how to manage odontogenic infections

1. Odontogenic infections

2. PERIAPICAL PATHOSIS
• Peri apical pathosis means the lesions of
the periapical part of the periodontal
membrane around the apex of the root of
tooth.
– Periapical Periodontitis -- periodontal
abscess – sub periosteal abscess –
dentoalveolar abscess ( vestibular or
cutaneous – over skin).
– Dental Granuloma.
– Cysts/tumour etc.

3. Odontogenic Infections
Infection related to teeth

4. ETIOLOGY
1. Pulp disease.
2. Periodontal disease.
3. Secondarily infected cysts or odontomes.
4. Remaining root fragment.
5. Residual infection.
6. Pericoronal infection.

5. TYPES
ACUTE
In the acute stage infection may remain intra
bony or spread into soft tissues in
following clinical forms:
1.Abscess.
1.Circumscribed collection of pus in a pathological
tissue space.
2.Thick walled cavity containing pus.
3.staphylococci & anaerobes--- large accumulation
of pus--- pointing & drainage.

6. Abscess

9. 2.Cellulitis.
1.This is spreading infection of loose CT.
2.It is a diffuse, erythematous, mucosal or
cutaneous infection.
3.It is result of streptococci & does not result in large
accumulation of pus.
4.Streptococci produce streptokinase,
hyaluronidase & streptodornase.

11. 3.Fulminating infections.
1.Spread of infection in various primary spaces in
the orofacial region.
2.Here secondary spaces along the pathway of least
resistance are involved.
3.Spread of deep cervical spaces and beyond.

12. Acute Peri Apical Abscess1
• This is due to vascular dilatation, an exudate of
neutrophil leucocytes & oedema in the peri apical
region.
• it is due to persistent irritation from chronic pulp
or acute virulent infection, or less host
resistance.

13. Etiology Acute Peri Apical Abscess
– Infective necrosis of pulp
Caries.
Traumatic exposure.
– Sterile necrosis–
blow on teeth.
• Chemical or thermal

14. CLINICAL FEATURES
Acute Peri Apical Abscess
1- History of previous pulpitis.
2- Carious or heavily filled tooth.
3- tender and felt extruded in socket.
4- When pus has formed severe throbbing
pain
5- sensitive to percussion.
6- Over lying gum may or may not be swollen
7- Mobility may or may not be present

15. TREATMENT
Acute Peri Apical Abscess
– Antibiotics ,Analgesics & Drainage through
pulp chamber.
– Extraction or endodontic treatment.

16. Acute Dento Alveolar Abscess
.
When pus does not remain confined to the peri
apical region.
– It perforates the cortex and comes to lie under
periosteum--- SUB PERIOSTEAL ABSCESS.
– The perforating abscess come into the soft tissues
then called as ACUTE DENTOALVEOLAR ABSCESS

17. CLINICAL FEATURES
Acute Dento Alveolar Abscess
• Pain– depend on the stage of disease.
• Sub mucosal swelling in the sulcus or palate.
• Fluctuation may come after few days.
• If untreated may point or burst producing a
discharging
sinus.

19. Radiographic features
Acute Dento Alveolar Abscess
• Little informative in acute phase except
little widening of periodontal ligament.
• But previous pathology if present will be
seen.

21. Treatment
acute dento alveolar abscess
• Same i.e. endo- or ext-.
• Intra or extra oral drainage

22. CHRONIC PERI APICAL
PERIODONTITIS1
• When the irritation in the peri apical
tissues persists either due to,
– incomplete resolution
– treatment of acute periodontitis or pulpitis
leading to necrotic pulp
– a forgotten blow or massive fillings or
unsuccessful R.C.T lead to chronic
periodontitis.
• This goes on painlessly and chronic

25. Skin Sinus Due Chronic infection
from deciduous molar

26. FACIAL SPACE INFECTION
• Fascia–lined areas-- potential spaces that
do not exist in healthy persons.
• Filled by pus or exudation during infection.
• Neurovascular structure - compartments.
• Loose areolar CT------ Clefts

27. Primary facial spaces
• Primary spaces are adjacent to tooth bearing
area & are directly involved by infection.
• Primary maxillary spaces.
• Canine
• Buccal
• Infratemporal.
• Primary mandibular spaces.
• Submental.
• Buccal.
• Submandibular.
• Sublingual.

31. Secondary spaces
MASTICATORY SPACES
– Masseteric.
– Pterygomandibular.
– Superficial & deep temporal.
CERVICAL SPACES
– Lateral pharyngeal
– Retropharyngeal
– Prevertebral

32. Lethal complications
Orbital & periorbital cellulitis.
Cavernous sinus thrombosis
Ludwig’s angina
Cervical cellulitis ( Lung Abscess &
Mediastinitis)

33. LUDWIG’ S ANGINA

35. Cavernous Sinus Thrombosis

38. Orbital & periorbital cellulitis

40. Cervical Cellulitis

44. PRINCIPLES OF
MANGEMENT OF
ODONTOGENIC
INFECTIONS

45. 1. Determine the severity of infection.
2. Evaluate host defenses.
3. Decide on the setting of care.
4. Treat surgically.
5. Support medically.
6. Choose and prescribe antibiotic therapy.
7. Administer the antibiotic properly.
8. Evaluate the patient frequently.

46. For appropriate treatment of
odontogenic infection
• Microbiology odontogenic infection
– Poly microbial nature
– Oxygen tolerance microbes
• Natural history of odontogenic infection
– Pathway of infection
• Low grade well localized
• Deep facial life threatening

47. Microbiology of odontogenic
infections
microorganism species
Aerobic (6%) S. Milleri – viridan gp
S.Angionosus,
intermedius and
constellatus
Misc.
Gram + Cocci
Anaerobic(50%) Anaerobic streptococcus
Peptostreptococcus
Prevotella
Porphyomonas
Fusobacterium
Gram +ve Cocci
Gram –ve rods
Mixed (44%)

48. Stages of infection
Inoculation stage
(Edema) 0-3 days
Facultative aerobes Hyaluronidase – spread
through connective
tissue- initiating cellulitis
stage
Cellulitis stage 1-5 days Mixed but Anaerobic
bacterias start
predominating
Inflammatory response
(Exudate)
Abscess stage 4-10 days Anaerobic bacterias
Resolution stage Natural / I&D

49. Natural history of odontogenic
infection
• Pulp/periodontal – periapical infection –
erosion of bone-soft tissues – vestibular-
facial spaces

51. Stages of infection

52. I. SEVERITY OF INFECTION
Three major factors must be considered in
determining the severity of an infection of
the head and neck:
• Anatomic Location
• Rate of progression
• Airway compromise.

53. I. SEVERITY OF INFECTION
(cont.)
1. Complete history:
1. CC
2. Onset
3. Duration
4. Rapidity of progress
5. Self medication ( if any)
6. General out look

54. 2. Physical examination:
1. Vital signs
1. temperature
2. Pulse rate
3. BP
4. RR
2. Swelling ( By palpation)
1. Doughy to indurated
2. Fluctuant
3. Extra oral Exam (Esp. Neck)
4. Intra oral Exam ( source of infection)
5. Distinction b/w abscess & cellulites

55. II. Evaluate state of Pt’s Host
Defense Mechanisms
• Diabetes
• Steroid therapy
• Organ transplant
• Malignancy
• Chemotherapy
• Chronic Renal Disease
• Malnutrition
• Alcoholism
• End-stage

56. III. Hospitalization
• Rapidly progressing Infection
• Difficulty in breathing
• Difficulty in swallowing
• Severe trismus
• Buccal & submandibular space infection

57. IV. Antibacterial therapy
• Need for antibiotic administration
– Seriousness of Infection
– Adequate I & D can be achieved
– State of pt’s host defenses
• Routine empirical therapy
– Known microbes

58. • Routine C & S testing
– Rapid onset & spread
– Infection not resolving
– Recurrent Infection
– Compromised host defenses
• Narrowest spectrum antibiotics
• Antibiotics with low toxicity
• Bactericidal antibiotics ( if possible)

59. V. Administration of antibiotics
• Proper dose & proper interval
• Peak plasma level 4-5 times MIC for
bacteria
• The interval 5 times the plasma half life of
drug
• Out pts course 6-7 days
• In pts potential administration

60. VII. Medical support
• Stress due pain & swelling – reduce host
defense
• Control of pain
• Control dehydration

61. VI. Surgical treatment
• Primary goal removal of the cause
• I & D for abscess plus C & S testing
• I & D for Cellulitis (Initial & Late)
• I & D for Complex infection ( Secondary &
Cervical spaces)

72. VIII. Post treatment evaluation
• Monitor
– Drain in place
– Medications
– Relief of signs & symptoms
• No response
– Inadequate surgery
– Depressed host defense
– Antibiotic problems – non compliance, low dose,
wrong bacterial diagnosis & wrong antibiotic
– Drug not reaching the site