antibiotic therapy