2. Pulpitis
Pulp becomes infected by
Carious exposure,
Leaking restorations ,
Dentinal tubules ,
Fractures or cracks.
Leading to an inflammatory
response(i.e.chemotaxis,enzymatic breakdown with
release of antigens)
3. Antigens in the surrounding tissue.
Leads to an immune response from the tissue-antibodies.
The response destroys much of the peripical
tissue leading to the formation of various types of
apical periodontal lesions.
6. Apical periodontitis
It is the inflammation of the periodontal ligament around the root apex.
The common causes are
Spread of Infection following pulp necrosis
Occlusal Trauma,
Chemical irritation(Overextended R.C.T medicaments)
There are two types-Acute Apical Periodontitis(AAP)
Chronic Apical Periodontitis(CAP)
7. Acute
periodontitis
Previous h/o pulpitis
Thermal changes do
not induce pain
Tooth is elevated
from the socket with
tenderness
Chronic
periodontitis
•AKA periapical granuloma
•Sequale of pulpitis or acute
periapical periodontitis.
•Tooth involved is usually
non-vital & maybe tender
8. Treatment
Acute periodontitis-
If there is occlusal trauma-selective grinding
If pulpally involved-R.C.T/Extraction
Chronic periodontitis(Periapical granuloma)-
Extraction of involved teeth
R.C.T/R.C.T with apisectomy
If left untreated it will transform intoApical periodontal
cyst
9. Apical granuloma
A “granuloma” is, literally, a mass made up of granulation
tissue.
Most common type of pathologic radiolucencies.
It is the result of a successful attempt by the
periapical tissues to neutralize and confine the
irritating toxic products that are escaping from
the root canal.
More inflammation at the center of the lesion
The Periphery of the lesion shows fibrosis (healing)
10. Radiographically-well-circumscribed
radiolucency somewhat rounded and surrounding
the apex of the tooth
It is difficult to differentiate from a radicular cyst
radiographically.Both have large, well defined
radiolucency with radiopaque (sclerotic) border.
11. Apical periodontal cyst(AKA
Radicular cyst,Periapical
cyst,Dental cyst,Root end cyst)
It is usually a sequale of Periapical Granuloma
It is a true cyst,since the lesion consists of a pathological cavity lined by
epithelium and is often fluid filled.
The epithelium is from cell rests of Malassez.
Clinical features:
Usually asymptomatic
Most common in maxillary anteriors.
May undergo acute exacerbation of the inflammatory process and develop rapidly
into an abscess,then cellulitis.
12. Radiographic features:
A thin radiopaque line around the periphery of
radiolucent area seen, indicating a reaction of the
bone to the slowly growing mass
Cannot differentiate between Granuloma and cyst
radiographically.Diagnosis is based on histologic
examination.
Treatment :
Extraction of involved tooth & curettage of socket
Rct with apisectomy
13. Periapical abscess(AKA
Dentoalveolar abscess,Alveolar
abscess)
It is an acute or chronic suppurative processs of the periapical region.
It is a sequalae of A.A.P or a periapical granuloma .
Phoenix abscess is an acute exacerbation of chronic periapical lesion.
Chronic abscess is an asymptomatic,well-circumscribed area of
suppuration that shows little tendency to spread from local area.
Clinical features :
Intially- Tenderness,which is relieved by application of pressure.
Later-Extreme pain & slight extrusion from socket.
Rapid extension to adjacent marrow spaces may occur,resulting in
osteomyelitis.
14. Radiographically:
Ill-defined radiolucent area at the apex of the tooth.
Treatment:
Drainage of abcess:
Opening the pulp chamber
Extraction
If left untreated it can lead to osteomyelitis, cellulitis.
15. Osteomyelitis
Inflammation of bone & its marrow contents.
Though the dividing line between osteomyelitis and an
abscess is unclear,osteomyelitis is usually reserved for
infections that spread through the bone to a larger
extent.
Predisposing factors :
Fracture due to trauma,RTA, radiation damage,
ostopetrosis,gun-shot wounds,Paget’s disease.
Systemic conditions: DM, sickle cell anemia, chronic
alcoholism,malnutrition,acute leukemia.
16. Acute suppurative osteomyelitis
It is a serious sequale of periapical infection resulting in the diffuse spread of infection
throughout the medullary spaces with subsequent necrosis of varible amount of bone.
Common causes:
Dental infection
Abscess(if virulent and not walled off)
Acute exacerbation of a granuloma or cyst
Clinical features:
In the maxilla,tends to be localised to involved tooth but in the mandible it is more
diffuse & widespread.
Pain, trismus, paresthesia of lip, elevation of temp,regional lymphadenopathy,loose and
tender involved teeth
Wbc is elevated, pus from gingival margin.
17. Radiographically:
Changes can be seen after 1-2 weeks.Ill-defined margins
& moth eaten appearance.
Treatment :
Debridement , Drainage & Drugs(antibiotic therapy)
Surgical removal for lesions with large sequestrum.
If left untreated,may proceed to Periostitis,soft-tissue
abscess or cellulitis.
18. Chronic suppuartive osteomyelitis
Clinical features are similar to those of acute osteomyelitis,except that all signs and
symptoms are milder.
Occurs in people with high tissue
reactivity.
Commonly occurs in children &
young adults,in the mandibular
1st molar.
There maybe no clinical
symptoms other than mild pain
associated with an infected pulp.
Path of entry of infection maybe diffuse
periodontal disease.
Commonly occurs in older
people,especially in edentulous
mandibular jaws.
Often there are no clinical
features,sometimes due to acute
exarcebation of chronic infection,there
is vague pain,unpleasant taste,mild
suppuration,fistula formation to
mucosal surface.
Chronic Focal Sclerosing
Osteomyelitis(Condensing osteitis)
Chronic Diffuse Sclerosing
Osteomyelitis
19. Radiographically:
Well circumscribed radio-opaque
mass of sclerotic bone extending
below the root apex of the roots.
Intact lamina dura
P.D.L ligament space widening(to
diff. From benign
cementoblastoma)
Diffuse,patchy,sclerosis of bone,often
described as “cotton-wool” appearance.
Treatment:
Affected tooth is extracted or
treated endodontically.
Sclerotic bone,not attached to
tooth,remains after extraction.
Treatment is difficult.Conservative
approach is most reasonable.
Teeth involved in sclerotic lesion to be
extracted.
20. Chronic Osteomyelitis with
Proliferative Periostitis(Garre’s chronic
non-suppurative sclerosing
osteitis,periostitis ossificans)
Shows focal gross thickening of the periosteum,with
peripheral reactive bone formation due to infection or
irritation.
Clinical features:
Almost exclusive to mandible,in premolar and molar
region,of children and young adults.
Presents as pain in the jaw with a bony hard swelling on the
outer surface of the jaw.
21. Radiographically:
Occlusal radiograph shows focal overgrowth of bone
on the outer surface of the cortex,which maybe
described as duplication of the cortical layer of bone.
Intraoral radiograph will reveal a carious tooth
opposite the hard bony mass.
Treatment:
Extraction or R.C.T of infected tooth.
Biopsy to confirm diagnosis.
24. Non Surgical management of apical
lesions
The aim of non-surgical root canal therapy is
the elimination of infection from the root canal
and the prevention of re-infection by root filling
Periapical lesions develop as sequelae to pulp disease.
They often occur without any episode of acute pain
and are discovered on routine radiographic
examination.
25. All inflammatory periapical lesions should be initially
treated with conservative nonsurgical procedures.
The ultimate goal of endodontic therapy should be to
return the involved teeth to a state of health and
function without surgical intervention.
26. METHODS FOR NONSURGICAL
MANAGMENT OF PERIAPICAL
LESIONS
1. Conservative root canal treatment without
adjunctive therapy
2. Decompression technique
3. Active nonsurgical decompression technique
4. Aspiration and irrigation technique
5. Method using calcium hydroxide
6. Lesion sterilization and repair therapy
7. Apexum procedure
27. Conservative root canal treatment
without adjunctive therapy
Instrumentation should be carried 1 mm beyond the
apical foramen.
Establishes drainage and relieves pressure. Once the
drainage stops,fibroblasts begin to proliferate and
deposit collagen; this compresses the capillary
network, and the epithelial cells are thus starved,
undergo degeneration, and are engulfed by the
macrophages.
28. Causes transitory inflammation and ulceration of the
epithelial lining resulting in resolution of the cyst.
Weekly debridement and drying of the canals over a
period of two to three weeks, followed by obturation
has led to a complete resolution of lesions by 12 to 15
months.
29. Decompression technique
The placement of a drain into the lesion, daily
irrigation using 0.12% chlorhexidine, periodic length
adjustment, and maintenance of the drain, for various
periods of time
Advantages: Simple procedure,minimal damage,easily
tolerated.
Contraindicated: Large dental granulomas or any solid
cellular lesion.
30. Active nonsurgical decompression
technique
This technique uses the Endo-eze vacuum system
(Ultradent,Salt Lake, Utah) to create a negative pressure, which
results in the decompression of large periapical lesions.
The high-volume suction aspirator is connected to a micro 22-
gauge needle, which is inserted in the root canal and activated
for 20 minutes, creating a negative pressure, which results in
aspiration of the exudate.
When the drainage partially stops, the access cavity is closed
with temporary cement,which helps in maintaining bacterial
control.
Advantage: Minimally invasive, as the entire procedure is done
through the root canal and causes less discomfort for the patient
31. Aspiration and irrigation
technique
Aspiration of the cystic fluid from the periapcial lesion
using a bucco-palatal approach. An 18-gauge needle
attached to a 20 ml syringe is used to penetrate the
buccal mucosa and aspirate the cystic fluid.
A second syringe filled with saline is inserted through
the buccal wound and passed out through the palatal
tissue creating a pathway for the escape of the irrigant.
Disadvantage: Buccal and palatal wounds that may cause
discomfort to the patient.
32. Method using calcium hydroxide
Calcium hydroxide has bactericidal effects. It creates
favourable conditions for periapical repair and stimulates
hard tissue formation.
The four- fold effect of Ca(OH)2:
(a) anti-inflammatory activity,
(b) neutralization of acid products,
(c) activation of the alkaline phosphatase, and
(d) antibacterial action
Calcium hydroxide is used as an antibacterial agent for only
15 days, following which it is irrigated out of the canal using
sodium hypochlorite.
33. Lesion sterilization and repair
therapy
The Cariology Research Unit of the Niigata University
School of Dentistry has developed the concept of ‘Lesion
Sterilization and Tissue Repair (LSTR)’ therapy that uses
a triple antibiotic paste of ciprofloxacin, metronidazole,and
minocycline, for disinfection of oral infectious lesions.
Repair of damaged tissues can be expected if lesions are
disinfected.
The combination of drugs has been shown to penetrate
efficiently through dentine from the prepared root canals.
The commercially available drugs are powdered and mixed in a
ratio of 1:3:3 (3 Mix) and mixed either with macrogol-propylene
glycol (3 Mix-MP) or a canal sealer(3 Mix-sealer)
Disadvantage is tooth discoloration induced by minocycline.
34. Apexum procedure
The Apexum procedure uses two sequential rotary
devices, the Apexum NiTi Ablator and Apexum PGA
Ablator (Apexum Ltd, Or Yehuda, Israel), designed to
extend beyond the apex and mince the periapical
tissues on rotation in a lowspeed handpiece, followed
by washing out the minced tissue.
Significantly faster periapical healing is noted with
this technique.
35. Surgical management of apical
lesions
In the following slides I will talk about the principles
of management of apical lesions or odontogenic deep
fascial space infections,as laid down by The late Dr.
Larry Peterson.
36. There are eight sequential steps that are to
be followed with thoroughness and
good judgment to ensure a high level of
care for these occasionally life-threatening
infections.
37. The eight steps in the management of odontogenic
infections are as follows:
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.
38. OR
1.Severity of infection
2.Host defenses
3.Care setting
4.Surgical treatment
5. Medical support
6. Prescribe antibiotics
7.Administer antibiotics properly
8.Evaluate Frequently
39. Step 1:
Determine the Severity of Infection
Three major factors must be considered
in determining the severity of an infection of the head
and neck:
1.Anatomic location
2.Rate of progression
3.Airway compromise.
40. Anatomic Location
The anatomic spaces of the head and neck can be
graded in severity by the level to which they threaten
the airway or vital structures, such as the heart and
mediastinum or the cranial contents.
44. The Danger space
It is found between the buccopharnygeal fascia and alar
fascia,posterior to retropharygeal space,it gets its
common name from the risk that an infection in this
space can spread directly to the thorax, it is sometimes
also referred to as the Alar space.)
45. A severity score (SS) was devised that assigned a
numerical value of 1 to 4 for involvement
of each of the anatomic spaces involved,be it low(1),
moderate(2), severe(3) or extreme severity(4),
respectively.
46. Severity score = 1 (low risk to airway or vital structures)
Vestibular
Subperiosteal
Space of the body of the mandible
Infraorbital
Buccal
Severity score = 2 (moderate risk to airway or vital structures )
Submandibular
Submental
Sublingual
Pterygomandibular
Submasseteric
Superficial temporal
Deep temporal (or infratemporal)
47. Severity score = 3 (high risk to airway or vital structures)
Lateral pharyngeal
Retropharyngeal
Pretracheal
Severity score = 4 (extreme risk to airway or vital
structures)
Danger space
Mediastinum
Intracranial infection
48. Rate of Progression
Characteristi
c
Inoculation Cellulitis Abscess
Duration 0–3 3–7 Over
days days 5 days
Pain Mild–moderate Severe Moderate–severe
and generalized
Size Small Large Small
Localization Diffuse Diffuse Circumscribed
Palpation Soft,doughy Hard, Fluctuant,
49. Necrotising fasciitis
A special note should be made of an especially rapidly
progressive infection called necrotizing fasciitis.
It is a rapidly spreading infection that follows the
platysma muscle down the neck and onto the
anterior chest wall.
50. Airway Compromise
The most frequent cause of death in odontogenic infections
is airway obstruction.
Complete airway obstruction is a surgical emergency.
Insufficient or absent air movement inspite of inspiratory
efforts will be apparent.Check O2 saturaltion levels.
One brief attempt at endotracheal intubation maybe
made,but a direct surgical approach to the airway by
cricothyroidotomy or tracheotomy is more predictably
successful.
Infection in the region of surgical airway access is not a
contraindication to an emergency cricothyroidotomy or
tracheotomy.
51. Step 2: Evaluate Host Defenses
Immune System Compromise:
The medical conditions that can interfere with proper
function of the immune system
Diabetes
Steroid therapy
Organ transplants
Malignancy
Chemotherapy
Chronic renal disease
Malnutrition
Alcoholism
End-stage AIDS
52. Other conditions that impair immune function:
Malnutrition,
Alcoholism,
Chronic renal disease.
53. Systemic Reserve
The host response to severe infection can place a
severe physiologic load on the body.
An elevated temperature at an advanced age is not only
a sign of a particularly severe infection, but also of
decreased cardiovascular and metabolic reserve, due
to the demands placed on the elderly patient’s
physiology by the high grade long standing fever
associated with the infection.
Evaluation of W.B.C count is important in determining
the severity of infection as well as in estimating the
length of hospital stay.
54. The physiologic stress of a serious infection can
disrupt previously well established control of systemic
diseases such as diabetes, hypertension, and renal
disease.
An otherwise mild or moderate infection may be a
significant threat to the patient with systemic disease,
and the surgeon should be careful to evaluate and
manage concurrent systemic diseases in conjunction
with direct management of the infection
55. Step 3: Decide on the
Setting of Care
Admission of a patient to hospital is indicated when:
Temperature > 101°F (38.3°C)
Dehydration -This can be assessed by elevated urine
specific gravity (over 1.030) or an elevated blood urea
nitrogen (BUN).
Infections in deep spaces that have a severity score of 2 or
greater, can hinder access to the airway for intubation by
causing trismus, directly compress the airway by swelling,
or threaten vital structures directly and indicates hospital
admission.
Need for general anesthesia
Need for inpatient control of systemic disease
56. Step 4: Treat Surgically
Secure the airway
Incision and drainage
Straight forward treatments, such as removal of the
involved teeth, intraoral incision and drainage, and
empiric antibiotic therapy, are almost always
successful.
Culture and Sensitivity Testing if economically viable.
57. Step 5: Support Medically
Hydration -Reestablishment of electrolyte balance. A
70 kg patient with a fever of 102.2°F would have a daily
fluid requirement of about 3,100 mL.
Nutrition,
Control of fever-
Initial temperature- Above 39.4’C or 103’F fever,it can
become destructive by increasing metabolic and
cardiovascular demands, beyond physiologic reserve
capacity of the patient.
Administration of acetaminophen or aspirin
58. Step 6: Choose and Prescribe
Antibiotic Therapy
Severity of Infection Antibiotic of Choice
Outpatient Penicillin
Clindamycin
Cephalexin
In case of penicillin allergy:
Clindamycin
Moxifloxacin
Metronidazole alone
Inpatient Clindamycin
Ampicillin + metronidazole
Ampicillin + sulbactam
In case of Penicillin allergy:
Clindamycin
Moxifloxacin
Metronidazole alone
59. Step 7: Administer the
Antibiotic Properly
The tissue-serum level of antibiotics determines their
effectiveness.
Orally administered antibiotics achieve much lower
serum levels at a slower rate than when they are
injected directly into the vascular system
intravenously.
60. Step 8: Evaluate the Patient
Frequently
In outpatient infections that have been treated by tooth
extraction and intraoral incision and drainage, The
most appropriate initial follow-up appointment is
usually at 2 days postoperatively for the following
reasons:
1. Usually the drainage has ceased and the drain can be
discontinued at this time.
2. There is usually a discernible improvement or
deterioration in signs and symptoms.
61. For odontogenic deep fascial space infections that are
serious enough for hospitalization, daily clinical
evaluation and wound care are required for at least two
to three days.
If there are no signs of clinical improvement in these
2-3 days, then it may be necessary to begin an
investigation for possible treatment failure.
One of the best methods of re-evaluation is the
postoperative C.T scan.
62. Severe odontogenic infections can be the most
challenging cases that an oral and maxillofacial
surgeon will be called on to treat.
Often the patient with a severe odontogenic infection
has significant systemic or immune compromise, and
the constant threat of airway obstruction due to
infections in the maxillofacial region raises the risk of
such cases severely
63. The eight steps in the treatment of severe odontogenic
infections, first outlined by Dr. Larry Peterson, remain
the fundamental guiding principles that oral and
maxillofacial surgeons must use in successful
management of these cases.
The surgeon’s mind must always remain open to the
possibility of treatment failure, an error in initial
diagnosis, antibiotic resistance, and previously
undiagnosed medically compromising conditions.
64. References
Nonsurgical management of periapical lesions-
Marina Fernandes, Ida de Ataide,Department of
Conservative Dentistry and Endodontics, Goa Dental
College and Hospital, Bambolim, Goa - 403 601,
IndiaJournal of Conservative Dentistry | Oct-Dec 2010
| Vol 13 | Issue 4
Peterson's Principles of Oral and Maxillofacial Surgery
2nd Ed 2004.