Q1)Dry socket

 Introduction
o Also called as Fibrinolytic alveolitis;alveolar osteitis, localized osteitis alveolalgia, alveolar
Osteomyelitis.
o It involves part or whole of the walls of socket; or the lamina dura.
o Geoffrey Howe, defined it as well recognized, but ill understood complication of extraction of
teeth.
 Characteristics:
o The condition is characterized by acute pain, bony walls of the socket are denuded of blood clot
 Etiology:
o Not clear/obscure.
o Trauma and infection; together.
 They cause inflammation of marrow spaces of alveolar bone.
 That liberates tissue activators which convert plasminogen in blood clot to plasmin. This
dissolves blood clot and releases kinins from kininogen; which is present in blood clot.
 The final result is of dissolution of blood clot and severe pain
 Predisposing factors:
o Infection of socket occurring either before, during or after the extraction— may be an exciting
factor
o Trauma: It is true that the condition may follow the use of excessive force during extraction.
o Vasoconstrictors: vasoconstrictors used in LA solution may predispose to dry socket, by
interfering with blood supply of bone, and they point out that the condition occurs more
frequently under LA than GA. Thus, vasoconstrictors cannot be the basic cause of the condition,
but may well be a contributing factor
o Mandibular teeth show higher incidence of dry sockets than maxillary teeth. Mandible has much
more dense bone and is less vascular than,maxilla.
o Bacteriological origin: A number of bacteria are known to possess fibrinolytic activity.
Treponema denticola may have an etiological role in the genesis of dry socket
o Pregnant women and those taking oral contraceptives appear to be more susceptible than
others
 Precaution
o Scaling of the teeth; any gingival inflammation should be treated prior to extraction
o Minimum amount of local anesthetic solution necessary for producing analgesia should be
administered
o Teeth should be removed in the least traumatic manner possible
o Prophylatic use of antibiotics especially metronidazole from the day of extraction for 3–4 days
reduces the incidence of dry socket significantly. It also has been shown to provide prompt relief
from pain; if given in large doses for 5 days
 Management
o Wound debridement
 o Nerve blocks—preferred to LA infiltration
o Aim: (i) Relief of pain, and (ii) Speed of resolution
o Procedure:
 Irrigation of debris and debridement:
 Socket is irrigated with warm normal saline and all degenerating blood clots are removed.
 Sharp bony margins should be either excised with rongeur forceps or smoothened with a bone
file or a drill
 Medicated dressing/Iodoform gauze or composed of zinc oxide eugenol on cotton wool should
be packed loosely and not tightly; as it may set hard and be difficult to remove. The dressing is
composed of: Eugenol, Balsam of Peru, Chlorobutanol, and Benzocaine
 Dressing—first 24 hours; then every alternate day; then every 3–4 days for more than 2 weeks
 Broad-spectrum antibiotics
 Other measures: Analgesics, and hot saline mouth baths
 Regular follow-ups
 If pain persists; it may require chemical cauterization of exposed bare painful bone
 Procedure:
 Isolation and drying of dry socket
 Application of small quantity of carbolized resin on the bony walls of the socket
 Zinc oxide eugenol cotton wool dressing is inserted over the caustic and left in situ for 3 days.
 The dressing relieves pain, but delays healing.
 Alternatively, Whitehead’s varnish on a piece of ribbon gauze can also be used and left in situ for
2–3 weeks. It is not very effective in controlling pain. At the time of removal of the pack the
socket will be seen granulating

Q2)Syncope

 Description
o Syncope is the most commonly encountered medical emergency in dental practice.
o Syncope is defined as sudden, transient loss of consciousness with spontaneous recovery.
o Extreme anxiety, fear, and pain are common predisposing factors in a dental setting.
o There is inadequate supply of blood to the brain due to vagus mediated reflex bradycardia with
or without peripheral vasodilatation.
o The signs and symptoms of syncope include light headedness, dizziness, pallor, nausea,
sweating, visual disturbances and fainting.
o Pulse is slow and feeble due to bradycardia and hypotension.
o Stress reduction protocols for managing anxiety, good communication, and reassurance are
effective tools to prevent episodes of syncope.
o The management consists of positioning the patient into supine position with legs slightly raised.
Aromatic ammonia from the emergency kit may be used as respiratory stimulant. This increases
the cerebral perfusion and the patient quickly regains consciousness. Patient’s airway should be
assessed and other vital signs monitored. Oxygen may be administered through Ventimask® or
nasal cannula.
Q3)Tooth extraction in a diabetic patient

 Introduction
o Diabetes mellitus is caused by an absolute or relative deficiency of insulin in the body.
o It can be classified into type 1 (insulin dependent) and type 2 (noninsulin dependent).
o Type 1 is more commonly seen in young patients and type 2 in adults.
o A patient can be classified as a diabetic, when his fasting glucose levels are constantly above 140
mg/dL.
o The nature of problems faced by the surgeon during the management of a known diabetic
patient is:
 Optimal blood sugar levels are to be maintained during the procedure, as well as
postoperatively to prevent hypoglycemia or hyperglycemia and ketoacidosis. Both the
conditions may be lifethreatening to the patient.
 The patient is prone to infections and has to be given adequate preoperative and postoperative
broad-spectrum antibiotic coverage to prevent infections.
 The patient may have additional systemic complications like renal failure, cardiac disorders,
ophthalmic problems and generalized vascular disease due to long-standing diabetes.
o For surgical purpose, a diabetic can be classified in three groups:
 Sugar levels controlled by diet and oral hypoglycemics.
 Sugar levels controlled by insulin.
 “Brittle diabetes”, usually of juvenile onsets, whose metabolic needs are labile and have
sequelae of long-standing disease such as renal failure, retinopathy, and generalized vascular
disease.
o Elective surgeries can be usually performed without complications in the first two types. In the
third type, although the management remains same, a more rigid control is to be exercised
intra- and postoperatively.
o Preoperative Investigations
 Chest radiograph—posteroanterior view
 Electrocardiogram
 Blood investigations like:
 Blood sugar fasting and postprandial
 Glucose tolerance test
 Renal profile: Such as blood urea nitrogen, serum creatinine, serum electrolytes.
 Urine analysis for sugar and acetone.
 If the patient is on oral hypoglycemics, he must be shifted to insulin on the day of surgery. The
general principle for the management of the patient under general anesthesia is to provide at
least 200 g of carbohydrate with adequate insulin to cover this need.
o Intra- and Postoperative Management
 Check the patient’s blood and urine sugar levels on the morning of surgery, with the help of
hemoglucose strips and urostrips or glucometer.
  Prepare a sliding insulin scale to be followed intraoperatively based on the patients sugar levels
 Pre- and postoperative broad-spectrum antibiotic coverage.
 Intra- and postoperative close monitoring of the blood and urine sugar levels.
 Prevent the patient from going into ketoacidosis or hypoglycemia.
 Signs of hypoglycemia: The patient is apprehensive, restless, agitated, the skin is moist and pale,
and there is tachycardia. The patient then lapses into coma.
 Treatment:
 In a conscious patient, oral carbohydrates are given to correct the glucose levels.
 In an unconscious patient, intravenous administration of 50% glucose solution restores
consciousness in 5–10 minutes or 1 mg glucagon IM restores consciousness in 15 minutes.
 Signs of diabetic ketoacidosis: Vomiting, tachypnea, Kussmaul (deep, rapid breathing at regular
intervals) breathing, dehydration and circulatory collapse.
 Treatment:
 Administration of insulin to normalize body metabolism and restoration of body fluids and
electrolytes.
 Shift the patient at the earliest possible to his regular oral feeds and antidiabetic medications.

Q4)Ludwigs angina

 Description
o It is the name given to a massive, firm, brawny cellulitis/induration, and acute, toxic stage,
involving simultaneously, the submandibular, sublingual and submental spaces bilaterally.
o It was first described by Wilhelm Friedreich Von Ludwig (1836).
o As the definition suggests, only the bilateral involvement of above mentioned spaces is
considered to be classical, disease entity.
 Etiology

The following causes can be attributed to Ludwig’s angina:

o Odontogenic: This is the cause in majority of cases

 The most common teeth involved are mandibular 2nd and 3rd molars.
 Acute periodontal abscess: Deep abscess may involve sublingual spaces.
 Acute pericoronal abscess: In relation to erupting mandible 3rd molars, which can extend to the
following spaces:
 Submandibular space
 Buccal space
 Sublingual space
 Pterygomandibular space.
 Infected mandibular cyst also can spread to form Ludwig’s angina.
o Iatrogenic: Use of a contaminated needle for giving local anesthesia.
o Traumatic injuries to orofacial region: These can be in the form of: (a) mandibular fractures, the
chances of developing Ludwig’s angina are more, if the fracture is compounded and
comminuted, (b) deep lacerations or penetrating injuries such as punctured wounds.
 o Osteomyelitis secondary to compound mandibular fractures; or acute exacerbation of chronic
osteomyelitis of mandible may develop into Ludwig’s angina.
o Submandibular and sublingual sialadenitis : Acute or chronic infection from these glands.
o Secondary infections of oral malignancies: The associated malignancies of the region may give
rise to secondary infection, leading to the condition.
o Miscellaneous causes: It includes rare causes such as:Infection in the tonsils or pharynx such as
purulent tonsillitis, etc.Foreign bodies such as fish bone, etc.Oral soft tissue lacerations.
o Cervical lymphoid tissues.
 Pathology
o The condition is a cellulitis—a diffuse inflammation of soft tissues which is not circumscribed or
confined to one area, but in contrast to the abscess, tends to spread through tissue spaces and
along fascial planes.
o Such type of spreading infection occurs in the presence of organisms that produce significant
amounts of hyaluronidase and fibrinolysins, which act to break down or dissolve, respectively
hyaluronic acid and fibrin.
o Streptococci, being the potent producers of hyaluronidase are always associated with classical
or true Ludwig’s angina.
 Involvement
o Most cases originate in association with mandibular second and third molars.
o The bone around these teeth is usually thicker on the buccal aspect than lingual side.
o The apices of these teeth are placed below the mylohyoid line of mylohyoid muscle, so that
infection tends to spread primarily to submandibular space. Hence, the submandibular space
plays a vital role in development and progress of the disease.
o The subsequent spread of the disease is determined by the muscles in the area.
o The condition usually follows a submandibular space infection caused by a periapical infection,
or pericoronitis around mandibular third molar.
o The infection then spreads to the sublingual space on the same side, around the deep part of
the submandibular gland.
o The submental space is involved by lymphatic spread. The condition can also occur in converse
manner, i.e. by spread from the sublingual spaces to the submandibular spaces
 Clinical Features

The following signs and symptoms are present with varying degree of severity

o General examination: It includes: (i) general constitutional symptoms: patient looks toxic, very ill
and dehydrated. There is pyrexia, anorexia, chills, and malaise; (ii) marked pyrexia; (iii) difficulty
in swallowing (dysphagia); (iv) impaired speech, and hoarseness of voice.
o Regional examination:
 Extraoral examination
 Firm/Hard brawny (board-like, woody hard) swelling in the bilateral submandibular and
submental regions, which soon extends down the anterior part of the neck to the clavicles.
 Swelling is nonpitting, minimally or nonfluctuant associated with severe tenderness.
 Classically, the swelling shows ill-defined borders with induration.
 Severe muscle spasm may lead to trismus with restricted mouth opening and also jaw
movements.
 Typically mouth remains open due to edema of sublingual tissues leading to raised tongue
almost touching the palatal vault.
 In extreme circumstances, tongue may actually protrude from the mouth; the tongue
movements are reduced.
 Airway obstruction.
 Respiratory rate may be seen to be raised; breathing being shallow with accessory muscles of
respiration being used.
 There may be dilation of alae nasi, raising of thoracic inlet by the scalenes and
sternocleidomastoid muscles and in-drawing of the tissues above the clavicle.
 Cyanosis may occur due the progressive hypoxia
 Fatal death may occur in untreated case of Ludwig’s angina within 10–24 hours due to asphyxia.
o Intraorally, the swelling develops rapidly, which involves (i) the sublingual tissues, and distends
or raises the floor of mouth, woody edema of the floor of the mouth and tongue (ii) tongue may
be raised against palate; (iii) increased salivation, stiffness of tongue movements, difficulty in
swallowing; (iv) backward spread of infection leads to edema of glottis, resulting in respiratory
obstruction/embarrassment.
 Stridor being the alarming sign of this fatal extension needing emergency intervention to keep
airway patent.
 There is reduced control of muscles and jaw posture— salivation is excessive and saliva may be
even seen drooling.
 Part of the tongue may get pushed backward making swallowing even liquid very difficult or
even impossible.
 Oral opening and jaw movements may be reduced.
 Progressive dyspnea is caused by backward spread of infection, until in the untreated case,
edema of the glottis causes a complete respiratory obstruction.
 Spread
o From the sublingual spaces, the infection may spread backwards in the substance of the tongue
in the cleft between the hyoglossus and genioglossus muscles along the course of sublingual
artery. By this route the infection reaches the region of epiglottis and produces swelling around
the laryngeal inlet.
o Due to anatomical continuity of various spaces with submandibular space, the infection may
track to submasseteric, and pterygomandibular spaces; and more posteriorly, parapharyngeal,
paratonsillar spaces; and worsening airway compromise.
o Infection from the submandibular region, can spread downwards along and beneath the
investing layer of deep cervical fascia, towards clavicle and subsequently to mediastinum
o Uncommonly, infection can spread below and reach close to carotid sheath, pterygopalatine
fossa, leading to cavernous sinus thrombosis with subsequent meningitis.
 Fate of Ludwig’s Angina
 o Ludwig’s angina, if untreated, can be fatal within 12–24 hours; death arising from asphyxia.
o Established cases may become more complicated with involvement of other spaces. The other
causes of death include: septicemia/ septic shock, mediastinitis, and aspiration pneumonia,
which are also caused by the complications of the disease.
 Principles of Treatment
o It should be taken as a life-threatening emergency situation. It is best treated by aggressive
intervention.
o The treatment is based on the combination of the following factors:
 early diagnosis,
 maintenance of patent airway,
 intense and prolonged antibiotic therapy,
 extraction of the offending teeth, and
 surgical drainage or decompression of fascial spaces.

Q5)Heat and cold therapy in oral surgery

 Description
o In Oral surgery heat and cold therapy is very important both in preoperative and postoperative
conditions.
o In the large majority of cases, it is practically indispensable. The actual application of hot or cold
compresses, of course, is usually performed by the nursing staff; but the oral surgeon, who has
assumed the responsibility of a surgical operation, is equally responsible to prescribe the proper
procedure of the application of the heat or cold, as he would be to prescribe other medication.
o The theory of heat and cold therapy is not difficult to understand
o Heat or cold, properly applied, is very helpful and will make the patient more comfortable.
o Heat and cold therapy is used routinely for hospitalized patients in all oral surgery cases, and, as
a rule, it is quite well understood by those in charge when heat or cold should be applied; but on
account of the possibility of a misunderstanding, the oral surgeon should check daily, and be
sure that the proper treatment is being carried out.
o Heat and cold therapy is indicated in inflammatory and infectious processes, which should be
thoroughly understood.
o Inflammation is the direct result of injury to human tissue ; it is defined as a succession of
phenomena exhibited in living tissue following trauma or bacterial invasion.

Q6)Alveolar abscess

 Introduction
o It is inflammatory reaction in pulpal infection and necrosis characterized by rapid onset
,spontaneous pain, tenderness of the tooth to pressure ,pus formation and eventual swelling of
associated tissues.
 Causes
o Trauma-Chemical or mechanical
o Bacterial invasion of dead pulp tissue from carious lesion
o Failed RCT
o BACTERIOLOGY • Streptococci • staphylococci •
 Symptoms
o First symptom maybe Tenderness of the tooth that maybe relieved by continued slight pressure
on the extruded tooth to push it back to the socket.
o Later patient has severe throbbing pain with swelling of overlying tissue.
o The tooth become more painful ,elongated and mobile
o As the infection progresses the swelling enlarges
o If left untreated the infection may progress to chronic apical abscess wherein the contain pus
may break through to form a sinus tract usually opening in the labial or buccal mucosa.
o It may further progress onto osteomyelitis or cellulitis.
o General systemic manifestation maybe seen
 patient appear pale, weakened from pain and loss of sleep.
 Pyrexia and patient may complain of headache
 Diagnosis
o By clinical examination and subjective symptoms given by the patient.
 Radiographic
o shows defective restoration or cavity
o Shows widening of the pdl space
 Diagnosis confirmation
o Electric pulp test or by thermal test
o The tooth doesn’t respond to electric pulp test or cold test
o Tender to percussion ,apical mucosa is tender to palpation and the tooth maybe mobile and
extruded
 Differential diagnosis
o Periodontal abscess -vital tooth periodontal pocket formation pus may exude from the sulcus on
pressure respond to vitality test Caries may not be present
 Treatment
o Surgical treatment
 Immediate Rx is incision and drainage
 Trephination maybe required
 If non restorable extraction is indicated
o Endodontic treatment
 Root canal treatment followed by crown
o Pharmacotherapy
 ANALGESIC AND ANTI-INFLAMMATORY NSAIDs
 Ibuprofen 200-800mg/ Diclofenac (sodium/potassium) 50-100mg
 DYNAPA-AQ 75mg IM
 OPIOIDS -Tramadol 50mg Codeine 60mg
 ANTIBIOTIC -Caps Amox 500mg or any appropriate antibiotic
 o Post operative instructions
 Avoid chewing sticky foods .
 Avoid biting hard foods and hard substances.
 If possible, chew only on the opposite side of your mouth.
 Take medication as recommended by your dentist
 Rinse three times a day with warm salt water
 Maintain good oral hygiene

Q7)Bell’s palsy

 Definition:
o It is defined as an idiopathic paresis or paralysis of the facial nerve of sudden onset (unilateral
lower motor neuron paralysis of sudden onset, not related to any other disease elsewhere in the
body).
 Sex predilection: Women are more affected than men.
 Age: It can occur at any age but more seen in the middleaged people
 Side involvement: It can be equally seen involving the right or left nerves. It is unilateral
 Etiology
o Although Bell’s palsy, by definition, is an idiopathic condition, there are abundant etiological
theories put forward from abnormal immune response to reactivated herpes simplex virus in
the geniculate ganglion.
 Clinical Features
o There is sudden onset; usually, patient gives history of occurrence after awakening early in the
morning.
o Unilateral involvement of the entire side of the face is seen.
o Abrupt loss of muscular control on one side of the face.
o Inability to smile, close the eye, or wink or raise the eyebrow on the affected side.
o Whistling is impossible.
o The corner of the mouth droops, causing drooling of saliva.
o In an attempt to close the eyelid, the eyeball rolls upward, so that the pupil is covered and only
the white sclera is visible (Bell’s sign).
o Inability to wrinkle the forehead or elevate the upper or lower lip.
o The eye waters due to inability to close.
o There is widening of the palpebral fissure, loss of blinking reflex.
o There is obliteration of the nasolabial fold.
o The face appears distorted and mask-like appearance to the facial features.
o Speech becomes slurred.
o Occasionally, there is loss or alteration of taste.
 Prognosis
o Initially, unilateral facial weakness affecting all parts of the facial musculature is noticed. This
gradually worsens over 2–3 days, reaching a maximum in about 2 weeks.
o Remission begins within 3 weeks of onset in 85% of cases with remainder taking as long as 6
months. Spontaneous recovery is known to occur in Bell’s palsy.
 Management
o Physiotherapy:
 The effect of facial paralysis or Bell’s palsy is wasting or muscle atrophy.
 Physiotherapy is, therefore, indicated to maintain the muscle tone and should be instituted as
early as possible.
 It consists of electrical stimuli by galvanism, gentle massage and facial exercises.
o Medication
 If the patient is seen within 2–3 weeks of onset of symptoms:
 Tab prednisolone in doses of 1 mg/kg for 10–14 days has been recommended with a gradual
tapering.
 Vitamins B1, B6, B12 may be administered. If the patient is seen after 3–4 weeks, then steroid
therapy is of no use.
o An audiogram should be performed; a CT or MRI and an EMG should be considered.
o If incomplete eye closure is present, artificial lubrication, taping the eye or perhaps the
placement of a spring, gold weight or tarsorrhaphy might prevent visual loss from exposure
keratitis.
o A baseline ophthalmologic examination is often helpful to determine further therapy.
o Chronic sequelae—may be in the form of hyperkinesia or hypokinesia.
 In hyperkinesia—offending muscle groups are denervated or botulinum toxin can be used.
 Clostridium botulinum toxin (Botox) is a neurotoxin, that temporarily interferes with
acetylcholine release from motor nerve endplates, causing skeletal muscle paralysis. The effect
lasts 4–6 months. Botulinum toxin has been useful in the treatment of facial paralysis by
weakening the contralateral side to allow centering of the mouth, more symmetry on smiling
and treatment of hypertrophic platysmal bands.
 Hypokinesia may require nerve transfers, muscle transfer or static slings.
o If electroneurography reveals a greater than 90% loss of compound action potential within first
2 weeks following onset of paralysis, facial nerve decompression is recommended. After this
period, surgery is not beneficial.
o Nerve decompression—can be carried out internally or externally.
o Internal decompression: The nerve is exposed in the fallopian canal; pressure in the canal is
relieved by exposing the nerve and the epineural sheath is opened to visualize the nerve fibers
and release adhesions or re-establish continuity.
o External decompression—is done by releasing of epineural sheath from surrounding scar tissue,
bone or a foreign body.
o Nerve anastomosis—reanimation: Anastomosis of the central end of hypoglossal or spinal
accessory nerve with the distal end of the facial nerve is done.
o Nerve grafting: Whenever there is evidence of neuroma or loss of portion of a nerve, nerve
grafting can be considered.
Q7)Inferior alveolar nerve block

Pterygomandibular Block

Other common names: Inferior alveolar nerve block,

mandibular nerve block.

Nerves anesthetized:

Inferior alveolar nerve along with its terminal branches:

(i) incisive nerve and (ii) mental nerve.

Lingual nerve.

Long buccal nerve (Figs 9.21A and B).

Areas anesthetized:

Inferior alveolar nerve: It supplies (i) mandibular

teeth up to the midline, (ii) body of the mandible,

(iii) inferior portion of the ramus of the mandible,

(iv) buccal mucoperiosteum, mucous membrane,

anterior to mandibular first molar, and (v) skin of the

chin, skin of lower lip, and mucosa of lower lip.

Lingual nerve: It supplies (i) mucosa of anterior

two-thirds of the tongue, (ii) mucosa of floor of the oral cavity, (iii) lingual soft tissues and periosteum,

(iv) sublingual and submandibular salivary gland.

Long buccal nerve: It supplies (i) buccal

mucoperiosteum in the region of mandibular molars

or buccal mucoperiosteum posterior to mental

foramen, (ii) adjacent part of vestibular mucosa,

(iii) adjacent part of buccal mucosa, (iv) mucosa of

retromolar fossa.
Indications:

Procedures of multiple mandibular teeth in one quadrant.

When buccal soft tissue anesthesia is required

(anterior to mandibular first molar).

When lingual soft tissue anesthesia is required.

Contraindications:

Acute inflammation or infection in the area of injection.

Patients who might bite either the lip or the tongue

(young children or mentally handicapped adults).

Anatomical landmarks:

Soft tissue landmarks:

Sulcus mandibularis, mucobuccal fold in the region of

mandibular premolars and molars

Buccal pad of fat

Retromolar triangle area

Pterygomandibular raphe (Fig. 9.22A).

Bony landmarks (Fig. 9.21B):

External oblique ridge

Internal oblique ridge

Anterior border of ramus of the mandible

Coronoid process

Coronoid notch

Occlusal plane of mandibular molars, and

Contralateral premolars.

Approximating structures when needle is in final position:

Superior to the following: Inferior alveolar vessels

and nerve, insertion of the medial pterygoid muscle,

mylohyoid vessels and nerve.

Anterior to the deeper lobe of the parotid gland.

Medial to the medial surface of ramus of the mandible.

Lateral to the following: Lingual nerve, medial

pterygoid muscle, sphenomandibular ligament.

Types of techniques: There are two techniques:

1. Direct technique: In this technique, the inferior

alveolar nerve is anesthetized first, hence it is known

as “direct technique”.

2. Indirect technique: In this technique, the inferior

alveolar is anesthetized in the third position. It is also

known as three positional block technique.

Technique for locating the landmarks: A 25 gauge

long needle is recommended. The target area is the

inferior alveolar nerve as it passes downward toward the

mandibular foramen, but before it enters the foramen

(Fig. 9.22B). For the right-sided block, the operator sits/

stands (at 8 o’clock position facing the patient). For the leftsided

block, the operator sits/stands at 10 o’clock position

by the side of the patient.

The height of injection:

Place the index finger or thumb of the left hand on the

external oblique ridge or the anterior border of the

ramus of the mandible.

When the finger contacts the anterior border of the

ramus, it is moved up and down until the greatest

depth of the anterior border of the ramus is identified.

This area is called the coronoid notch.

An imaginary horizontal line extends from the

coronoid notch to the pterygomandibular raphe and

determines the height of injection and is parallel to

and 6–10 mm above the occlusal plane of mandibular

molars.

The palpating finger is then moved lingually across

the retromolar triangle and onto the internal oblique

ridge. The finger, still in line with the coronoid notch

and in contact with the internal oblique ridge, is moved

to the buccal side, taking with it the buccal sucking pad.

This gives better exposure to the internal oblique ridge,

the pterygomandibular raphe and the pterygotemporal

depression.

When palpating the intraoral landmarks with the

thumb/finger, the operator may place the index finger/

thumb extraorally behind the ramus of the mandible, thus

holding the mandible between the thumb and the index

finger. In this manner, the anteroposterior width of the

ramus may be assessed.

Direct technique: The syringe and the needle is then

inserted at the previously described height of insertion

from the opposite side the mouth, at a level bisecting the

finger and penetrating the tissues of the pterygomandibular

space.

The depth of the needle penetration can be determined

by estimating when the tip of the needle has been

advanced half the distance between the palpating thumb

and index finger. During insertion, the patient is asked to

keep the mouth wide open. The needle is penetrated into

the tissues until gently contacting bone on the medial

surface of the ramus of the mandible.

The needle is then withdrawn about 1 mm, aspiration

done, to avoid intravascular administration of the solution,

and 0.8–1 mL of the solution is deposited slowly (in 60

seconds). The needle is then withdrawn slowly and when

about one-half of its inserted depth has been withdrawn,

the syringe is taken on the ipsilateral side, without

withdrawing the needle outside the mucosa, 0.5 mL of the

solution is injected in this area to anesthetize the lingual

nerve (Figs 9.23A to C).