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282 PART V ORALANDMAXILLOFACIALSURGERY
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lasting, direct bone-to-implant anchorage in man, Acta Orthop Scand52:155–170,1981.
AlbrektssonT, Dahl E, Enbom L, et al.: Osseointegrated oral implants. A Swedish multicenter study of 8139 consecutively
inserted Nobelpharma implants, J Periodontol59:287–296,1988.
AlbrektssonCJ, Sennerby L: What is osseointegration? In Worthington P, Evans JR, editors: Controversies in oral and maxil-
lofacial surgery, Philadelphia, 1997, Saunders.
AndersonG, Andreasson L,BjelkengrenG: Oral implant rehabilitation in irradiated patients without adjunctive hyperbaric
oxygen, Int J Oral Maxillofac Implants13:647–654,1998.
Ata-Ali J,Ata-AliF,Ata-AliF: Do antibiotics decrease implant failure and postoperative infections? A systematic review and
meta-analysis, International J Oral & Maxillofac Surg43(1):68–74,2014.
BachG,NeckelC, Mall C,KrekelerG: Conventional versus laser-assisted therapy of periimplantitis: a five-year comparative
study, Implant Dent9(3):247–251,2000.
Bagheri SC, Bell RB, Khan H: Current therapy in oral and maxillofacial surgery,StLouis,2012,ElsevierSaunders.
BeckerW,BeckerBE, Alsuwyed H, et al.: Long-term evaluation of 282 implants in maxillary and mandibular molar posi-
tions. A prospective study, J Periodontol70:896–901,1999.
BlockMS: Color atlas of dental implant surgery,ed3,MarylandHeights,Missouri,2011,SaundersElsevier.
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Surg49:482–492,1991.
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TRIGEMINALNERVEINJURY
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David W. Lui, A.Omar Abubaker, Kenneth J. Benson
1. What are the three major classifications of nerve injury?
1. Seddon classification: neuropraxia, axonotmesis, neurotmesis
2. Sunderland classification: first- to fifth-degree injury
3. Mackinnon classification: classes 1 to 6
2. Can you describe the Seddon classification of nerve injury?
See Table 27-1.
3. Can you describe the Sunderland classification of nerve injury?
• First-degree injury: Damage is confined to within the endoneurium with no axonal degertion.
• Second-degreeinjury:Damageextendsthroughandincludestheendoneuriumwithnosignicant
axonal degeneration.
• Third-degreeinjury:Damageextendstotheperineurium.
• Forth-degreeinjury:Damagetotheentirefasciclethatextendsthroughtheperineuriumtotheepi-
neurium, but the epineurium remains intact. There is axonal, endoneurial, and perineurial damage
with degeneration of the fascicles.
• Fifth-degreeinjury:Completeornearcompletetransectionofthenervewithepineurialdiscontinu-
ity and likely neuroma formation.
4. What is a Mackinnon class 6 nerve injury?
MixednerveinjuryinvolvingacombinationoftheSunderlandtypesofnerveinjuries.
5. What is Wallerian degeneration?
Wallerianoranterogradedegenerationisaseriesofmolecularandcellulareventstriggeredthrough-
outthedistalnervestumpandwithinasmallreactivezoneatthetipoftheproximalstump.The
primaryhistologicchangeinvolvescytoskeletalfragmentationofbothaxonsandmyelin.
6. What are the four types of neuroma based on gross morphology?
Lateraladhesiveneuroma,lateralexophyticneuroma,neuroma-in-continuity,andamputation
neuroma.
7. What is dysesthesia?
Anunpleasantabnormalsensationthatiseitherspontaneousorprovoked.
8. What is the difference between analgesia and anesthesia?
Analgesia is an absence of pain in response to stimulation that would normally be painful. Anesthe-
sia is the absence of perception of stimulation by any noxious or nonnoxious stimulation of skin or
mucosa.Itisdividedintogeneral(central),regional,andlocaltypes.
9. What is allodynia?
Allodyniaispainduetoastimulusthatdoesnotnormallyprovokepain.Unlikehyperalgesia,hyper-
pathia,andhyperesthesia,allodyniamayincludeemotionallyinducedsensationsinthenerve-injured
patient.
10. What is anesthesia dolorosa?
Anesthesia dolorosa is pain in an area or region that is anesthetic.
11. What is hyperalgesia?
Hyperalgesia is an increased response to a stimulus that is normally painful.
12. What is hyperesthesia?
Hyperesthesiaisanincreasedsensitivitytoanynoxiousornonnoxiousstimulationofskinormucosa,
excluding the special senses; it includes allodynia and hyperalgesia.
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Table 27-1. Seddon Classification of Nerve Injury
NEUROPRAXIA AXONOTMESIS NEUROTMESIS
Sunderland I II, III, IV V
Nervesheath Intact Intact Interrupted
Axons Intact Some interrupted All interrupted
Wallerian degeneration None Yes,someaxons Yes,allaxons
Conductionfailure Transitory Prolonged Permanent
Spontaneousrecovery Complete Partial Poor to none
Timeofrecovery Within 4 weeks Months None, if not begun by
Adapted from Meyer RA, Bagheri SC: Clinical evaluation of peripheral trigeminal nerve injuries, Atlas Oral Maxillofac
Surg North Am 19:15–33, 2011.
13. What are the symptoms of hyperesthesia?
Patients describe a shooting, flashing, burning pain produced by normally nonpainful stimuli.
14. What is hyperpathia?
Hyperpathiaisapainfulsyndromecharacterizedbyincreasedreactiontoastimulusandincreased
thresholdforresponse.Itcommonlyisinducedbyrepetitivemechanicalpressuresandcharacterized
byfaultyidenticationandlocalizationofstimuli.
15. What is hypoalgesia?
Hypoalgesia is diminished pain response to a normally painful stimulus.
16. What is paresthesia?
Paresthesiaisanabnormalsensation,eitherevokedorspontaneous,thatisnotnecessarilyunpleas-
ant or painful, as in dysesthesia.
17. What is sympathetically mediated pain (SMP)?
SMPisthrobbing,diffuse,andhyperalgesicpainperpetuatedbyabnormalreexactivityinsympa-
theticpathwaysfollowingperipheralnerveinjury.Theclassicsyndromesofcomplexregionalpain
syndrometypeIandII(formerlyknownasreexsympatheticdystrophyandcausalgia,respectively)
aretheorizedtoinvolvebothperipheralandcentralmechanisms.
18. What are the symptoms of SMP?
The symptoms are often described as burning, hot, lancinating pain. Patients also complain of
increased pain intensity during stressful periods.
19. What is Tinel’s sign?
Tinel’ssignisaprovocativetestofregeneratingnervesproutsinwhichlightpercussionoverthe
nerveelicitsadistaltinglingsensation.Itisusedasasignofsmallberrecoverybutispoorlycorrelatedwithfunctionalrecoveryandeasilyconfusedwithneuromaformation.
20. What is deafferentation pain?
Deafferentationpainispaininabodyregionofpartialorcompletetraumaticperipheralnervedecit
inwhichretrogradecentralneuropathyhasoccurred.Deafferentationmechanismshavebeenimpli-
cated in phantom pain, hyperpathia, and allodynia.
21. How many axons and fascicles are in the inferior alveolar nerve?
Approximately 7000 to 12,000 axons and 10 to 24 fascicles.
22. What is the incidence of inferior alveolar and lingual nerve injury during removal of
third molars?
Theincidenceofinferioralveolar,lingual,and,lessfrequently,longbuccalnerveinjuryduring
mandibularthirdmolarremovalrangesbetween0.6%and5.0%.Ingeneral,theincidenceofinferior
alveolarnerve(IAN)injuriesishigherthanthatofthelingualnerve;inonestudy,incidencewas1.2%
fortheIANand0.9%forthelingualnerve.Factorssuchasage,surgicaltechnique,andproximityof
3 months
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Figure 27-1. Neurosensorytestingprotocolfornerveinjurypatientswithdecreasedsensationwithoutdysesthesia.
(Modified from Meyer RA, Bagheri SC: Clinical evaluation of peripheral trigeminal nerve injuries, Atlas Oral Maxillofac Surg
North Am 19:15–33, 2011.)
thenervetothetoothinuencetheincidenceoftheseinjuries.Morethan96%ofpatientswithlingual
nerveinjuriesrecoverspontaneously.
23. What factors are associated with a higher incidence of lingual nerve injury during
the course of third molar removal?
Linguallyangledimpactionsareespeciallyvulnerabletonerveinjuryduringtheirremovalbecauseof
theerosionorabsenceofthelingualcorticalplatebyinfectionorcystexposingthenervedirectlyto
damageduringinstrumentationtoremovethetooth.
24. What is the average rate of an injured axon’s forward growth?
Approximately 1 to 2 mm/day.
25. What are the potential clinical manifestations of a trigeminal nerve injury?
• Nonpainfulanesthesiaandhypoesthesia
• Nonpainfulhyperesthesia
• Painfulanesthesiaandhypoesthesia
• Painfulhyperesthesia
26. What is the recommended protocol for neurosensory testing in nerve injury pa-
tients with decreased sensation without dysesthesia?
See Fig. 27-1.
27. What is the recommended protocol for neurosensory testing in nerve injury pa-
tients with painful sensation?
See Fig. 27-2.
28. What is the recommended nonsurgical treatment of chronic trigeminal dysfunc-
tion and dysesthesia?
See Fig. 27-3.
29. How should open nerve injuries be managed?
Ifanopeninjuryisobserved,itisbestmanagedwithimmediateprimaryrepair.Delayedprimary
repairisperformedwithintherstfewpostoperativedays.Adelayedsecondaryrepairisperformed
more than 3 weeks after injury.
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Unpleasant altered sensation
Brushstroke-evoked pain
(Level A)
No pain response
Pain response: Allodynia
Repetitive stimulus-evoked pain
(Level B)
No pain response
Pain response: Hyperpathia
Noxious mechanical stimuli
(Level C)
'd Pain response:
No pain response
Figure 27-2. Neurosensorytestingprotocolfornerveinjurypatientswithpainfulsensation. (Modified from Meyer RA,
Bagheri SC: Clinical evaluation of peripheral trigeminal nerve injuries, Atlas Oral Maxillofac Surg North Am 19:15–33, 2011.)
Normal pain response
Hyperalgesia
Decreased altered sensation
Direction and 2-point discrimination
(Level A)
Normal Abnormal
Contact detection
(Level B)
Impaired
Normal
Mildly
impaired
Normal
Moderately
impaired
Figure 27-3. Nonsurgical treatment of chronic trigeminal dysfunction and dysesthesia. NSAIDs, Nonsteroidal antiinflam-
matory drugs; TCAs, tricyclic antidepressants; TENS, transcutaneous electrical neural stimulation. (Modified from Allig
CC, Schwartz E, Campbell RL, et al.: Algorithm for diagnostic assessment and surgical treatment of traumatic trigeminal
neuropathies and neuralgias, OralMaxillofacSurgClinNorthAm 4:555, 1992.)
Pain sensitivity
(Level C)
↑Threshold
↓Response
Severely
impaired
Abnormal
Moderately
impaired
Abnormal
No response
Anesthetic
CHAPTER 27 TRIGEMINALNERVEINJURY 287
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30. When should closed (unobserved) nerve injuries be addressed surgically?
Unobservednerveinjuriesshouldberepairedifthepatienthas:
• Intolerableanesthesiaofmorethan3months
• Painfulsymptomsthatpersistmorethan4monthsthatmayberelievedwithproximalanestheticblock
• Intolerabledeteriorationofsensationbeyond4monthsandnoimprovementofsensationbeyond
4 months
31. What other method of nerve repair can be done if primary repair is not possible?
Aninterpositionalfreenervegraftandnerveguidance.
32. What are the general principles of delayed nerve repair?
Repairmustbecompletedwithouttension.First,extraneuraldecompressionisperformedtoremove
allirritative,foreign,orcompressiveforcesfromnervecontact.Next,thenervemustbeinspectedfor
continuity.Ifnervecontinuityisseen,thenervemaybeinspectedwithanepineuralincisionatthesite
ofinjury.Internaldecompression(neurolysis)isperformedandcompletedbyclosingtheepineurium.If
neuroma-in-continuityistooextensive,excisionofneuromaalongwithpartofthenerveisperformed.
A direct neurorrhaphy is performed in a tension-free manner.
33. What are the types of nerve repair?
• Epineural
• Perineural
• Groupfascicular
34. Which type of nerve repair is appropriate for the IAN?
Mixedmotorandsensorynervesarebesttreatedwithperineuralandgroupfascicularsuturing.The
sensoryIANcanbetreatedwiththeepineuralsuturetechnique.
35. What does coaptation refer to in nerve repair?
Bringingindividualnervefasciclesintothebestpossiblealignment.Directneurorrhaphycanonlybe
performedwhenthenerveistensionfree.
36. If a defect is too large for a direct neurorrhaphy of the IAN, which nerves may be
considered as donors for free nerve graft?
Thesural,greaterauricular,andmedianantebrachialnervesareconsidered.
37. What factors govern the choice of donor site for free nerve repair?
• Accessibility
• Lengthrequired
• Diameterofdonornervecomparedwiththehostnerve
• Patientpreference
• Fascicularnumberandpattern
38. Which nerve is the best donor site for an interpositional graft for an IAN defect of
approximately 25 mm?
Thesuralnerve.Thesuralnervecanprovideupto30mmofgraftharvest.Itprovidessensationtothe
posteriorandlateralaspectsofthelegandfoot.Italsohasupto50%feweraxonsandsmalleraxonal
sizethantheIAN.
39. Which free nerve may be used as a donor site for smaller defects (up to 15 mm
long) of the IAN?
Thegreaterauricularnervecanbeusedforshortgaps(upto15mm).Thisnervegraftisagood
matchwiththeIANintermsofaxonalsizeandaxonalnumbers.However,comparedwiththehost
nerve,thegreaterauricularnerveishalfthediameterandhashalfthefascicles.Acablegraft(two
parallelstrands)maybeusedtoprovideabettersizematch.
40. How much nerve should be harvested for a nerve graft?
Becauseofprimarycontracture,thelengthoftheharvestednerveshouldbeatleast25%longerthan
the defect.
41. When is delayed nerve repair in the maxillofacial region indicated?
If a wound is grossly contaminated or if the mechanism of injury may cause scarring of the proximal
anddistalends.Examplesofsuchinjuriesarebluntavulsioninjuriessuchasgunshotwoundsand
injuriessustainedinmotorvehicleaccidents.
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Table 27-2. Success Rate of Microsurgical Repairs of Inferior Alveolar and
Lingual Nerve Injuries
PATIENTS SUCCESS* (%) RANGE (%) SEM
Hypoesthetic
• IAN N = 192 85.4 66-94 3.68
• Lingualnerve N = 131 87.0 50-91 5.66
Hyperesthetic
• IAN N = 124 55.6 25-80 7.01
• Lingualnerve N = 74 67.5 50-100 6.82
*Success is defined as (1) minimum recovery of gross touch perception and (2) global pain reduction of >30%.
Overall success rate (N = 521) is 76.2%.
SEM, Standard error of the mean; IAN, inferior alveolar nerve.
Adapted from LaBanc JP, Gregg JM: Trigeminal nerve injuries: basic problems, historical perspectives, early
success, and remaining challenges, Oral Maxillofac Clin North Am 4:227–283, 1992.
42. How is the term anastomosis applied to nerve injuries?
Trickquestion.Anastomosisisnotappropriatenomenclaturewhendiscussingnerverepair.Vessels
areanastomosed,andnervesarerepairedorreconstructed.
43. What type of suture material is most compatible for nerve repair?
Aninertandnonresorbablesuturematerial,suchas8-0or9-0monolamentnylon(Ethilon)orpoly-
propylene(Prolene).
44. What potential alloplastic nerve conduits may be used in nerve reconstruction?
Forguidednervegrowthupto3mm,thefollowingnerveguidesmaybeusedforrepair:
• TypeIcollagentubes
• Expandedpolytetrauoroethylene
• Polyglycolicacidtubes
45. What method is used for locating the great auricular nerve?
A line is drawn connecting the mastoid process and angle of mandible. A perpendicular line is then
drawntobisectthemastoid-mandibleline.Thegreatauricularnerveapproximatesthissecondline.
46. What is the success rate of microsurgical repairs of inferior alveolar and lingual
nerve injuries?
See Table 27-2.
47. What is the most significant factor of functional neurosensory recovery?
Timingofsurgicalintervention.
BiBliography
AlligCC,SchwartzE,CampbellRL, et al.: Algorithm for diagnostic assessment and surgical treatment of traumatic trigemi-
nal neuropathies and neuralgias, Oral Maxillofac Surg Clin North Am4:555,1992.
Donoff R:Surgicalmanagementofinterioralveolarnerveinjuries(part1):caseforearlyrepair,J Oral Maxillofac Surg
53:1327–1329,1995.
Elusten K,StevensM:Diagnosisandmanagementofinterioralveolarnerveinjury,Compendium16:1028–1038,1995.
Greg J:Neurologicalcomplicationsofsurgeryforimpactedteeth.InAllingCC, Helfric JF, Alling RD, editors: Impacted teeth,
Philadelphia, 1993, Saunders.
Gregg J:Surgicalmanagementofinferioralveolarnerveinjuries(part2):casefordelayedmanagement,J Oral Maxillofac
Surg53:1330–1335,1995.
Gregg JM: Nonsurgical management of traumatic trigeminal neuralgia and sensory neuropathies, Oral Maxillofac Surg Clin
North Am4:375–392,1992.
LaBanc J:Reconstructivemicroneurosurgeryofthetrigeminalnerve.InPetersonLJ, et al.: Principles of oral and maxil-
lofacial surgery, Philadelphia, 1992, Lippincott.
LaBanc JP, Gregg JM: Glossary, Oral Maxillofac Surg Clin North Am4:563,1992.
LaBanc JP,VanBovanRW:Surgicalmanagementofinferioralveolarnerveinjuries,Oral Maxillofac Surg Clin North Am
4:425–438,1992.
CHAPTER 27 TRIGEMINALNERVEINJURY 289
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Meyer RA, Bagheri SC:Clinicalevaluationofperipheraltrigeminalnerveinjuries,Atlas Oral Maxillofac Surg North Am
19:15–33,2011.
Miloro M: Microneurosurgery. In Miloro M, Gali GE, Larsen PE, Waite PD, editors: Peterson’s principles of oral and maxil-
lofacial surgery,Hamilton,ON,2004,BCDecker.
Zuniga JR, Essick GK:Acontemporaryapproachtotheclinicalevaluationoftrigeminalnerveinjuries,Oral Maxillofac Surg
Clin North Am4:353–367,1992.
OROFACIAL INFECTIONS
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AND ANTIBIOTIC USE
A. Omar Abubaker
CHAPTER 28
1. What is the source of the bacteria that cause the most odontogenic infections,
and what is the incidence of these infections?
Odontogenic infections are caused mostly by indigenous bacteria that normally live on or in the host.
When such bacteria gain access to deeper tissues, typically in the majority of cases through decayed
or nonvital teeth, they cause odontogenic infection.
In a recent retrospective study of an 8-year period, the number of patients admitted for treat-
ment of severe odontogenic infection represents 4% of all patients admitted to an OMFS service, with
1.7% requiring intensive medical and surgical therapy and a 0.012% mortality rate.
2. What are the predominant bacteria found in the oral cavity?
See Box 28-1.
3. Which species of bacteria cause odontogenic infection?
Most of the microorganisms associated with odontogenic infections are gram-negative rods (fusobac-
teria, bacteroides). Some are gram-positive cocci (streptococci and peptostreptococci), and 25% are
aerobic, mostly gram-positive streptococci. About 60% are anaerobic bacteria. Almost all odontogenic
infections are caused by multiple bacteria (an average of five species). Fusobacterium sp. is associated with severe infections (Fig. 28-1 and Table 28-1). In a recent study, 42 patients were treated with
surgical incision and drainage and antibiotics. The specimens from all of these patients were sent for
culture and sensitivity tests and for gram-positive and gram-negative aerobes. Forty microorganisms
were isolated. There were 28 aerobes and 10 anaerobes. Two fungi were also identified. The most
common bacteria isolated were Staphylococcus aureus, Klebsiella, Escherichia coli, and Peptostrep-
tococcus. The key takeaway point here is that antibiotics alone cannot resolve odontogenic infection
satisfactorily. Quick recovery of patients results from proper basic management including early
drainage/decompression, which is equally important.
4. Which staphylococci are clinically important to orofacial infections?
Of the 23 species of staphylococci, only three are clinically important to orofacial infections: Staphylo-
coccus aureus, Staphylococcus epidermidis, and Staphylococcus saprophyticus.
5. What is coagulase? Which Staphylococcus species produces coagulase?
Coagulase is an enzyme that coats the bacteria with fibrin and reduces the ability of the host cell to
phagocytize it. S. aureus is the only coagulase-positive staphylococcus.
6. What is the basis for microbiologic diagnosis of odontogenic infection?
Initially, an empirical diagnosis of the causative organism of odontogenic infection is made based on
the presumption of involvement of bacteria typical for the site (oral flora). The microbiologic diagnosis
stems from this presumption and can be confirmed via Gram stain and culture.
7. What is Gram staining? What is its clinical significance?
Each specimen obtained from a patient with an infectious process initially should be stained according
to the protocol developed by Hans Christian Joachim Gram. The process involves staining, decolorizing, and re-staining the specimen with a different stain. The organisms are categorized into one of
four groups based on their stain retention and morphology: gram-positive cocci, gram-negative cocci,
gram-negative rods, or gram-positive rods. Because Gram staining can be completed within a few
minutes, it usually narrows the list of likely causative organisms immediately, whereas culture and
sensitivity testing and biochemical identification may take 1 to 5 days to complete. After the staining
process, organisms that retained their initial stain will remain violet (gram-positive), whereas those
that lost the initial stain will be re-stained red (gram-negative).
290
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Box 28-1. Predominant Bacteria Found in the Oral Cavity
Aerobes Anaerobes
Gram-positive rods Gram-positive rods
Corynebacterium Actinomyces
Rothia Lactobacillus
Diphtheroids Propionibacterium acnes
Gram-negative rods Bifidobacterium
Eikenella corrodens Eubacterium
Haemophilus Clostridia
Enterobacteriaceae Gram-negative rods
Klebsiella Bacteroides
Pseudomonas B. gingivalis
Escherichia B. intermedius
Gram-positive cocci B. endontali
Streptococcus B. oralis
Alpha-hemolytic B. melaninogenicus
Strep. salivarius Fusobacterium
Strep. mitior F. nucleatum
Strep. sanguis Wolinella
Strep. mutans Capnocytophaga
Strep. milleri Gram-positive cocci
Beta-hemolytic Peptostreptococcus
Strep. pyogenes Streptococcus
Enterococci Gram-negative cocci
Staphylococcus Veillonella
Staph. aureus
Staph. epidermidis
Gram-negative cocci
Neisseria
Branhamella
Spirochetes
Treponema
Fungi
Candida
Adapted from Peterson LJ: Microbiology of head and neck infections, Oral Maxillofac Surg Clin 3:247–258, 1991.
8. Are there any factors that predict successful treatment and hospital length of stay
(LOS) of odontogenic infection in children?
In a recent study of 106 children with odontogenic infection, LOS was significantly shorter in patients
who had a tooth extracted within 48 hours versus patients who had a tooth extracted at 48 hours or
longer, and LOS was significantly shorter in patients with upper face and left face infections than lower
face infections and right face infections, respectively. Patients with a primary first molar infection had
the shortest LOS; patients with a white blood cell count less than 10,000 cells/mm3 had shorter LOS.
9. How do morphologic findings relate to bacterial categories?
See Table 28-2.
10. What is the pattern of progression of odontogenic infections?
Early infection is often initiated by high-virulence aerobic organisms (commonly streptococci), which
cause cellulitis, followed by mixed aerobic and anaerobic infections. As the infections become more
chronic (abscess stage), the anaerobic bacteria predominate, and eventually the infections become
exclusively anaerobic.
11. What is cellulitis?
Cellulitis is a warm, diffuse, erythematous, indurated, and painful swelling of the tissue in an infected
area. Cellulitis can be easy to treat but can also be severe and life threatening. Antibiotics and removal
of the cause are usually sufficient. Surgical incision and drainage are indicated if no improvement is
seen in 2 to 3 days, or if evidence of purulent collection is identified.
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