Management of complications of wisdom removal

1. Copy right 2021
Wisdoms complications
Copy Right 2024

2. Dr.Islam Kassem
BDS,MSc,MFDS RCS Ed, MOMS RCPS Glasg
FFD RCSI,FDS RCPS GLasg
Senior Consultant OMFS
Head of OMFS Alamin Hospital
Examiner for RCPS Glasg
Trainer in the Egyptian Fellowship
IMAXFAX center

3. Our team

4. • There is no conflict of interest in this lecture
• I have no monetary benefit from this lecture.
• No implied sponsorship by any company to the
speaker
• all photographed patients were treated by the
speaker and consented for photographing and
public publishing

5. My advice

6. Copy Right 2020
Wisdom of wisdoms

7. is a tooth that fails to erupt into its
normal functioning position in the
dental arch within the expected
time.
Impacted teeth

9. Alternatives to Removal
1. Restoration
2. Periodontal therapy
3. Operculectomy
4. Removal of another tooth
5. No treatment

10. Evaluation
Mesioangular Vertical Distoangular
Horizontal Inverted Transverse

11. Whinters lines

12. Principles of Surgery

14. Full thickness flap Partial thickness

16. Treatment and
Management

17. Lingual splitting
technique
I.Kassem

18. Minimal force please

19. ■ Formation of blood clot filling the socket.
■ Organization of the clot.
■ Epithelialization of the surface of the wound.
■ Formation of woven bone in the c.t. filling the socket (1 month → 2months in adult ).
■ Replacement of woven bone by trabecular bone and remodeling of the alveolus.
Healing of Extraction wounds

20. 1. Infection.
2. Prolonged bleeding due to a clotting
defect.
3. Formation of an oro-antral fistula.
4. Proliferation of a malignant tumor.
5. Radiotherapy.
6. Immunodeficiency.
7. Scurvy.
Delayed healing of extraction wounds

21. Damage with Electromagnetic Radiation
Two ways to cause damage
1. Ionizing radiation
• Able to break bonds (i.e. DNA causing mutations)
2. Intensity
• Thermal heating of tissue (i.e. microwave heating
food)

22. Energy Production - Components
NADH Dehydrogenase
ATP Synthase
Cytochrome bc1
Complex
Cytochrome c Oxidase
Red light at 660nm and Infrared light at 830/840nm
Cytochrome C Oxidase Absorption

23. Laser Therapy Dosage - Arndt-Shultz Law
Physiological
Activity
Strength of Stimuli
A B
C
D
A. No light gives no effect
B. Small amount of light also has no effect
C. Maximal effect at the apex of the curve
D. Inhibitory amount of light inhibits healing
Control
H+ H+
H+
H+
H+
H+
ADP ATP
Electron Transport Chain

24. Effect of Red and Infrared Light
H+ H+ H+ H+ H+ H+
H+
H+
H+
ADP ATP
Laser Therapy Effects
Primary
– The light is absorbed by
cytochrome c oxidase
Secondary
– Release of NO into
endothelium of blood
vessels
– Small increases in free
radicals
– Increased proton gradient
in mitochondria
Clinical
– Wound Healing,
Acceleration of the
Inflammatory Process and
Pain Influence
Put title of slide here

25. Low level laser management
of BRONJ case report
Laser Med Sci J ,2012
Kassem et Al

27. Immediate after surgical
repair

28. Complications of dental extraction
■ Local complications.
■ Systemic complications.
■ Intra – operative complications.
■ Post – operative complications ( immediate or delayed. )
■ Complications related to:
Patient factor, surgeon factor, surgery or instrumentations.

29. 1. Fracture of the tooth.
2. Fracture of the jaw:
a. Isolated molar.
b. Buried tooth.
c. Thin mandible – edentulous.
d. Excessive force.
Local complications

30. ikassem@dr.com

31. 3. Damage to soft tissue:
a. Instruments slips off the tooth.
b. Lower lip may be crushed between the teeth.
c. The handles of the forceps or pressure of the
hand supporting the jaw can cause bruising.
4. Opening of the maxillary antrum.
5. Fracture of the maxillary tuberosity.

33. 6. Loss of tooth:
a. Displaced into the loose tissue on the lingual
side of the lower molar.
b. May be swallowed.
c. May be inhaled.
7. Removal of a permanent tooth germ.
Extraction of deciduous molar with apical
infection which causes the permanent –
premolar tooth germ to become attached by
fibrous tissue to the periodontal membrane of
the overlying tooth.

35. 8. Excessive bleeding:
a. Tissue damaged – careless extraction.
b. As a result of haemorrhagic disease.
c. Infection.
9. Local infection:
a. Localised ostietis (dry socket ).
b. Osteomylietis.

36. 10. Loss of root fragement:
a. Displaced into the inferior dental
canal.
b. Displaced into the medullary
cavity.
c. Displaced into the antrum.
d. Displaced into a cystic cavity.

37. 11. Access:
a. Small mouth.
b. Crowded or mall-positioned teeth.
c. Trismus.
12. Pain:
a. Has L.A. worked – give more if needed.
b. Regional block – infiltration or inter-
ligumentary.
Intra – operative complications

38. 13. In ability to move the tooth:
X-Ray → :
a. Look for bulbous or diverging
roots.
b. Very long roots.
c. Ankylosis or sclerotic bone. 14.
Breaking the tooth or alveolar bone.
15. Damage to other teeth / tissues and
extraction of the wrong tooth.

39. Dislocation
Management
Hipocrate Method

40. New method

41. (The most frequent painful
complication of extraction )
Dry Socket ( Alveolar osteitis )

42. Aetiology:
Excessive trauma.
Impaired blood supply ( lower jaw > Upper jaw )
Local anaesthesia.
Oral contraceptive ( oestrogens component causes
increase in serum fibrinolytic activity)
Osteosclerotic disease.
Radiotherapy.
Smoking.

43. Pathology:
Destruction of the blood clot either by:
Proteolytic enzymes produced by bacteria.
Excessive local fibrinolytic activity.
Anaerobes are likely to play a major role.
Destruction of the clot leaves an open socket,
infected food and other debris accumulate.

44. ■ Pathology:
■ The necrotic bone lodges bacteria which
proliferate freely, Leucocytes unable to
reach them through the avascular
material.
■ Dead bone is gradually separated by
osteoclasts.
■ Healing is by granulation tissue from the
base of the walls of the socket.

45. Clinical features:
Pain usually starts few days after extraction.
Sometimes may be delayed for few days or more.
Deep – seated, severe and aching or throbbing in
character.
Mucous membrane around the socket is red and tender.
No clot in the socket ( Dry ).

46. Clinical features:
When debris is washed away, whitish, dead bone may
be seen or may be felt as rough area with a probe.
Sometimes the socket becomes concealed by
granulation tissue growing in from the edge.
Pain may continues for week or two and rarely longer.

47. ■ Prevention:
1. Minimal trauma.
2. Squeezed the socket edge firmly after
extraction.
3. In case of dis-impaction of 3rd molars
dry socket is more common:
- Minimum stripping of the periosteum.
- Minimum damage to the bone.
- Use prophylactic antibiotic.

48. ■ Prevention:
4. In patient who have had radiotherapy, every
possible precaution should be taken.
5. In osteosclerotic disease:
■ Little damage to bone (surgical extraction).
■ Prophylactic antibiotic.
6. Stop smoking for two days post extraction.

49. ■ Treatment:
■ Explain to the patient and warn them.
■ The aim of the treatment is to keep the
open socket clean and to protect the
exposed bone:
1. Irrigate the socket by antiseptic solution.
2. Fill the socket with an obtudant dressing
containing some non irritant antiseptic.
3. Frequent use of mouth wash.

50. ■ Treatment:
■ A great variety of dry socket dressing has been
formulated:
1. Iodoform - containing preparation.
2. Alvogyl – which is easy to manipulate.
( The dressing should be: Obtudant, antiseptic, soft
to adhere to the socket walls and absorbable ).
■ In many cases, irrigation of the socket and
replacement of the dressing has to be repeated
every few days.

51. IAN contains both sensory and motor fibres
Within the mandibular canal, the nerve is about 3
mm in diameter, and its course varies from person
to person
It can run with a gentle curve toward the mental
foramen, or it can have an ascending or descending
pathway (Snell, 2000)
A 2-mm safety zone between the apical part of the
implant and the upper border of the inferior alveolar
canal is strongly recommended by most implant
manufacturers and clinicians (Kraut and Chahal,
2002)
Nerve injury

56. Can happen concomitantly with bleeding of
the inferior alveolar artery, which could reduce
vision of the operating field and may cause
hematoma formation and compression of the
nerve trunk
Some authors suggest that infiltration
anaesthesia should be done without IAN block
To ensure that the patient has enough
sensation to realise when the drill trip is in
close proximity to the mandibular canal
(Annibali et al 2009).

59. Several methods used to localize the IAN to avoid its’ injury. These
include:
 Conventional radiography, tomography, and computerized tomography (CT)
 Surgical exposure of the mental nerve by blunt dissection to allow direct vision
of the nerve and to estimate the distance between the mandibular ridge crest
and the IAN, but the irregular intra-osseous course of the nerve limits the value
of this surgical technique (Anderson et al, 1991)
Clinicians must also bear in mind that the crest of the ridge may
contain very thin bone that cannot be used for implant support
(Alhassani and AlGhamdi, 2010)
In 70% of cases, IAN canal follows the lingual cortical plate of the
mandibular ramus and body (Kim et al,2009)
A bifid inferior alveolar canal has been reported (0.08 – 0.95%), it
can manifest more than one mental foramen on radiographs (Su-Gwan,
2011)

60. In posterior mandible region, the lingual nerve can be
damaged if the lingual flap that is raised is not retracted
carefully.
In 15-20% of cases, the lingual nerve is found at or coronal to
the crest of bone lingual to the mandibular third molar (Pogrel
and Goldman, 2004).
Is usually located 2 mm horizontally from the cortical plate in
the flap and 3 mm apical to the crest.
Is in contact with the cortical bony plate 22% of the time
(Behnia et al, 2000).

61. Is less likely to undergo spontaneous regeneration than is the
IAN, which is protected within the inferior alveolar canal
Easier to avoid damage to the IAN than to the lingual nerve,
which is not visualized on radiographs and whose relationship to
the posterior portion of the mandible varies (Kraut and Chahal,
2002)
To avoid its damage, an elevator should be used to protect the
nerve located in the flap underneath the periosteum, and the
elevated tissue should be managed gently to avoid inducing a
transient traction injury
If possible, lingual vertical releasing incisions should be avoided
(Greenstein et al, 2008)

62. Traumatic nerve injury and neurosensory impairment may occur intraoperatively or postoperatively; during
all phases of dental implant surgery, including anaesthetic administration, incisions, soft tissue reflection,
osteotomy preparation, bone augmentation, implant placement, suturing or even soft tissue swelling after
surgery Misch and Resnik (2012).
Local anaesthetic (LA) administration prior to implant therapy is responsible for 25%-29% of nerve injuries (Al
Sabbagh et al, 2015). Juodzbalys et al (2011) mentions 3 mechanisms by which this may occur:
Direct trauma to the nerve - barbing of the needle
Trauma to the epineurial blood vessels - causing haemorrhage and resultant compression of nerve fibres
Chemical damage from the anaesthetic and its components
Aetiological factors

63. Intraoperative (Direct)
1. Mechanical by injection needle, implant drill, root body, bone debris, haematoma and/or instrumentation, which may
have 2 effects :
A. Direct mechanical injury – pressure, encroachment, transection or laceration of the nerve itself
B. Indirect mechanical injury – haematoma, compression and secondary ischaemia
2. Thermal and Chemical factors will both cause direct nerve destruction
Postoperative (Indirect)
1. Thermal stimuli and Peri-implant infection will cause inflammation and secondary ischemia leading to degeneration
of the nerve structures
2. Haematoma can cause tissue scaring and secondary ischemia of the neurovascular bundle resulting in nerve
degeneration.
Aetiology for Inferior Alveolar Nerve injury

64. Classification of neuropathy
There is no classification of neural damage that is
particularly related to the oro-facial areas, but
peripheral nerve damage classification by Seddon and
Sunderland is however relevant in this region
In 1943, Seddon described a triple classification of
mechanical nerve injuries to characterize the
morphophysiologic types of mechanical nerve injuries.
Seddon’s classification is based on the time span and
completeness of sensory recovery

65. Neuropraxia: characterized by a rapid and virtually complete return of sensation or function, and no degeneration of the axon. It
may be the result of nerve trunk manipulation, traction, or compression of a nerve. Normal sensation or function returns within 1
week following the nerve injury. The response to this type of injury is paresthesia.
Axonotmesis: characterized by axonal injury with subsequent degeneration or regeneration. Traction and compression are the
usual mechanisms of this type of injury. These may cause severe ischemia, intrafascicular oedema, or demyelination. Complete
recovery can occur in 2 to 4 months, but improvement leading to complete recovery may take up as long as 12 months. The
psychophysical response to this type of injury is an initial anaesthesia followed by a paresthesia as recovery begins.
Neurotmesis: characterized by severe disruption of the connective tissue components of the nerve trunk with a serious
compromise to sensory and functional recovery. The cause of this injury is traction, compression, injection injury, chemical injury,
or in a complete disruption of the nerve trunk laceration and avulsion. The psychophysical response to this injury is immediate
anaesthesia. With this type of nerve injury there is a poor prognosis for recovery.
Seddon’s Classification

66. Sunderland (1951) classified nerve injury based on the degree of
tissue injury and further highlights the importance of each structural
component of the nerve trunk. He also further added on to the
Seddon's Classification in a sense, and divided Seddon's last stage
(neurotmesis) into three subcategories .There are therefore five
grades of nerve injury according to Sunderland's system (cited in
Juodzbalys et al, 2011).
The Seddon and Sunderland classifications were only made on the
anatomical positions of the nerve bundles and some authors (Renton
et al, 2013) mention that perhaps a new classification on injury
method (i.e. compression, stretching etc.) is necessary.

67. Happy birthday

69. Diagnosis
❑ Neural damage and its complications are extremely unpleasant for both the patient and the
dentist, with effects varying from mild paresthesia to complete anaesthesia and/or pain.
❑ Many functions such as speech, eating, kissing, make-up application, shaving and drinking could
be affected (Juodzbalys et al, 2011).
❑ Once it happens it is important for the clinician to recognise, diagnose and provide appropriate
care and management of these complications or disturbances.
❑ If a nerve injury is suspected, the clinician should perform a basic neurosensory examination of
the neuropathic area and ascertain whether the patient experiences pain, altered sensation or
numbness and document these findings.
❑ Renton and Devine (2013), discuss the greater clinical relevance as achieved when
the patients’ report is used, in combination with subjective and objective
neurosensory tests.

70. Key areas of assessment include:
 Pain – discomfort, altered sensation and numbness
(anaesthesia)
 Functional implications – eating, speaking, drinking, kissing,
tooth brushing or avoidance thereof
 Psychological – personality traits, anxiety, stress, post-
traumatic stress disorder, anger or paranoia

71. Renton and Devine (2013) outline a step by step patient
examination including clinical data reflecting patient
feedback as well as subjective clinical somatosensory tests:
1. Exam of extra-oral and intra-oral tissues
2. Confirmation of the dermatome affected – run closed
college tweezers over the affected dermatome from the
unaffected regions into the affected extra-oral and intra-
oral regions, whilst asking the patient to indicate (verbally)
when the sensation either decreases or increases.
3. Accurately map the neuropathic area, particularly intra-
orally as this may reinforce the diagnosis of the possible
cause of the nerve injury (local anaesthetic versus surgical
trauma) and record the percentage (%) of the dermatome
affected extra-orally and intra-orally.

72. 4. Identify the extent of injury: Size of neuropathic area – % of dermatome
affected by neuropathy
5. Identify any scarring of tissues associated with recurrent tissue trauma
6. Mechanosensory tests: The authors believe the most important neurological signs
worth detecting are:
Subjective function:
 Light touch: Using a tissue corner drawn gently over normal and neuropathic
areas.
 Sharp blunt discrimination: Positive response (>3 out of 5 repeats) using a
dental probe repeating alternating sharp/blunt stimulation while asking the
patient to differentiate compared with unaffected side.
 Pressure point pain
 Moving point allodynia: pain on moving tissue or sable brush over neuropathic
area
 Two-point discrimination can be undertaken crudely with college forceps and
normal parameters are published. Moving point discrimination using a Sable
brush no 9 compared with unaffected side.

73.  Elicited altered sensations and/or pain at rest and on stimulation:
A. Anaesthesia: no sensation on assessment
B. Hypoaesthesia: reduced sensation on assessment
C. Hyperaesthesia: increased sensation on assessment
D. Allodynia: pain response to nonpainful stimuli (usually to touch and or
cooling)
E. Hyperalgesia: increased pain response to painful stimuli (usually acute
enhanced discomfort to sharp blunt/pin prick test when compared with
normal unaffected side)
7. Radiation of altered sensory effects or pain
8. Additional thermal tests can be implemented using ethyl chloride or damp
tissue to confirm cold allodynia, which is a common sign for peripheral sensory
neuropathy.
Objective tests including somatosensory – evoked potentials, nerve conduction
studies and reflexes.

74. Subjective clinical sensory testing methods and
IAN structures assessed (Juodzbalys and Wang, 2011).

75. Chair-side Diagnosis
In a report by Svensson et al (2011) a simple chair-
side screening examination technique is proposed to
be used (without the need for sophisticated
equipment) or as a useful adjunct to the
comprehensive clinical sensory testing techniques as
discussed by Juodzbalys and Wang (2011) and
Renton and Devine (2013) in their diagnosis of
sensory disturbances.
Affected dermatomes – Mapping

76. Proposed screening examination of oro-facial
somato-sensory function (Svensson et al, 2012)
The patient is asked to report their
experience of spontaneous pain,
dysesthesia and paraesthesia and of
stimulus-dependent pain when
presented with a natural stimulus on
the tissues inside the mouth as well
as on the skin extra-orally.
The outcome can either be assessed:
 as “YES” or “NO” or
 measured on a scale of zero to five:
■ 0 =never,
■ 1 = hardly noticed,
■ 2 = slightly,
■ 3 = moderately,
■ 4 = strongly and
■ 5 = very strongly and is further compared to
the response from the same stimuli on the
contralateral, unaffected side.

77. For appropriate management of neural
complications, the exact cause of injury should be
established
If intraoperative (osteotomy preparation or during
implant placement) nerve injury is suspected, it must
be recorded, and a thorough neurosensory
examination should be performed as soon as the
local anaesthesia effect has worn off (Kraut and
Chahal, 2002).
Radiographs should be taken to ascertain the
implant’s position.
Management

78. Situations that can lead clinicians to suspect possible nerve
injury during surgery include:
 Pain, electric-shock type feeling or altered sensation during
bone drilling or implant placement
 slippage of the drill itself or implant deeper than planned
 sudden give during preparation (penetration of canal wall)
 presence of excessive bleeding, especially if nerve proximity
is suspected. If the inferior alveolar blood vessel is ruptured,
it may be advisable not to place the implant and to wait 2 –
3 days to ensure no nerve damage has occurred. The implant
can be placed thereafter into the formed granulation tissue
which should not compromise the success of the implant
(Khawaja and Renton, 2009)

79. On day following surgery, if a patient relates
symptoms of altered perception, it needs to be
determined whether they are due to:
 the presence of the root impinging on the nerve
 as a result of local anaesthesia
 soft tissue or buccal flap manipulation
 oedema (Greenstein et al, 2008).
Again, any of the above information must be
documented

80. If it is suspected that the implant is the cause of altered
perception, it should be removed as soon as possible
If the implant causing the problem is already
osseointegrated, it can be removed by a trephine drill
As an alternative, an apicectomy of the implant could even
be done
If uncertain with regard to implant penetration into a nerve
canal, a CT scan may be needed to provide additional
information
If the twist drill or the implant did not encroach upon the
canal, it is possible that bone was merely compressed,
thereby placing pressure on the nerve. The implant should
then be slightly withdrawn several turns (Greenstein et al,
2008)
This should also be done as soon as possible to prevent or
minimize permanent nerve damage

81. due to an inflammatory reaction in the injured nerve
To control this, a course of steroids can be prescribed:
Oral prednisolone of 1 mg per kg per day (maximum 80 mg) for first
week and then lowering the dose by 10 mg daily over the following week
An alternative would be a large dose of non-steroidal anti-inflammatory
drugs such as:
800 mg ibuprofen 3 times daily for 3 weeks
Adjunct drugs such as clonazepam, carbamazepine or vitamin B-
complex might alleviate neuritis via their known neuronal anti-
inflammatory actions(Khawaja and Renton, 2009)
If improvement is noted at three weeks on the basis of a repeated
neurosensory examination, the clinician can prescribe an additional three
weeks of anti-inflammatory drug treatment (Kraut & Chahal, 2002)

82. Perceptions of pain and temperature are usually the first 2
sensations to recover, whereas other sensations may take longer
Follow-up appointments should take place at 4, 8, and 12 weeks
after placement and each visit should include documentation of
subjective symptoms, oral-facial function and atrophic or
cutaneous changes
Any improvement in the patients’ condition should be recorded,
along with results of a neurosensory examination and the patient’s
description thereof
It is important medico-legally to document the level or depth of
neurosensory dysfunction at each visit

83. Patient should be referred for microsurgery if total
anaesthesia persists or if after 16 weeks, dysesthesia
(painful sensation) is still present
Early referral will allow for early management before
distant degeneration of the nerve takes place
Many studies have reported favourable patient responses
to IAN microsurgery. All have emphasized the need for
surgery before Wallerian degeneration (a process that
results when a nerve fibre is cut or crushed) of the distal
portion of the IAN has occurred; because this degeneration
is a slow process, and repair is possible even 4 to 6 months
after the injury has occurred (Kraut & Chahal, 2002)

84. Strauss et al in 2006 concluded that 50% of the patients
who underwent microsurgical repair of the IAN reported
significant improvement,
42.9% reported slight improvement,
and only 7.1% reported no improvement.
They also reported that highly significant improvements
were still achieved after 1 year of microsurgical intervention.

85. The patients’ ability to cope with the neuropathy and
pain, functional problems and their psychological
status will direct the need for intervention
Most patients present with neuropathic pain post-
therapy and are managed with medication and
counselling or reassurance
Nerve injuries can have a significant negative effect on
the patients’ quality of life and the fact that it was
caused by the clinician would compounds the negative
psychological effects for these injuries
Patients need psychological treatment which involves
immediate explanation of the situation, professional
support and realistic expectations on the way forward

86. Laser Therapy
Historically referred to as:
• LLLT (low level laser therapy)
• LILT (low intensity laser therapy)
• Laser Biostimulation
• Low power laser therapy
• Cold laser therapy
• Note: LLLT best term for searching PubMed,
the Nat’l Institutes of Health Public database
• Search: “ PubMed “

87. Contact is Most Effective
Treatment Technique
NON-CONTACT:
DEEP
CONTACT:
DEEPER
CONTACT WITH
PRESSURE:
DEEPEST
Laser vs. Ultrasound (US)
● LLLT better than low-intensity pulsed ultrasound
(LIPUS) or US on bone repair
○ LLLT created repair bone →formation
○ LLLT produced healthier, stronger bone
○ LIPUS →bone resorption (weaker)
J Rehab Res & Dev, Volume 41 Number 5, September/October 2004
Photomed Laser Surg. 2006 Dec;24(6):735-40
Lasers Med Sci. 2010 Jun 3.

88. Laser vs. Ultrasound
● LLLT more effective than US.
● Better ↓ symptoms, pain and faster healing.
● Laser more effective than US at stim healing, reducing
pain.
Photomed Laser Surg. 2009 Jan 26.
Laser vs. Electrical Stimulation
FACT: Laser more effective at pain reduction &
stimulating healing than electric stim.
● Phys Ther. 2006 Jul;86(7):955-73.
● J Appl Oral Sci. 2006 Apr;14(2):130-5
● Photomed Laser Surg. 2006 Feb;24(1):45-9.
FACT: Laser as effective or more effective than electric
stim and electrical acupuncture.
● BMC Musculoskelet Disord. 2007 Jun 22;8:51.
● FACT: Effective to use electrical stimulation while
painting with laser; accomplishes a synergistic effect.
● J Appl Oral Sci, Apr;14(2):130-5.

90. Islam Kassem
ikassem@dr.com
01559900333