BOARD REVIEW
ENDODONTICS
I. Diagnostic Procedures
-75% of patients requesting emergency treatment for relief of pain have pulpal or periapical disease, and, thus, are candidates for endodontic therapy.
-50% of these are vital pulps; 25% are necrotic pulps.
-Patient cannot always localize the painful tooth. With an increase in severity and duration of pain, the patient loses the ability to locate the painful tooth.
-Anterior teeth practically never refer pain to the opposite jaw.
-Posterior teeth can refer pain to the opposite jaw on the same side (upper to lower or lower to upper).
-Posterior mandibular teeth can refer pain to the ipsilateral ear.
-No referral of pain across the midline.
-Anterior teeth seldom refer pain to posterior teeth and posterior teeth seldom refer pain to anterior teeth.
-So, pain in anterior is from anterior teeth, pain in posterior is from posterior teeth, posterior teeth can refer pain from maxilla to mandible or mand to max, ant teeth do not refer pain from max to mand or from mand to max, and pain is not referred across the midline.
-Pain should describe pain as sharp, dull, or throbbing (dull and throbbing are pulpal signs)
-Lingering pain will signify an irreversible pulpitis.
-The following correlate well with a diagnosis of irreversible pulpitis:
1. previous hx of pain
2. spontaneous pain
3. lingering pain
-The electric pulp tester and thermal tests only test the nerve function of a tooth. They do not indicate the actual vitality of the tooth. The thermal tests are more valuable in differentiating b/w reversible and irreversible pulpitis.
-Hot thermal pulp tests:
1. burlew wheel (can raise the internal temp of tooth 20º in 20sec.
2. “hot” gutta percha
3. “hot” ball burnisher
-Cold thermal pulp tests:
1. ice stick (32º F): not reliable on teeth with full coverage
2. dichlorodi(tetra)fluoroethane: (-14ºF): Endo ice
3. carbon dioxide snow (119º): Dry ice
4. hot or cold liquids: isolate tooth with rubber dam and can use ice water, hot water, or coffee. The temp of the water or coffee cannot be greater than 140ºF.
-Test cavity: only use when all other diagnostic tests have yielded equivocal results.
-Transillumination, magnification & illumination, and staining: identify fractures (also percussion, and wedging (tooth slooth)).
-Maxillary sinusitis: percussion sensitivity over the max sinus, pain bending over, running, or going downstairs. Topical anesthetic on a cotton roll inserted into the patient’s nostril on the effected side may confirm a diagnosis of max sinusitis.
-Radiographic diagnosis: The state of health of pulp tissue, even if it’s necrotic, cannot be determined radiographically.
II. Final diagnosis
A. Pulpal diagnosis
1. Reversible:
a. localized inflammation
b. localized increase in intrapulpal pressure
c. threshold stimulation for A-delta nerve fibers is lowered
d. exaggerated, non-lingering response to stimuli
e. pulp tissue is able to accommodate increased pressure and repair the damage
f. (+) EPT, (+) cold (non-lingering), (+) hot (non-lingering), perc & palp (-)
g. txmnt: remove caries, perm restoration (if recent restoration, check occlusion)
2. Irreversible
a. localized area of necrosis that cannot be repaired or walled off
b. spreads throughout the pulp causing inflammation in adjacent areas
c. usually have pre-existing chronic pulpitis which has decreases the ability of the pulp to respond favorably
d. the presence of inflammatory mediators lowers the threshold of stimulation for all intrapulpal nerves
e. PMNs are involved and they cause exacerbation of the inflammation
f. Pain lingers after thermal stimulation of A-delta nerve fibers spontaneous dull, aching pain caused by stimulation of unmyelinated C-fibers in the pulp proper
g. Mediators of inflammation (bradykinin) directly stimulate the fibers
h. (+) EPT, (+) cold (lingering), (+) hot (lingering), maybe perc and palp sensitive
i. txmnt: pulpotomy (must obtain hemorrhage control) or total pulpectomy
3. Total necrosis
a. if caused by inflammation that started in the pulp (caries for ex), it most probably will spread to the periradicular tissues
b. if caused by trauma that severs the blood supply to the tooth, a dry necrosis may result that may not spread to the periradicular tissues
B. Periradicular diagnosis
1. Acute periradicular periodontitis
a. inflammation of PDL caused by tissue damage; extension of pulpal pathosis or occlusal trauma
b. pressure on tooth (occlusion/percussion) is transmitted to the fluid which pushes on nerve endings in the PDL
c. tooth may be elevated out of its socket because of the buildup in fluid pressure in the PDL
d. usually don’t see radiographic changes b/c it happens so quickly
e. pain will remain until bone is resorbed, the fluid is drained, or the irritants are removed
f. pulp tests are essential and results must be correlated with other diagnostic information in order to determine if inflammation is of pulpal origin or from occl trauma
g. (+/-) EPT, (+-) cold, (+/-) hot, (+) perc, maybe (+) palp
h. may see a widened PDL on radiograph
i. txmnt: total pulpectomy & occl adjustment
2. Acute periradicular abscess
a. large numbers of bacteria get past the apex into the periradicular tissues
b. implies a breakdown of the immune system because the body should have been able to contain the microbes inside the root canal system
c. acute inflammatory response; PMNs are the dominant cells
d. results in local collection of purulent exudate
e. may not have radiographic evidence of bone destruction b/c fluids are rapidly spread away from the tooth
f. clinically, swelling to various degrees is present along with pain and a feeling that the tooth is elevated in the socket
g. systemic symptoms (fever, malaise) can also be present
h. the infection may spread along facial planes to form a cellulitis
i. (-) EPT, (-) cold, (-) hot, (+) perc, (+) palp
j. may/may not see changes on radiograph with respect to PDL
k. txmnt: pulpectomy, drainage, and appropriate analgesics & antibiotics if necessary
3. Chronic periradicular periodontitis (asymptomatic)
a. periradicular granuloma
-relatively low grade, long standing lesion formed to neutralize irritants from the canal system and wall them off from the rest of the body
-the soft tissue lesion will keep expanding at the expense of the surrounding bone as long as the irritants keep emanating form the root canal system
-microscopically composed of lymphocytes, plasma cells, and macrophages surrounded by an un-inflamed fibrous capsule made up of collagen, fibroblasts, and capillary buds
-clinically, the lesion is asymptomatic and is detected radiographically by a periradicular radiolucency
-(-) EPT, (-) cold, (-) hot, (+/-) perc, (+/-) palp
-see periradicular RL on radiograph
-txmnt: can appt. for NSRCT since it’s asymptomatic
b. periradicular cyst
-if the inflammation stimulates the epithelial rests of Malassez to begin dividing, a cyst may develop within the granuloma
-“bay cyst”: lumen communicates with the apical foramen that may heal with NSRCT
-“true cyst”: lumen doesn’t communicate with the apical foramen and requires surgical root canal txmnt
4. Chronic suppurative periodontitis
a. an apical lesion that has established drainage by breaking through the cortical plate of bone and the overlying periodontal tissues
b. clinically, a sinus tract is present
c. the patient is usually asymptomatic
d. (-) EPT, (-) cold, (-) hot, (+/-) perc, (+/-) palp
e. radiographically, see a periradicular RL and a sinus tract
f. txmnt: appt for NSRCT or OHI
5. Phoenix abscess (recurrent chronic periradicular periodontitis)
a. an acute periradicular abscess superimposed on a pre-existing chronic periradicular periodontitis
b. an acute exacerbation of a previously existing chronic lesion
c. like a periradicular abscess, except you have a radiolucency associated with the tooth
d. the patient experiences the same symptoms as periradicular abscess
e. (-) EPT, (-) cold, (-) hot, (+) perc, (+) palp
f. see periapical RL on radiograph
g. txmnt: total pulpectomy, drainage, appropriate analgesics & antibiotics
6. Chronic periradicular periodontitis with symptoms
a. a periradicular granuloma or cyst that is showing signs of becoming acute
b. pain to occlusion, palpation, or percussion
c. histologically, the tissue would show an increased # of PMNs
d. (-) EPT, (-) cold, (-) hot, (+/-) perc, (+/-) palp
e. txmnt: total pulpectomy
7. Focal sclerosing osteomyelitis (condensing osteitis)
a. a very low grade pulpal inflammation which results in an increase in the bone density rather than resorption
b. clinically, the patient is usually asymptomatic
c. see increased bone density on radiograph
d. RCT is not indicated unless there is other evidence of pulpal inflammation
e. Radiopacity may persist after RCT and extraction of the tooth
f. (+/-) EPT, (+/-) cold, (+/-) hot, may have perc & palp sensitivity
g. txmnt: appt. for NSRCT
III. Emergencies during endodontic treatment
A. After initiation of endodontic therapy
1. Before obturation: a flare up
Etiology:
a. over-instrumentation
b. inadequate debridement
c. missed canal
d. hyperocclusion
e. debris extrusion
f. procedural complications
2. After obturation
Etiology:
a. debris extrusion
b. over-instrumentation
c. over-filling
d. under-filling
e. missed canal
B. Analgesics
1. Mild pain
-OTC meds: ASA 325mg, Motrin 200mg, or Tylenol 650-1000mg
2. Moderate pain
-NSAID: max effective dose: Motrin 400, 600, or 800mg
-if NSAID is contraindicated, use Tylenol 1000mg
-Narcotic: Tylenol #3 (60mg codeine)
3. Severe pain
-NSAID combined with a narcotic or Tylenol with a narcotic
C. Antibiotics
1. Indicated when the patient presents systemic signs of infection (fever, increased respiration or lymphadenopathy. Also indicated when the patient is immunocompromised.
2. Indications: systemic involvement, compromised host resistance, fascial space involvement, or inadequate surgical drainage.
3. Penicillin is antibiotic of choice (inhibits cell wall synthesis)
4. Clindamycin (PCN allergy) inhibits protein synthesis
5. Metronidazole (Flagyl) is bactericidal and degrades DNA in organism
IV. Management of Traumatic Injuries to the Dentition
-Most dental injuries occur from falling while playing or running (16-25%).
-The central incisors are the most common teeth involved in traumatic injuries (80%).
-Boys tend to injure their teeth more often than girls (1.5:1 to 3:1).
A. Definitions
1. Apexification: a method of inducing the formation of a calcified barrier or continued apical development of an incompletely formed root in which the pulp is necrotic.
2. Apexogenesis: physiological development and formation of the root-end. This term is frequently used to describe vital pulp therapy performed to permit the continuation of this process.
3. Avulsion (exarticulation): the complete separation of a tooth from its alveolus by traumatic injury. Ellis class VI.
4. Calcific metamorphosis: a pulpal response to trauma characterized by rapid deposition of hard tissue within the canal space.
5. Calcium hydroxide (CaOH): an odorless white powder frequently used as an intracanal medicament in non-surgical endodontic procedures and also secondary to traumatic injuries. This appears to encourage calcification and can be used in pulp capping, pulpotomy, apexogenesis, and apexification procedures in the permanent dentition. CaOH also appears to inhibit inflammatory and resorptive responses and demonstrate antimicrobial activity.
6. Extrusion: movement of a tooth in an incisal or occlusal direction. This can be intentional, physiologic, or traumatic.
7. Fractures: the following are classified according to the WHO classifications:
a. Enamel fracture: involves enamel only (enamel chipping and incomplete fractures (cracks)). Ellis class I.
b. Crown fracture w/out pulp involvement: an uncomplicated fracture involving enamel and dentin only. Ellis class II.
c. Crown fracture with pulp involvement: a complicated fracture involving enamel, dentin, and exposure of the pulp. Ellis Class III.
d. Root fracture: limited to fracture involving roots only (cementum, dentin, and pulp). Could be horizontal which shows bleeding from the sulcus. Ellis class IV.
e. Crown-root fracture: included uncomplicated and complicated types, the former w/out and the latter w/ pulp exposure. In both cases, enamel, dentin, and cementum are involved.
8. Infraction: an incomplete crack of enamel w/out the loss of tooth structure.
9. Luxation: the dislocation of a tooth from its alveolus resulting from acute trauma. Ellis class V. Types of luxation:
a. Extrusive luxation: a partial displacement of the tooth out of its socket (partial avulsion).
b. Intrusive luxation: an axial displacement of the tooth into the alveolus accompanied by fracture of the alveolar socket.
c. Lateral luxation: a displacement of the tooth in a direction other than axially, accompanied by fracture of the alveolar socket.
d. Subluxation: injury to supporting tissues resulting in abnormal loosening of a tooth or teeth w/out displacement.
e. Concussion: an injury to the tooth supporting structures w/out abnormal loosening or displacement of the tooth.
10. Resorption: a condition associated with either a physiologic or a pathologic process resulting in a loss of dentin, cementum, or bone. Types of resorption:
a. External: resorption initiated in the periodontium and initially affecting the external surfaces of a tooth. This may be further classified as surface, inflammatory, or replacement. It can also be classified by location (cervical, lateral, or apical). It may/may not invade the pulp.
b. Inflammatory: a pathologic loss of cementum, dentin, and bone resulting in a defect in the root and adjacent bony tissue.
c. Internal: a pathologic resorption initiated in the root canal.
d. Replacement (ankylosis): loss of cementum, dentin, and periodontal ligament with the ingrowth and fusion of bone to the root defect.
e. Surface: a physiologic process causing small superficial defects in the cementum and underlying dentin that undergo repair by deposition of new cementum.
B. Intraoral exam
1. Soft tissue exam: check for lacerations, palpate intraoral bony contours, palpate soft tissues for imbedded foreign objects, and check for swelling.
2. Hard tissue exam: check each tooth for alignment, mobility, and fracture. Check for abnormal occlusion, gingival hemorrhage from the sulcus, and the alveolus. Percuss each tooth.
3. Pulp vitality testing:
-**thermal and electric pulp tests may be unreliable for 6-12 months, but it’s important to obtain baseline readings.
-Previous negative responses can turn positive and previous positive responses can turn negative.
-Immediately after trauma, more than 50% of teeth with luxation injuries do not respond to the EPT.
-Repeat vitality testing at close intervals for at least one year after the injury.
-Traumatized teeth, in the absence of radiolucencies and sinus tracts, should be considered to have vital pulps---even if they test non-vital.
C. Radiographic exam
1. Examine the x-ray for luxation injuries, horizontal root fractures, periradicular radiolucencies, the stage of root development, and evidence of root resorption.
2. Occlusal films, a pano, and periapical films a 0, +15, and –15 degrees from the vertical axis of the tooth will help in the diagnosis and location of horizontal root fractures. Use the bisecting angle technique for these films.
3. Radiographs of soft tissue can aid in locating foreign bodies in soft tissue.
D. Post-traumatic complications
1. Discoloration: may/may not be indicative of pulpal necrosis. Pulpal hemorrhage is extravasated red blood cells and hemolysis.
2. Pulpal necrosis:
a. Type of injury:
-intrusion: 96%
-extrusion: 64-98%
-subluxation: 26%
b. Root development
-incomplete: 17%
-complete: 68%
3. Calcific metamorphosis: common causes:
a. Luxation injuries: 20-25%
b. Root fractures: 69-86%
c. More common with an open apex.
d. Less than 10% become necrotic.
e. Prophylactic endo is not indicated
E. Treatment of fractures to hard dental tissues
1. Crown infraction
a. baseline vitality tests
b. radiographs
c. recall: 1,3,6, & 12 mos
2. Crown fracture (enamel only)
a. baseline vitality tests
b. remove sharp edges
c. restore w/ acid etch composite
3. Uncomplicated crown fracture (exposure of dentinal tubules, no pulpal exposure)
a. baseline vitality tests & radiographs
b. cover exposed dentin with CaOH
c. acid etch composite or amalgam restoration
4. Complicated crown fracture
a. txmnt depends on several factors:
-open vs closed apex
-time since injury
-size of pulp exposure
b. If pulp exposure and open apex, do apexogenesis if still vital.
c. If exposure is small, can place a pulp cap with CaOH w/in 3-4 hrs after injury
d. If exposure is large and tooth is vital, can do a Cvek pulpotomy. Here, remove 2mm of coronal pulp tissue with a high speed diamond bur, cover with CaOH, then with glass ionomer, and an acid etch composite. Restore with minimal trauma to tooth. The pulpotomy is done to maintain the vitality and allow the root to completely form. After root completion, perform root canal filling, if needed.
e. If the exposure is large and the tooth is not vital, perform apexification procedure to induce apical closure. After apical closure, fill the canal with gutta percha.
f. Recall 6, 12, & 24 mos. If pulp becomes necrotic during this time, a pulpectomy and apexification will be required. Perform NSRCT if pulp becomes necrotic and apex is closed.
5. Uncomplicated crown-root fractures (not involving pulp)
a. baseline vitality tests and radiographs
b. pulpal protection
c. CaOH or GI to seal dentinal tubules
d. Apply final restoration
6. Complicated crown-root fractures (involve the pulp)
a. txmnt depends on a variety of factors:
-open vs closed apex
-level of fracture
b. Txmnt modalities may vary from extraction of one or both segments, apexogenesis, apexification, ortho extrusion, crown lengthening surgery, RCT with gutta percha obturation, and appropriate restorative materials.
7. Horizontal root fractures
a. 20-40% undergo pulpal necrosis
b. Clinical exam: tenderness to percussion, bleeding from gingival sulcus, mobility or displacement of the coronal segment. Some will not respond to vitality testing.
c. Radiographic exam: the fracture line may/may not be present at the initial exam, but may be apparent on follow-up radiographs.
d. The radiographic exam should include an occlusal film and 3 PAs (0, +15 and –15 degrees) from the vertical axis of the tooth.
e. Occlusal films are best for diagnosing fractures in the apical 1/3 and PAs using the bisecting angle technique are best for detecting cervical 1/3 fractures.
f. Txmnt:
-immobilize with rigid splint for 6-12 weeks
-monitor for changes in pulp vitality (EPT, tooth color, symptoms, periradicular radiolucencies)
-if pulp remains vital, no further txmnt will be required
F. Treatment of concussion and luxation injuries
1. Concussion
a. baseline vitality tests and radiographs
b. relieve the occlusion
c. recall 1,3,6, & 12 mos
2. Subluxation
a. baseline vitality tests and radiographs
b. relieve occlusion
c. stabilization, if needed, for 7-14 days with physiologic splint (flexible ortho wire or nylon fishing line)
d. recall 1,3,6, & 12 mos
3. Intrusive luxation
a. txmnt:
-spontaneous eruption (if very immature apex, allow tooth to re-erupt and observe for replacement resorption)
-surgical reposition and splint with physiologic splint for 6 weeks
-perform RCT w/in 14-21 days with CaOH for one yr
-after 1mo, fill w/ gutta percha
4. Extrusive luxation
a. txmnt:
-radiographs
-reposition tooth
-physiologic splint for 7-14 days
-if apex is immature, observe for revascularization of the pulp
-root canal txmnt
5. Lateral luxation
a. txmnt:
-reposition tooth
-stabilization with physiologic splint for 7-14 days
-perform RCT if displacement is more than 5mm
G. Treatment of avulsion (exarticulation) injuries
-these are 1-16 % of traumatic injuries to the permanent dentition
-7-13% of traumatic injuries to the deciduous dentition
-7-11 yrs of age is the most common age group
1. Healing responses:
a. normal PDL and cementum repair
b. surface resorption
c. inflammatory resorption
d. replacement resorption (ankylosis)
-see lack of PDL space
-a moth-eaten appearance of the root
-may hear a metallic percussion sound
2. Txmnt:
a. depends on the health of the PDL cells on the root surface of the avulsed tooth.
b. The #1 priority is to protect the viability of the PDL
c. The treatment is based on the 1995 Guidelines of the AAE
-re-plant immediately, if possible
-if contaminated, rinse with water b/f replanting
-if immediate replantation is not possible, place tooth in the best transport medium available.
-best transplant medium is Hank’s Balanced Salt Solution (HBSS)---others are milk, saline, or saliva (if none available, use water)
-the storage medium is more important than the extraoral time. Short periods of dry storage result in resorption.
-Milk is superior to saliva for storage of the avulsed tooth
d. Management in the dental office:
-Replant as soon as possible if extraoral time is less than 1hr.
-Keep PDL on the tooth moist.
-If the tooth has been in any physiologic storage media (HBSS, milk, or saline), replant immediately.
-DO NOT HANDLE THE ROOT SURFACE.
-Rinse any debris off the root surface with HBSS or saline.
-The presence of an intact and viable PDL on the root surface is the most important factor in assessing healing w/out root resorption.
-Management of the socket: DO NOT CURETTE OR VENT THE SOCKET. If a clot is present, aspirate gently w/out entering the socket and irrigate with saline. After replantation, gently compress the bony plates together.
-Management of the soft tissue: suture if any laceration are present
-Stabilization: splinting is indicated in most cases. Place a physiologic splint for 7-10 days (longer if there is excessive mobility after this time period). Do not do rigid fixation b/c this will cause replacement resorption (ankylosis)
e. Endodontic txmnt:
-tooth with open apex and less than 1hr extraoral dry time:
-replant in an attempt to revitalize the pulp
-recall q3-4 wks for evidence of pathosis
-if path noted, clean and fill canal with CaOH
(apexification)
-tooth with open apex and greater than 1hr extraoral time:
-replant after soak in SnF2 for 5-20min
-clean and fill canal with CaOH
-recall q6-8 wks
-tooth with closed apex and less than 1hr extraoral time:
-remove pulp in 7-14 days
-medicate canal with CaOH for 6-12 mos
-obturate canal after this time
-tooth with closed apex and greater than 1hr extraoral time:
-perform RCT either intraorally or extraorally
-prior to replantation, remove tissue tags from the root surface and soak the tooth in an accepted Fl solution
V. Root canal morphology and access preparation
A. Weine’s classification system
1. Type I: one canal leaving the pulp chamber and one canal exiting apex
2. Type II: two canals leaving the pulp chamber and one canal exiting apex.
3. Type III: two canals leaving the pulp chamber and two canals exiting apex.
4. Type IV: one canal leaving pulp chamber and two canals exiting apex (most common in mand 1st premolars).
B. Anatomy for specific teeth
1. Max central: 100% Type I.
2. Max lateral: mostly Type I.
a. 53% of roots curve distal, 33% are straight
3. Max canine: virtually 100% Type I.
4. Max 1st premolar:
a. one canal : 9%
b. two canals: 85%
c. three canals: 6%
5. Max 2nd premolar:
a. one canal: 48%
b. two canals: 24%
c. three canals: 1%
6. Max 1st molar:
a. 40-70% have 4 canals
b. 50% have 2 canals in MB root (MB1 & MB2) (usually Type II)
7. Max 2nd molar:
a. 30-40% have 2 canals in MB root (usually Type III)
8. Mand incisors: 40% have 2 canals (usually Type II)
9. Mand canine: only 20% have 2 canals
10. Mand 1st premolar:
a. one canal: 75%
b. two canals: 24%
c. three canals: 1%
11. Mand 2nd premolar:
a. one canal: 98%
b. two canals: 2%
b. two canals: 2%
12. Mand 1st molar:
a. two canals: 5%
b. three canals: 65%
c. four canals: 30%
d. Type III in mesial: 60%
e. Type II in mesial: 40%
13. Mand 2nd molar:
a. one canal: 1%
b. “C”-shaped: 4%
c. two canals: 5%
d. three canals: 80%
e. 4 canals: 10%
f. Type III in mesial: 40%
g. Type II in mesial: 60%
h. Type I in distal: 85%
C. Root canal instrumentation (cleaning and shaping)
-Flexibility is lost in files at size 30.
-Irrigation to the apex is achieved only after a size 35 file.
-Flare so a spreader can get to within 1 to 1.5mm of W.L.
1. Circumferential filing (serial filing) with step-back:
-File at W.L. up to 3 sizes greater than the first one to bind.
-Prepare coronal 1/3 with gates-gliddens
-Step-back with recapitulation to prepare mid 1/3
2. Balanced force technique:
-Insert file to W.L. using clockwise rotation passively.
-Apical pressure and counter clockwise rotation once at the W.L. point (moved 120º in a counter clockwise motion---this is where the cutting is done)
-This uses flexible triangular files.
-It also uses a “safe-tip” rather than a pyramid.
3. Crown down pressureless technique:
-Prepare coronal 1/3 with large files and irrigation.
-Use gates-gliddens to flare (#s2 & 3).
-Start larger instrument (#40) and work toward apex.
-The last 3mm is prepared with a #25 file.
D. Sonics & Ultrasonics
-Some show greater cutting efficiency.
-Some show decreased post-op pain.
-Experience superior debridement in canal irregularities.
-Increased antimicrobial effect.
-Increased disinfection due to heat, good aid for removing foreign objects or silver points.
-Ultrasonic instruments: vibration above audible range: greater than 20,000Hz (25–40 KHz). Powered by an electrical current through plates.
-Sonic instruments: vibration in audible range---less than 20,000Hz (1-8KHz). Powered by compressed air through a rotor shaft.
-These produce acoustic streaming: like scrubbing bubbles that create a flow to remove debris from the walls.
E. Files
1. Files:
-square
-method: twist
-flutes: 1-2mm
-technique: back and forth
2. Reamers:
-triangular
-method: twist
-flutes: 0.25mm
-technique: twist
-reamers have fewer flutes than files do (1/2 to 1 fewer per mm).
-useful to remove gutta percha with chloroform.
3. Hedstrom:
-round
-method: machined (milled)
4. Flex-R:
-rhomboid
-method: twist
-technique: balanced force
5. K-flex:
-diamond
-method: twist
6. Broaches:
-smooth barbed notched steel; removes soft tissue only!
F. File dimensions
1. D0: an imaginary plane that does not exist on the file.
2. D1: file size at the tip of the file (ex: .08mm for a size 8 file).
3. The length of the part of the file with the cutting flutes is always the same (16mm). The flare of the blade is also always the same regardless of the size of the instrument.
4. The diameter of the file where the cutting flutes end (16mm) is known as D2 or D16 and it is the diameter at the tip plus .32mm (ex: for a #8 file it’s .08 + .32 = .40). This means that the taper of the instruments is 0.02mm per mm.
G. Irrigants
1. Sodium hypochlorite (NaOCL):
-dissolves vital, necrotic, and fixed tissues.
-has a long shelf-life.
-it’s highly antimicrobial.
-it’s a lubricant.
-avoid in a open apex, as it is irritating to periradicular tissues.
2. EDTA (ethylene diamine tetra-acetic acid):
-a calcium chelating agent (replaces Ca with Na).
-it chelates dentin, making it more soluble.
-it removes the smear layer opening dentinal tubules.
3. RC-Prep (15% EDTA, 10% urea peroxide, carbowax, and a water soluble base:
-the urea peroxide serves as both a chelating agent & for irrigation.
-this must be de-activated or it can cause periradicular bone loss.
-it can also remain in the tubules if not washed out.
4. Saline:
-this has no bactericidal properties.
-it will not dissolve necrotic material, but is the kindest to tissues.
5. Others:
-Glyoxide
-Hydrogen Peroxide
VI. Obturation of the Root Canal System
A. Reasons to obturate
1. prevent re-infection.
2. create a favorable biologic environment.
3. seal within the system any irritants that cannot be fully removed during canal cleaning and shaping procedures.
4. prevent material leakage from the canal into the periradicular region.
B. Indications for obturation
1. Patient is asymptomatic.
2. The temporary filling is intact.
3. The canal is dry or can be easily dried.
4. The canal is properly prepared.
C. Indications for one-visit endodontics
1. Teeth with vital pulps.
2. Teeth with associated sinus tracts.
3. Teeth with necrotic pulps that are asymptomatic.
4. The canal can be easily dried.
D. Contraindications for one-visit endodontics
1. Teeth with necrotic pulps that are symptomatic.
2. Teeth with associated periradicular swellings.
3. Re-treatment of teeth with previous silver cone fills.
4. The canal cannot be dried.
E. Filling materials
-Can be pastes (ZoE) or solids (G.P.).
-Pastes can be used if it’s a pedo case or if patient has a latex allergy due to the rubber in the gutta percha. MTA can also be used in this situation.
1. Gutta percha:
a. trans-polyisoprene
-alpha trans-polyisoprene: naturally occurring gutta-percha; brittle.
-beta trans-polyisoprene: commercially available gutta-percha. This is what we use to obturate the canal system.
-can convert alpha form to beta form by warming G.P. and then immediately immersing in cold water.
b. composition of gutta-percha
-gutta percha: 19-22%
-zinc oxide: 56-75%
-heavy metal sulfates: 2-17%
-waxes & resins: 1-4%
2. Root canal sealers:
a. Purpose:
-binding agent
-lubricant
-filler
-obturate lateral canals
b. Types: Roth’s, Grossman’s, Kerr, Tubliseal, & Sealapex
c. Roth’s cement sealer (contents):
-zinc oxide: 42% filler
-staybelite resins: 27% adhesive
-bismuth subnitrate: 15% pH, radiopacity
-barium sulfate: 15% radiopacity
-sodium borate anhydrous: 1% plasticity
-Eugenol 100%
d. Grossman’s sealer: the same as Roth’s, but contains silver.
3. Obturation
a. Lateral compaction (not condensation---we do not condense gutta percha).
b. Cold lateral compaction: dry canal with absorbent points.
c. The method which allows the deepest penetration of the spreader resulted in a seal closer to the prepared length. The spreader should penetrate to 1mm short of working length in an empty canal.
d. Gutta percha can be sterilized via a one-minute immersion in undiluted chlorox.
e. Obtura system:
-unitek: high temp (160ºC)
f. Ultrafil system:
-hygienic: low temp (70ºC)
g. Thermafil system:
-a solid-core carrier system
4. Chemically plasticized gutta-percha
a. Klorpercha
b. Chloropercha
c. Eucapercha
d. Custom-fit master cone
-dip apical 2-3mm of the master cone into chloroform for 1 sec.
-allow master cone to dry, place sealer into canal, and re-insert master cone.
-laterally compact gutta-percha with spreader.
5. Silver points
a. Corrosion products have been shown to form at the end of failed silver point cases.
b. These products have been shown to be cytotoxic.
VII. Radiographic Techniques and Interpretation
A. Reducing exposure
1. Use lead apron with thyroid collar.
2. Use E-speed film (1/5 the exposure of D-speed)
B. Factors affecting the radiographic image
1. Density: the degree of blackness in the processed film
-to increase density, increase exposure time, increase kVp, increase mA, and decrease the source-to-film distance.
-factors affecting density: subject, area of mouth, developing conditions, light leaks, and the type of film used.
2. Contrast: relative difference in densities
-this is altered by the kVp
-long scale contrast has many shades of gray (low contrast) at about 90kVp (desirable in caries detection).
-short scale contrast has fewer shades of gray (high contrast) at about 70kVp (**desirable in endodontic treatment).
3. Image sharpness: ability to produce sharp outlines of the object being
radiographed.
-factors affecting sharpness: keep source-to-object distance long (long cone), keep object-to-film distance small, and avoid motion.
-most importantly, maintain parallelism---keep object and film parallel and direct x-ray beam at right angles to the object and film.
C. Techniques
1. Paralleling technique
a. Film is parallel to long axis of tooth.
b. Central ray is directed at right angle to object and film.
c. Requires paralleling device.
2. Bisecting angle technique
a. central ray is directed perpendicular to the bisector of the angle formed by the long axis of the tooth and film.
3. The ideal out of the two is the paralleling technique. The bisecting angle allows for more cone cuts.
D. Buccal object rule
1. When 2 different radiographs are made of a pair of objects, the image of the buccal object moves, relative to the lingual object, in the same direction that the x-ray beam is directed.
2. This rule can determine:
a. position landmarks
b. position of hidden root apices
c. number, location, size, shape, and direction of root canals
d. it can distinguish b/w anatomic landmarks and pathosis
e. it can determine the position of root fractures, perforations, and resorption
f. it can distinguish between external and internal resorption
g. it can locate foreign bodies after trauma
E. Angulation
1. Increasing the vertical angulation will shorten the roots.
2. Decreasing the vertical angle will elongate the roots.
3. The horizontal angulation is changed mesially as you move posteriorly.
VIII. Endodontic Surgery
A. Rationale
If tooth cannot be otherwise debrided or obturated. Techniques include curettage and root end resection w/ a retrograde filling.
B. Indications for endo surgery
1. Relief of pain
2. Drainage
3. Anatomy complications:
a. calcifications
b. dilacerations
c. buccal root fenestrations
4. Iatrogenic:
a. broken instruments
b. ledges
c. perforations
d. prosthetic posts
5. Diagnostic purposes (biopsy)
6. Root fracture visualization
C. Contraindications for endo surgery
1. Poor prognosis
2. Non-restorability
3. Patient not medically capable of withstanding txmnt.
4. Short roots
5. Mand molars---b/c you remove a large amnt of buccal bone
6. Proximity of the neurovascular bundle
D. Flap designs
1. Semilunar
a. major portion in attached gingiva
b. it’s fast and easy
c. it requires the least amount of access
d. it’s not adaptable to enlargement
e. a greater force of retraction is needed
f. visibility is limited
g. does not involve marginal and interdental gingiva
h. crestal bone is not exposed
i. can be used for an extremely long root in certain situations (long maxillary canine)
j. excessive scarring
2. Luebke-Ochsenbein
a. Vertical releasing incisions on each side
b. need a minimum of 5mm of attached gingiva
c. scalloped horizontal incision just below the gingival margin
d. cannot be extended
e. does not expose crestal bone
f. minimizes gingival recession where crowns are in place and esthetics is a concern
g. will get a disruption of the blood supply to the marginal gingiva resulting in a reliance on collateral circulation
3. Triangular
a. one vertical releasing incision
b. this is the least confining as it can be extended
c. excellent landmarks for suturing
d. may result in gingival recession, but has excellent wound healing potential
4. Trapezoidal
a. requires 2 vertical releasing incisions and one horizontal incision in the sulcus
b. the advantages are the same as the triangular; plus a reduced tension.
5. Principles of flap design
a. Incision should be made with a firm stroke.
b. Incision should not cross an underlying bony defect that existed prior to surgery, or is produced by surgery.
c. Vertical incisions are made in the concavities b/w bony eminences.
d. Termination of the vertical incision at the gingival crest must be at the line angle of the tooth.
e. Do not extend the vertical incision beyond the depth of the muco-buccal fold.
f. The base of the flap must be as wide as the width of the free edge (supra-periosteal blood vessels run vertically, try not to transect them).
g. Periosteum must be reflected as an integral part of the flap.
h. The retractor must rest on bone and not impinge on soft tissue.
E. Root end resection
1. Remove diseased root tip.
2. The traditional 45º bevel has been replaced by a less steep angulation of a bevel (0-20º)
3. Resect the entire root end: remove 3mm if possible, but remember to leave 3mm for root end preparation and root end filling (may need to resect less if a post is close to the apex).
4. Increasing the depth of root end filling significantly decreases apical leakage. Increasing the bevel will increase leakage.
F. Root end preparation
1. 3mm prep into the canal, centered in the long axis of the root.
2. Use ultrasonics at medium power
G. Root end filling materials
1. gutta percha
2. amalgam (not used much anymore)
3. IRM (powder: 80% zinc oxide & 20% polymethylmethacrylate; liquid: 99% eugenol & 1% acetic acid)
4. Super EBA (powder: 60% zinc oxide, 30% alumina, & 6% natural resin; liquid: 37.5% eugenol & 62.5% ortho-ethoxybenzoic acid)
5. ZoE
6. Cavit
7. GI
8. MTA (new): tri-calcium silicate, tri-calcium aluminate, di-calcium silicate, tetra-calcium aluminoferrite, bismuth oxide, and gypsum.
-composition: 75% Portland cement
20% bismuth oxide
5% gypsum
-It is recommended that after completion of root end filling, 50% citric acid should be applied (pH 1) to the root end for 2 minutes to demineralized the dentin and expose collagen for attachment and new cementum deposition.
IX. Endodontic Retreatment
A. Clinical success
1. No tenderness to percussion or palpation.
2. Normal mobility.
3. No sinus tracts or concurrent perio disease.
4. Tooth function.
5. No signs of infection or swelling.
6. No evidence of subjective discomfort.
B. Radiographic success
1. Normal to slightly thickened PDL.
2. Elimination of previous rarefaction.
3. Normal lamina dura in relation to adjacent teeth.
4. No evidence of resorption.
C. Causes of endodontic failure
1. Inadequate seal of the root canal system.
2. Untreated or contaminated canal space.
3. Broken instruments or fragments which do not allow successful canal cleaning and sealing.
4. Vertical root fracture.
5. Trauma (resorption, fracture, or avulsion).
6. Periodontal involvement.
7. Host factors (non-odontogenic pathology or systemic conditions).
8. Misdiagnosis: another tooth is etiology.
D. Non-surgical retreatment
1. Retreatment prognosis is poorer than for the original RCT.
2. Retreatment often requires greater technical ability than for the original RCT.
3. Remove poor quality restorations to ensure caries removal and lack of leakage.
4. Retain satisfactory restorations for esthetics and function.
E. Access considerations
1. Post and cores must either be removed or get through for NSRCT.
2. Reduce post retention: ultrasonics, reduce coronal dentin walls.
3. Problems with access: failure to gain proper access to the pulp chamber and root canal system.
4. Removing crowns:
-section with bur
-ultrasonics
-Roydent bridge remover
-Richwill crown & bridge remover (sticky material)
-Clevedent crown & bridge remover
F. Retreatment techniques for gutta percha removal
1. A hot instrument can be used.
2. The gutta percha can be drilled out.
a. gates gliddens
b. peeso reamers
3. Solvents
a. chloroform
b. methylchloroform (less carcinogenic)
c. eucalyptol (must be heated)
4. After softening with solvent, use files (one size smaller than the MAF)
5. Do not use ultrasonics: it does not facilitate gutta percha removal.
6. Removing pastes is more difficult: try ultrasonics or drills.
G. Retreatment techniques for Ag points
1. Try bypassing with solvents to soften the cementation.
2. Can use ultrasonics to loosen the point.
3. Grasping devices: Steiglitz Ag point pliers, double hemostat technique, or modified spoon excavator.
H. Retreatment with posts
1. Need to either remove or perforate through post to gain canal access.
2. Hazards: root fracture while removing post or root perforation while drilling through post.
3. Reducing post retention: coronal dentin wall should be relieved cautiously.
4. Undue force in pulling post: increased incidence of root fracture; apply forces along the long axis of the post.
5. Post & coronal restoration: attempt post removal after coronal restoration is relieved or removed.
6. Where appropriate, trim or trough around the post to reduce retention (ultrasonics is the key).
7. If ultrasonics is unsuccessful, may attempt core penetration.
I. Separated instruments
1. Visualizing the instrument with magnification greatly assists in planning the removal.
2. If able to grasp with another solid object, the removal is usually accomplished.
3. If unable to grasp, attempt to bypass
J. Calcified canals
1. Study angled radiographs.
2. The canal may be negotiable, despite lack of radiographic visualization.
3. Attempt to retreat non-surgically b/f considering surgery.
4. Telltale signs: bubbles are produced as NaOCl dissolves organic matter; discoloration is a characteristic of reparative dentin.
5. Flush RC-prep frequently with NaOCl.
X. Repair of Iatrogenic Problems and Treatment of Resorption Cases
-Perforation: a artificial opening in a tooth or its root, created by boring, piercing, cutting, or pathologic resorption, which results in a communication b/w pulp canal and the periodontal tissues.
A. Causes of perforations
1. Caries
2. Resorption
3. Iatrogenic
a. during access
b. during instrumentation
c. during post preparation
B. Types of perforations
1. Access
a. furcation
b. lateral
2. Instrumentation
a. mid-root
b. apical
3. Post preparation
C. Contributing factors to access perforations
1. Inadequate pre-op assessment
2. Calcified chamber and canals
3. Tooth alignment/malalignment
4. Full crown restorations
D. Contributing factors to instrumentation perforations
1. Excessive canal enlargement
2. Curved canals
3. Apical debris
E. Perforation prevention during instrumentation
1. Be aware of the “danger zone”: located 1.5mm apical to orifice of mesial root of mand 1st molars (the thickness here is 1.2-1.3 mm thick).
2. Use frequent irrigation and patency files.
3. Pre curve files.
4. Use files in strict sequence.
5. Consider NiTi files and balanced force instrumentation technique.
F. Perforation prevention during post space preparation
1. Use heat vice engine driven instruments to remove gutta percha.
2. Evaluate root curvature prior to post space preparation.
3. Use a post less than 1/3 the width of the root.
4. Remember the 3-D morphology of the canal space
G. Perforation diagnosis
1. Slow steady hemorrhage from the teeth.
2. Patient tastes NaOCl.
3. Sudden pain in previously comfortable patient.
4. Place file in suspected perforation and expose radiographs.
5. Sudden increase in W.L.
6. Blood on the side of the paper point.
7. Use apex locator: more reliable in radiograph, especially if perf is located on buccal or lingual.
H. Factors affecting the prognosis of a perforation
1. Location
a. Apical perfs have less chance of contamination through the gingival sulcus.
b. Cervical perfs often become contaminated after epithelial down-growth.
c. Time: immediate repairs have a much better prognosis.
d. Size: the larger the size of the perf, the more area that must be sealed.
e. Sealability: need moisture control, visibility, access, and control of the repair material.
I. Perforation repair techniques
1. Internal matrix: must be resorbable, control hemorrhage, prevent overfills and underfills, be biocompatible, be sterile, and stimulate bone formation.
2. Internal matrix materials:
a. Collaplug or collatape: synthetic collagen formulations.
b. CaOH: good when perf defect has been present for some time and has bacterial contamination.
c. Gelfoam: mushy
d. Hydroxyapatite: expensive
e. Indium foil: used historically with amalgam---not used now.
f. Calcium phosphate cement
g. Tricalcium phosphate
h. DFDBA (demineralized freeze dried bone allograft): expensive
3. Perforation repair materials:
a. Amalgam: used historically---not used now.
b. ZoE: too much eugenol.
c. IRM: less eugenol than ZoE, so less tissue irritation.
d. EBA: less eugenol than IRM.
e. Cavit: eventually resorbs and should not be used.
f. Gutta percha: used for apical perfs w/ or w/out an internal matrix.
g. Composite: light curing can be a problem in mid-root perfs.
h. Glass ionomer: popular for coronal and mid 1/3 perfs, good flow characteristics.
i. MTA (mineral trioxide aggregate): the latest and greatest. The sealability is better than IRM, EBA, and amalgam. Research has shown that cementum attaches to MTA. It has the consistency of wet sand and a long working time (4 hrs). It’s Portland cement (75% by weight). It contains tricalcium silicate, bismuth oxide, dicalcium silicate, tricalcium aluminate, tetracalcium aluminoferrite, and gypsum.
J. Root resorption
-may be transient or self-limiting
-may be progressive or have an unknown etiology, but associated with trauma, replantation, ortho movement or chronic inflammation.
-use buccal object rule to distinguish internal from external resorption.
-Types of root resorption:
1. Internal: initiated within the pulp space
-unknown etiology, but may be trauma or caries
2. External: initiated in the periodontium
Types:
a. Surface: defects in dentin and cementum that undergo repair by
deposition of new cementum. Txmnt: none
b. Replacement (ankylosis): pathologic loss of cementum, dentin and
PDL with the ingrowth of bone into the defect and
the fusion of bone to cementum and/or dentin.
Txmnt: none
c. Inflammatory: pathologic loss of cementum, dentin and bone
resulting in a defect in the root and adjacent bony tissue. Types of
inflammatory resorption:
1. Cervical: stimuli from gingival sulcus or root surface
that begins in cervical region below epithelial
attachment. May occur after N.V. bleaching.
Txmnt: NSRCT, elevate flap or extract/re-implant.
2. Extracanal invasive: cervical resorption that spreads
from inside the tooth.
Txmnt: depends on extent and location. If
supraosseous, elevate a flap and restore or extrude and
restore.
3. Apical: from noxious products draining from root
canal.
Txmnt: NSRCT and CaOH to get stop.
4. Pressure: pulp not involved---see in permanent
dentition during tooth eruption.
Txmnt: remove source: ortho, impacted teeth and
tumors/cysts.
XI. Evaluation of Endodontic Success and Failure
A. Criteria for failure: Clinically
1. Persistent symptoms
2. Sinus tract or swelling
3. Percussion or palpation sensitivity
4. Extensive tooth fracture
5. Increased mobility or perio breakdown
6. Inability to function on tooth
B. Criteria for failure: Radiographically
1. Increase or no change in RL
2. Increase in PDL space
3. Loss of lamina dura
4. Root resorption
C. Causes of failure
1. Perforation
2. Obturation incomplete
3. Over-extension
4. Root canal missed
5. Periodontal disease
6. Another tooth
7. Split tooth
8. Trauma
D. Pre-operative causes of failure
1. Mis-diagnosis
2. Poor case selection
3. Poor prognosis
E. Operative causes of failure
1. Failure to obtain mechanical objectives
2. Failure to obtain biological objectives
3. Procedural accidents
a. perforations
b. ledges
c. separated instruments
d. longitudinal fractures
e. extruded material
F. Post-operative causes of failure
1. Occlusal or other trauma
2. Fractures
3. Inadequate final restoration
4. Non-endodontic causes
G. The endodontic triad
1. Microbe disinfection
2. Complete debridement: **the key to success
3. 3-dimmensional obturation
XII. Fascial Space Infections of Odontogenic Origin
A. Immediate life threatening signs
1. Respiratory impairment
2. Difficulty in swallowing
3. Impaired vision or eye movement
4. Change in voice quality
5. Severe lethargy
6. Decreased level of consciousness
***These signs may indicate a life-threatening condition and immediate referral to a specialist or physician in a hospital emergency room may be indicated.
B. Signs of serious infection
1. Severe infection spreading beyond the oral cavity into critical facial spaces
2. Systemic involvement
3. Rapidly progressing infections
4. Long-term chronic infections
5. Severe trismus
6. Moderate to severe dehydration
7. Treatment requiring advanced management
***These conditions may indicate the need for prompt, non-emergency, referral to a specialist or physician---do not delay action.
C. Serious general signs needing immediate referral
1. Toxic appearance (patient looks really sick)
2. Respiratory difficulty (sniffing position, using accessory muscles to breathe, stridor, or paradoxical breathing (rocking chair movement))
3. CNS changes (decreased level of consciousness, intense headache, stiff neck, vomiting, swollen eyelids, or abnormal eye signs)
4. Dehydration (postural hypotension, increased thirst, fever, loss of skin turgor, shrunken drawn face, or oliguria).
5. Malnutrition (continued weight loss, muscle wasting, edema of ankles and feet, dry sparse hair, lethargy, or swollen abdomen)
6. Vital signs:
a. Mild to moderate infection = >99.5ºF; if <102ºF, may not need antipyretics.
b. Usually no B.P. change with a mild to moderate infection.
c. Pulse rate is slightly elevated with a mild to moderate infection (b/w 90ºF to 100ºF). The pulse increases 10 beats/min for each degree of temp increase.
d. Respiratory rate is slightly elevated with mild to moderate infection (18-20/min). It will be significantly elevated with a severe infection and greater than 22/min that’s shallow and irregular requires immediate referral.
D. Bacterial infections
1. Mixed infections (75-90% of species are obligate anaerobes). The anaerobe/aerobe ratio is 3:1.
2. Bacteria mostly found in odontogenic infections are facultative anaerobes (Streptococci) and obligate anaerobes (Porphyromonas, Prevotella, Fusobacterium, Veillonella, Eubacterium, & Peptostreptococcus.
E. Classification of facial spaces (swelling of and below the mandible)
1. Mandibular buccal vestibule
a. Anatomic location: buccinator, mentalis, and oral mucosa.
b. Source of infection: mandibular apices above the buccinator and mentalis muscles.
c. Can spread to buccal space
d. Risk: low
2. Body of the mandible
a. Anatomic location: cortical plate and periosteum.
b. Source of infection: mand teeth
c. Can spread to buccal space, submandibular space, or sublingual space.
d. Risk: low
3. Mental space
a. Anatomic location: bilateral, superior (mentalis muscle), and inferior (platysma muscle).
b. Source of infection: mand incisors
c. Can spread to submental space or submandibular space.
d. Risk: moderate
4. Submental space
a. Anatomic location: superior (mentalis muscle, mylohyoid muscle), inferior (platysma muscle), and lateral (b/w the bellies of the digastric).
b. Clinical presentation: swelling beneath chin.
c. Source of infection: mand incisors
d. Can spread to sublingual space, submandibular space, or parapharyngeal spaces.
e. Risk: moderate
5. Sublingual space
a. Anatomic location: superior (FOM), inferior (mylohyoid muscle), lateral (lingual surface of the mand), and medial (hyoglossus, geniohyoid, & genioglossus muscles).
b. Clinical presentation: swelling in FOM, dysphagia, & elevation of the tongue.
c. Source of infection: mand incisors, canines, premolars, and the mesial root of the 1stmolar (apices lie above the attachment of the mylohyoid muscle).
d. Can spread to submandibular space, parapharyngeal spaces, and the pterygomandibular spaces.
e. Risk: moderate
6. Submandibular space
a. Anatomic location: superior (mylohyoid muscle), inferior (platysma), lateral (lingual surface of the mand), and medial (hyoglossus and mylohyoid).
b. Clinical presentation: submandibular swelling, mild trismus, toxic appearance, and systemic symptoms.
c. Source of infection: mand molars; the apices lie below the attachment of the mylohyoid muscle).
d. Can spread to parapharyngeal spaces, deep temporal space, pterygomandibular space, and fascial planes of the neck).
e. Risk: moderate
7. Ludwig’s angina
a. Anatomic location: bilateral cellulitis, submental space, sublingual space, and submandibular space.
b. Clinical presentation: indurated bilateral mand swelling, swelling of the neck, elevation of the tongue, resp difficulty, and systemic signs.
c. Source of infection: all mand teeth
d. Can spread to facial planes in neck, mediastinum, and can cause glottic edema leading to resp obstruction.
e. Risk: Very high
F. Classification of facial spaces (swelling of the lateral face and neck)
1. Maxillary buccal vestibule
a. Anatomic location: superior (buccinator muscle), lateral (buccinator muscle), and medial (lingual cortical plate).
b. Source of infection: max premolars and molars.
c. Can spread to buccal space.
d. Risk: low
2. Buccal space
a. Anatomic location: superior, medial, and inferior (buccinator muscle), lateral (skin of the cheek), and posterior (masseter muscle).
b. Clinical presentation: swelling of cheek
c. Source of infection: max/mand molars
d. Can spread to deep temporal space, superficial temporal space, lateral pharyngeal space, pterygomandibular space, or submasseteric space.
e. Risk: moderate
3. Temporal space (superficial and deep spaces)
a. Superficial
-clinical presentation: external swelling over temporal; above the zygomatic arch
b. Deep
-clinical presentation: minimal external swelling; trismus
c. Source of infection: infections spreading from the pterygomandibular space or the submasseteric space.
d. Risk: moderate
4. Other spaces
a. Parapharyngeal: will see uvula deflection, swelling of parapharyngeal wall, and a high fever. Source could be from other fascial spaces (peritonsilar abscess). Can spread to mediastinum, base of skull, foramen ovale, or the brain. High risk.
b. Cervical spaces: will see brawny swelling of the neck, resp difficulty, and obliteration of the sternal notch. Source could be a spread from other fascial spaces. It can spread to the posterior and anterior mediastinum. High risk.
G. Classification of facial spaces (swellings of the midface)
1. Canine space
a. Anatomic location: superior (levator anguli oris), anterior (orbicularis oris), and posterior (buccinator muscle).
b. Clinical presentation: extraoral swelling, obliteration of the nasolabial fold, and intraoral swelling.
c. Source of infection: maxillary canine or 1st premolar.
d. Can spread to cavernous sinus (causing a thrombosis), buccal space, deep temporal space, or periorbital area).
e. Risk: moderate
2. Other swellings that can lead to a cavernous sinus thrombosis: periorbital space swelling or swelling of the base of the upper lip.
3. Cavernous sinus thrombosis
a. Pathogenesis: angular vein, ophthalmic vein, pterygoid plexus.
b. An infection in the midface or infratemporal space results in increased intravascular pressure, reversed direction of venous blood flow, stasis in the cavernous sinus, thrombus formation, or release of thrombi into the circulatory system.
c. Clinical presentation: swelling of eyelids, exophthalmos, drowsiness, vomiting, stiffness in neck, and a very high fever.
d. Source of infection: midface region (base of upper lip, canine space infection, or a periorbital space infection), infratemporal space, pterygoid plexus, pterygomandibular space, and needle track infections.
e. Risk: Very high
H. Treating odontogenic infections
1. Determine whether you will treat or refer the patient.
2. Eliminate etiology of infection.
3. Incision and Drainage (I & D)
a. Indicated when an infection presents with significant facial swelling, cellulitis, or involvement with facial spaces. The area of swelling need not be fluctuant.
b. Rationale for I & D:
-Decrease the # of bacteria.
-Reduces tissue pressure (alleviates pain and improves circulation in the area).
-Prevents the spread of infection.
-Alters the oxidation-reduction potential.
-It accelerates healing.
c. Obtain specimen for culture and sensitivity: stat gram stain, aerobic C & S, and anaerobic C & S.
d. Incise in healthy tissue at the site of greatest fluctuation down to the level of apical bone (subperiosteal).
e. Try to encourage draining by gravity.
f. Leave a ½ to ¾ of an inch opening for draining (size of tip of index finger).
g. Do blunt dissection with curved hemostats gently through the deeper tissues and explore all parts of the abscess. Extend to roots of teeth responsible for the infection.
h. Insert sterile penrose tubing sutured to healthy tissue.
i. Perform total pulpectomy and place CaOH at time of I & D.
j. Ideally, have patient return for obturation appt before removal of drain.
k. If drain must be removed b/f obturation due to time factors, remove after resolution of the infection.
l. If cannot do stat C & S, select PCN as antibiotic of choice. If allergic to PCN, go to clindamycin.
XIII. Anesthesia and Pain relief
A. Akinosi technique:
1. Use a 25ga long needle.
2. Insert along the lingual aspect of the mandibular ramus adjacent to the maxillary tuberosity.
3. The needle will pass parallel to the ramus, aspirate and inject.
4. The disadvantage here is that there’s no bony contact to provide a landmark.
B. Gow Gates
1. This has a 98% success rate.
2. Patient has to open wide.
3. Target is the lateral border of the neck of the condyle (use the corner of the mouth and tragus of the ear notch as landmarks).
4. Penetrate distal to the max 2nd molar at the height of the palatal cusp.
5. Advance until bony contact with the neck of the condyle.
C. PDL injection
1. Decreases blood flow to nerve for about 20min.
2. Can induce localized external root resorption.
3. There may be slight damage where the needle penetrates, but not much migration (25 days to fully recover).
4. No longer use for dx.
5. Goes into intraosseous spaces.
D. Mylohyoid
1. Consider this when signs of anesthesia are present after inferior alveolar and long buccal.
XIV. Microbiology and Immunology
A. Immunology considerations
1. IgG (plasma cell): Principle antibody involved in protective reaction against microbes and their products.
2. IgM (plasma cell): also protective and is a larger molecule formed in response to large microbes.
3. IgE (mast cell): Involved in immediate hypersensitivity.
4. IgA: found in urine, colostrum, respiratory and GI tract secretions, tears, and saliva. Probably involved in antimicrobial/antiviral action.
5. IgD (B-lymphocyte): surface of B-lymphocytes (antibody producers) involved in switching from IgM to IgG production.
6. Undifferentiated mesenchymal cells start repair.
7. Some repair by fibroblasts.
B. Possible components in periapical reactions (pain, swelling, and bone destruction)
1. Microbial virulence factors: collagenase, hyaluronidase, streptokinase, irritating factors from filling materials.
2. Host tissue products: histamine.
3. Hypersensitivity reactions: antigens involved may be bactericidal products, host tissue, and medicaments.
XV. Pulpal and Periradicular Pathology
A. Dentin
1. Components:
a. 45% inorganic (hydroxyapatite)
b. 33% organic (collagen, ground substance)
c. 22% water
2. Types of dentin:
a. Secondary (physiologically formed)
b. Mantle
c. Circumferential
d. Predentin
3. Dentinal tubules:
a. Formed around odontoblastic processes (the diameter and # of dentinal tubules increase as you approach the pulp).
b. Peritubular dentin: highly mineralized; readily dissolved in acid.
c. Intertubular: organic
d. Dentinal fluid: direct communication b/w dentin and pulp.
B. Pulp
1. Zones of pulp:
a. Predentin: organic matrix; present as long as odontoblasts are present.
b. Odontoblastic layer: cell bodies; one cell thick; desmosomes impart syncytial function.
c. Cell-poor zone (zone of Weil): capillaries and unmyelinated nerve fibers; disappears during formation of reparative dentin.
d. Cell-rich zone: fibroblasts and reserve cells.
e. Pulp proper: collagen; fibroblasts, macrophages, nerves, and blood vessels.
2. Cells:
a. Odontoblasts: processes extend approximately 1/3 of the distance into the dentin; dentinogenesis.
b. Fibroblasts: most numerous cell of the pulp; not fully differentiated.
c. Fibrocyte: mature fibroblast.
d. Immunologic: lymphocytes, plasma cells, mast cells, and histiocytes.
3. Ground substance:
-The spread of inflammation is impeded by this gelatinous state.
4. Fibers:
a. Collagen
b. elastin
c. blood vessels
5. Vascular:
a. Arterioles via apical foramen
b. These form a capillary plexus in the cell-free zone
c. Venules and arterioles anastomose.
6. Innervation:
a. All afferent impulses from the pulp result in pain.
b. A-delta fibers:
-myelinated; fast (25m/sec)
-small diameter
-sharp pain; dentinal pain, low threshold
-tested by EPT and cold
c. C-fibers:
-unmyelinated, slow (1m/sec)
-large diameter
-true nociceptive; deep, aching pain
-may remain excitable in non-vital tissue (ex: + EPT in necrotic pulp)
d. Proprioreception in PDL spaces
7. The order in which nerves are anesthetized:
a. Pain
b. Temp
c. Touch
d. Proprioreception
e. Skeletal
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