TOOTH MOBILITY

Introduction
Healthy gums and teeth are essential for the power of speech and beautiful smile.

“Mouth is the mouthpiece of mind”.

Mobile teeth are concerned not only for the patient, but also to the dentist, because it is the critical stage where the tooth lies between two “S” i.e. to be saved or sacrificed.

Tooth mobility is an important feature of periodontal disease. This is evidenced by the large number of devices and method of tooth mobility assessment that have been developed and tested. Tooth mobility has been considered and investigated as an indirect measure of the functional condition of the periodontium as well as possible aggravating co-factor for periodontal disease. Tooth mobility is considered to be of paramount significance of establishment of diagnosis, prognosis and treatment plan.

Definitions
The degree of looseness of tooth beyond physiologic movement.

TERMINOLOGIES
1. Physiologic / Normal Mobility
It refers to the limited tooth movement or tooth displacement that is allowed by the resilience of an intact and healthy periodontium when a moderate force is applied to the crown of the tooth examined. (Muhlemann 1951).

2. Pathologic tooth mobility
It is any degree of perceptible movement of a tooth faciolingually, mesiodistally or axially when a force is applied to the tooth. (M.J. Perlitsh 1980)

3. Altered tooth mobility
It is an alteration of the mobility characteristics of a tooth, which represents a transient or permanent change in periodontal tissues. (Giargia and Lindhe 1997). An increased TM may be associated with different physiologic or pathologic phenomena while decrease mobility usually is result of therapy.

4. Functional mobility
Functional mobility is the movement of teeth during function or parafunction.
5. Normal tooth mobility
It is more during early mornings and progressively decreases. Muhlemann (1960) reported that tooth mobility was 0.4 – 0.12 mm for 500 gm force applied. The incisors have the highest (0.1 – 0.12 mm) and molars the lowest (0.4 –0.8mm). Children and females exhibit higher values than adults and males respectively.

6. Increased / Static tooth mobility
It is a form of stabilized mobility. It is usually due to TFO, but may be due to periodontal diseases. But the periodontal structures have become adapted to an altered functional demand. It is self limiting and normal for that tooth with remaining bony support.

7. Increasing / Progressive tooth mobility
It is of progressive nature and can be identified only through a series of repeated tooth mobility measurements carried out over a period of several dogs or weeks.

8. Hypermobility
A form of increased mobility persisting after completion of periodontal treatment. It is often referred to as “residual mobility”. It has 2 phases, a developing phases and a permanent phase.

9. Reduced tooth mobility
As seen in ankylosed tooth after failing replantation or if autogenous bone grafts are placed in contact with detached root surface.

STAGES OF TOOTH MOBILITY
Tooth mobility occurs in 2 stages, namely
1) Initial / Intra socket stage (ITM)
2) Secondary stage (STM)

 Initial / Intra socket stage (ITM):
When a small force is applied to the crown of a tooth, the resistance of tooth supporting structures against displacement of root is low in the initial phase of force application and crown is moved by 0.5 mm to 0.1 mm which was called initial tooth mobility (ITM) by Muhlemann (1954) and is the result of intra alveolar displacement of root.

ITM depends on structure and organization of periodontal ligament. In the pressure zone there is a 10% reduction in the width of the periodontal ligament and in the tension zone there is a corresponding increase. The magnitude of the “Initial tooth mobility” varies from individual to individuals from tooth to tooth, and is mainly dependent on the structure and organization of PDL. The ITM value of ankylosed teeth is therefore zero.

Secondary stage (STM) :
When a large force (up to 500 pounds) is applied to the crown, the fiber bundles on the tension side can not offer sufficient resistance to further root displacements. The additional displacement of the crown that is observed in “Secondary tooth mobility” is allowed by distortion and compression of the periodontal ligament in the pressure side.

Aetiology
Local and systemic factors are implicated.
Local factors:
1. Bone loss or loss of tooth support:
2. Trauma from occlusion:
3. Hypofunction:
4. Extension of inflammation from the gingiva or from the periapex into the periodontal ligament
5. Periodontal surgery temporarily increases tooth mobility
6. Pathology of jaws like tumors, cysts, ostemylitis etc.
7. Tooth morphology (Crown and root shape)
Flat contacting surface – thin, narrow septa – less bone support.
Convex or bell shape – flat and wide septa more bone support increase in number, size of roots – more one support.
8. Overjet and over bite are directly proportional to tooth mobilit

9.The spread of inflammation from an acute periapical abscess may increase tooth mobility in the absence of periodontal disease.

Systemic factors:
1. Age: Mobility is positively related to age of the individual (Wasserman 1973) changes in the PDL that have been reported with aging include decreases numbers of fibroblasts with more irregular structure.
2. Sex and Race: Slightly higher incidence seen in females and Negroes. (Wasserman 1973).
3. Menstrual cycle: Burdine and Friedman (1970) observed increased horizontal tooth mobility during 4th week of menstrual cycle.
4. Oral contraceptives: Studies by knight and wade, Das, Bhowmick and Dutta indicate that periodontal disease and attachment loss were more common among women on pills. However Friedman (1972) found tooth mobility to be less among ovulatory drug users.
5. Pregnancy: Ratietschak (1967) has reported tooth mobility in pregnancy and has attributed it to physico-chemical changes in periodontium.
6. Systemic disease: Certain systemic diseases aggravate periodontal disease i.e. Papillon Lefevere syndrome, Down’s syndrome, Neutropenia, Chediak Higashi syndrome, Hypophosphatasia, Hyperparathyroidism, Acute leukemia, Paget’s disease etc.
7. Bone factor concept of Glickman: “When a generalized tendency toward bone resorption exists, bone loss initiated by local inflammatory processes may be magnified. This systemic influence on the response of alveolar bone has been termed the bone factor in periodontal disease. The bone factor concept, developed by Irving Glickman in early 1950s, envisioned a systemic component in all cases of periodontal disease. In addition to the amount and virulence of plaque bacteria, the nature of the systemic component, not its presence or absence, influences the severity of periodontal destruction.
Although the term “Bone factor” is not in current use, the concept of a role played by systemic defense mechanisms has been validated, particularly by studies of immune deficiencies in severely destructive types of periodontitis, such as juvenile forms of the diseases.

Factors affecting development of tooth mobility:
1. Magnitude, frequency and character of masticatory forces.
2. Amount of fiber bundles, in the periodontium and strength of alveolar bone.
3. Physical resistance of the periodontium.
4. Direction of the masticatory stress.
5. Physiological and systemic factors, which influence metabolic process of cells such as blood circulation in periodontium, age, nutrition and general health.
6. Para-functional habits and forces.

MICROSCOPIC FEATURES OF TOOTH MOBILITY –
The excessive forces produce molecular physico-chemical alteration of the ground substance and fibrous components of the tissues, atrophic, degenerative and necrotic changes. Increased compression and tension of the periodontal ligament are seen. With severe tension, widening, thrombosis, hemorrhage and tearing of the periodontal ligament and bone resorption are seen. There is temporary depression, in mitotic and the rate of proliferation and differentiation of fibroblasts, collagen and alveolar bone.
Grant et al (1995) found significant proportions of Campylobacter rectus and Peptostreptococcus microbes and elevated levels of Porphyromonas gingivalis in pockets of mobile teeth than that of non mobile ones.

Dynamics of tooth mobility
Tooth mobility seems to occur in two stages (Muhlemann 1967):
1) First, there is an initial or intra vascular stage where movement within the socket is associated with redistribution of the fluids, interstitial contents and fibers.
2) The second stage occurs gradually and includes elastic deformation of the alveolar bone proper in response to increased forces.

FORCES ON TEETH:
1. Normal or Physiologic forces:
Teeth and their supporting structures are subjected to severe occlusal forces of up to 50 mg during mastication. The presence of tissue fluids and arrangement of PDL fibers are such that these intermittent heavy forces can be properly accommodated without tissue destruction. These forces are transmitted through PDL fibers to the alveolar bone proper.

2. Orthodontic or Pathologic forces:
When unidirectional orthodontic force exceeding the adaptive capacity is applied to a tooth, pressure is exerted on side of the periodontal ligament in the direction of the force and tension on the opposite site. In undermining resorption, bone is resorbed towards the socket with eventual resorption of the socket wall, where as on tension side, new bone is opposed on the socket lining maintaining the constant width of the periodontal space.

3. Jiggling Pathologic Forces:
Forces applied to a tooth during function and parafunction may exceed the adaptive capacity. These jiggling forces may move a tooth in a faciolingual, mesiodistal, or vertical direction, along the X, Y or Z axis. As a result of pressure being exerted in all direction, the entire periodontal ligament behaves as it is subjected to pressure only. A force that exceeds the tooth’s adaptive capacity leads to the lesion of trauma from occlusion.

CORRELATION BETWEEN TOOTH MOBILITY AND OCCLUSION
Trauma From Occlusion
“When occlusal forces exceed the adaptive capacity of the periodontal tissue, injury results.” The resultant injury is termed trauma from occlusion.
So occlusal trauma is described as trauma to the periodontium from functional and para-functional forces causing damage to the attachment apparatus of the periodontium by exceeding its adaptive and reparative capacities.

– Generally, two forms of occlusal trauma are recognized:

1. Primary occlusal trauma
It is a condition in which the pathologic occlusal forces considered the principal etiology for occlusal changes in the periodontium.

2. Secondary occlusal trauma
It occurs when the periodontium is already compromised by inflammation and bone loss. Teeth with a reduced adaptive capacity and compromised periodontium may then migrate when subjected to certain occlusal forces. Factors such as frequency, duration and velocity of those occlusal forces, not just their magnitude, may be of greater significance in the development of tooth hypermobility. This mobility is a common clinical sign of occlusal trauma.

TOOTH MOBILITY INDICES
a. Miller’s Index (1938):
i) The first distinguishable sign of movement.
ii) The movement of the tooth which allows the crown to deviate within 1 mm       of its normal position.
iii) Easily noticeable and allows the tooth to move more than 1mm in any direction or to be rotated or depressed in the socket.

b. Modified Miller’s index:
Scorer of 0, 0.5, 1, 1.5, 2.5, 3 are utilized.

c. Prichard’s index (1972)
i) Slight mobility.
ii) Moderate mobility.
iii) Extensive movement in a lateral or mesiodistal direction combined with vertical displacement in the alveolus.
iv) Or sign can be used for added refinement.

d. Wasserman’s Index (1973)
i) Normal
ii) Slight mobility less than 1 mm of buccolingual movement.
iii) Moderate mobility – up to approximately 2 mm of buccolingual movement.
iv) Severe mobility – more than 2 mm of movement.

e. Nyman’s Index (1975)
Zero degree – Normal – less than 0.2 mm
Degree 1 – Horizontal / Mesiodistal mobility of 0.2 – 1mm
Degree 2 – Horizontal / Mesiodistal mobility of 1-2 mm.
Degree 3 – Horizontal / Mesiodistal mobility exceeding 2mm and / or vertical mobility.

f. Flezar’s Index (1980)
Mo – Firm Tooth
M1 – Slight increased mobility
M2 – Definite to considerable increase in mobility but not impairment of
function.
M3 – Extreme mobility, a loose tooth that would be incomparable in
function.

g. Glickman’s Index (1972)
i) Normal mobility
ii) Pathologic mobility
iii) Grade I – slightly more than normal
Grade II – moderately more than normal
Grade III – Severe mobility faciolingually and or / mesiodistally combined   with vertical displacement.

h. Lovdal’s Index (1959)
First degree – teeth that were somewhat more mobile than normal.
Second degree – teeth showing conspicuous mobility in transversal but not axial direction. Third degree – teeth being mobile in axial as well as on transversal direction.

Measurement of tooth mobility
Measurement of tooth mobility is important to evaluate the condition of periodontium in research oriented studies and for diagnosis and treatment planning.
There are numerous mobilometers, to name a few.
1. Elbrecht’s indicator (1939)
2. Werner’s Oscillator (1942)
3. Dreyfus vibrator (1947)
4. Zinrner’s oscillograph (1949)
5. Manly’s device (1951)
6. Muhlemann’s Macro-periodontometer and Micro-periodontometer, Pictons gauge (1957)
7. Parfitt’s transformer (1958)
8. Joel’s technique (1958)
9. Goldber’s device (1961)
10. Korber’s transducers, USAFSAM periodontometer (O’Leary and Rudd 1963)
11. Pameijer’s device (1973)
12. Laser method (Ryden 1974)
13. Persson and Svensons device (1980)
14. Periotest (Schulte 1987, Simons AG, Germany)

PERIODONTOMETER: (Muhlemann 1957)
By means of the “Periodontometer” a small force (100 pounds) is applied to the crown of a tooth. The crown starts to tip in the direction of the force. The resistance of the tooth supporting structures against displacement of the root is low in the initial phase of force application and the crown is moved only5/100 to 10/100mm.
PERIOTEST
The Periotest device dynamically measures the reaction of the periodontium to a defined percussive force applied to the tooth produced by a tapping device.
It is connected by table to a unit which controls functions and analyses measurements. A metal rod housed in the interior of the hand piece, the tapping head is accelerated to a present speed of 0.2 m/s (meters per second) and maintained at constant speed by compensation for the influence of friction and gravitation. Upon impact, the tooth is slightly deflected and the tapping head is decelerated.
The contact time between the tapping head and the tooth varies between 0.3 and 2 ms (milli seconds). The contact time is shorter for teeth whose alteration ability of the periodontium is greater and which are less mobile. The tapping head is electro magnetically retracted into the hand piece. In 4 seconds, 16 exact defined tapping impulses are applied to the tooth and 10,000 signals for deceleration are registered and analyzed by the measuring unit. Invalid measurements are recognized as such and eliminated.
Since the contact times are not clinically meaningful, the unit displays a value called the “Perio test value” (PTV). The value is calculated from the contact time between tapping head and tooth and ranges from – 8 to +50, corresponding to four different degrees of mobility.

Goodson (1988) confirmed the correlation between PTV and clinical mobility index (MI). He showed the periotest differentiates between 39 units for the mobility indices 0 to 3.
In a comparative study, stepwise multiple linear regression analysis at Periotest values compared with clinical parameters demonstrated that the influence of bone loss is far more important than other clinical parameters, indicating that the periotest value dependent to a large extent on bone loss. The greater the alveolar bone height, the lower the periotest value.
Of the other diagnostic valves tested, the pocket depth is correlated somewhat more strongly with periotest value than recession and the papillary hemorrhagic index. The correlation between the PTV and bone loss was stronger in the maxilla than in the mandible. Periodontally healthy teeth also had higher periotest value in the maxilla.
In tooth with non inflammatory recession and simultaneously TMJ dysfunction syndrome contribute to a significant increase in the periotest values for incisors. This is possibility due to increased alveolar destruction by bruxism.
In addition, the high sensitivity of the periotest method provides a means for early recognition of changes in the periodontium on a result of periodontal diseases.
Even though standardization of the grading of mobility would be helpful in diagnosing periodontal disease and in evaluating the outcome of treatment, these devices are not widely used.
As a general rule, mobility is graded clinically with a simple method such as the following:
The tooth is held firmly between the handless of two metallic, instruments or with one metallic instrument and one finger, and an effort is made to more it in all directions.
“It is not the length of the excursive movement of the crown that is important from a biologic point of view, but the displacement of the root within the remaining periodontal ligament”. Increased crown displacement (tooth mobility) may also be detected in a clinical measurement where a “Horizontal” force is applied to teeth with angular bony defects / or increased width of the periodontal ligament. If this mobility is not gradually increasing – from one observation interval to the next – the root is surrounded by a periodontal ligament of increased width but normal composition. This mobility should be considered “Physiologic” since the movement is a function of the height of the alveolar bone and the width of the periodontal ligament.
Only progressively increasing tooth mobility which may occur in conjunction with trauma from occlusion and which is characterized by active bone resorption and which indicates the presence of inflammatory alterations with in the periodontal ligament tissue, may be considered “Pathologic”.

TOOTH MOBILITY REVISTED:
1) (According to Charles Anderegg and David Metzler, J.P. July 2001)
Our commonly used parameter, degrees of millimeter movement, gives incomplete diagnostic and prognostic information. Current methods of grading or classifying mobility give no indication of the mobility is pathologic, physiologic or adaptive in nature.
2) So adding the designator (A) for adaptive and (P) for pathologic to the current grading or classification scheme would add the critical element for determining necessary additional occlusal or periodontal treatment.
3) Pathologic mobility, as defined, would include any degree of movement that may be reduced or eliminated once the pathologic factors is identified and corrected. Such etiologic factors would include inflammatory disease such as periodontitis, occlusal factors, parafunctional habits and iatrogenic factors.
4) Adaptive mobility, as defined, would include the absence of an etiologic factor that might be improved upon to directly improve stability by decreasing or eliminating tooth mobility. While pathologic mobility would certainly require treatment, adaptive mobility might or might not. Progressing mobility, whether adaptive or pathologic, would of course require treatment to stabilize the situation.
5) So we feel that adding the designator (A or P) to current descriptive terminology would, in a broad sense, address the etiology of existing mobility and complement current methods used to measure the degrees of mobility.

TREATMENT OF INCREASED TOOTH MOBILITY
A number of situations will be described here which may call for treatment aimed at reducing an increased tooth mobility.

Situation – I:
Increased mobility of a tooth with increased width of the periodontal ligament but normal height of the alveolar bone:
– If a tooth is fitted with an improper fitting a crown restoration, occlusal interferences develop and the surrounding periodontal tissues become the seat the inflammatory reactions, i.e. trauma from occlusion.
– If the restoration is so designed that the crown of the tooth in occlusion is subjected to undue forces directed in a buccal direction, because resorption phenomena develop in the buccal – marginal and lingual – apical pressure zones with a resulting increase of the width of the periodontal ligament in these zones.
– The tooth becomes hyper mobile or moves away from the “traumatizing” position. The resulting increased mobility of the tooth should be regarded as a physiologic adaptation of the periodontal tissues to the altered functional demands.
Fig. (a). contact relationship between a mandibular and a maxillary premolar in occlusion. Occlusion results in horizontally directed forces (arrows) which may produce an undue stress concentration within the “brown” areas of the periodontium of maxillary tooth. Resorption of alveolar bone and a widening of the periodontal ligament can be detected, leading to increased mobility. Following adjustment of the occlusal correction, the horizontal forces are reduced. This results in apposition “red areas” and normalization of the tooth mobility.

Situations – II:
Increased mobility of a tooth with increased width of the periodontal ligament and reduced height of the alveolar bone:
– If a tooth with a reduced periodontal tissue support is exposed to excessive horizontal forces, inflammatory reactions develop in the pressure zones of the periodontal ligament with accompany bone resorption. These alterations are similar to those which occur around a tooth with normal height of the supporting structures (as seen in situation 1). The alveolar bone is resorbed, the width of the PDL is increased in the pressured tension zones and tooth becomes hyper mobile.
– If the excessive forces are reduced or eliminated by occlusal adjustment bone apposition to the “pre trauma” level will occur, the periodontal ligament will regain its normal width and the tooth will become stabilized.

Conclusion
Situations I and II oculusal adjustment is an effective therapy against increased tooth mobility when such mobility is caused by an increased width of periodontal ligament.

Situation – III:
Increased mobility of a tooth with reduced height of the alveolar bone and normal width of the periodontal ligament:
– In this case tooth mobility can not be reduced or eliminated by occlusal adjustment. If such increased tooth mobility does not interfere with the patients chewing function or discomfort, no treatment is required.
– If the patient experiments the tooth mobility as disturbing, however the mobility can in this situations be reduced only by splinting, i.e. by joining the mobile tooth / teeth together with other teeth in jaw into a fixed splint for example “A – splint”. A-splint, according to Glossary of Periodontal terms (1986) is an appliance designed to stabilize mobile teeth”. A-splint can be fabricated in the form of joined composite filling, fixed bridges removable partial prosthesis etc.

Situations – IV:
Progressive (increasing) mobility of a tooth (teeth) as result of gradually increasing width of reduced periodontal ligament:
– Often in cases of advanced periodontal disease the tissue destruction may have reached a level where extraction of one or several teeth cannot be avoided. Teeth which in such a dentition are still available for periodontal treatment may, after therapy, exhibit such a high degree of mobility or even signs of progressively increasing mobility – that there is an obvious risk that the forces elicited during function may mechanically disrupt PDL components and cause extraction of the teeth. Only by means of a splint will it be possible to maintain such teeth.
– In such cases fixed splint has two objectives.
To stabilize hyper mobile teeth and
To replace missing teeth.
– Splinting is indicated when the periodontal support is so reduced that the mobility of the teeth is progressively increasing. i.e., when a tooth or a group of teeth during functions are exposed to extraction forces.

Situations – V:
Increased bridge mobility despite splinting:
– In patients with advanced periodontal disease it can often be observed that the destruction of the periodontium has progressed to varying levels around different teeth and tooth surfaces in the dentition. They may also be distributed in the jaw in such a way as to made it difficult, or impossible, to obtain a proper splinting effect even by means of a cross arch bridge The entire bridges splint may exhibit mobility in frontal and / or lateral directions. Neither progressive tooth mobility nor progressive bridge mobility can be accepted.
– In cases of extremely advance periodontal disease, a cross arch splint with an increased mobility may be regarded as an acceptable result of rehabilitation. It requires particular attending regarding the design of the occlusion.
– In cases of severity advanced periodontal disease it is often impossible to anticipate in the planning phase whether a bridge / splint after insertion will show signs of instability and increasing mobility. In such cases, a provisional splint should always be inserted.
– Any alteration of the mobility of the bridge / splint can be observed over a prolonged period of time and the occlusion continuously adjusted. Until, after 4-6 months, it is known whether stability can be achieved (i.e. no further increase of the mobility).
– Conclusion: An increased mobility of a cross arch bridge / splint can be accepted provided the mobility does not disturb chewing ability or comfort and then mobility of the splint is not progressively increasing. Splints can be temporary, permanent, extracoronal, intra coronal, removable, fixed or fiber or resin bonded etc.
– However through are 2 schools at thought regarding mobility and splinting. Waerhaug and co-workers feel that increase in mobility do not necessarily represent a state of pathology and does not require splinting. But Muhlemann strongly advocates that increase in mobility is pathological which requires treatment. However, a study of Kegel et al (1979) revealed no difference in mobility reduction between splinted and unsplinted teeth over 17 weeks period.

LOCAL ANESTHESIA

INTRODUCTION

               An anesthesia is derived from the word (an-without Aisthetos-sensation it was given by oliver bendel in 1846.) Local anesthesia is a state of controllable,reversible insensibility in which sensory perception and motor responses are both markedly depressed. where as analgesia is the temporary abolition or diminution of pain reception. It allows patient to undergo surgical and dental procedures with reduced pain and distress.  It is also used for relief of non surgical pain and to enable diagnosis of the cause of some chronic pain condition. Anaesthetist sometimes combine both general and local anaesthesia techniques.

lignocaine with adrenaline

Anaesthesia is defined as  loss of sensation with or without loss of consciousness”.

There are two basic types of anesthesia

  1. General Anesthesia

general anesthesia

2. Local Anesthesia

local anesthesia

General Anesthesia Local anesthesia
Site of action CNS Peripheral nerves
Mechanism of action Block axonal conduction Depress  synaptic transmission
Route of adminstration Inhalational or I/V Topical application or local injection
Area of body involved Whole body Restricted area
Consciousness Lost Unalatered
Care of vital functions Essential Usually not needed

The effect of local anesthetic are most necessarily limited to sensory nerve fibers alone. When these drugs are brought into direct contact with the other parts of the mixed spinal nerves they can also affect in the functioning of the somatic  motor and sympathetic nerve fibers. This can then interfere with the tone of skeletol and smooth muscles innovated bthey these nerves.

In addition local aesthetis that are systematically absorbed from site of their application may be carried by the blood stream to the brain, heart, liver and other organ. The effect  of these drug on the centaral nervous system and circulatory system can then cause serious toxic reaction. Thus the anesthesiologist employs special technique of administrations which are intended to

  1. Place the local anesthetic solution at some presiced local point along the course of peripheral nerves.
  2. They will keep the drug systemic absorption at the rate so slow that it doesn’t goes up to the toxic levels.

There are many methods of inducing local anesthesia for example :

  1. Mechanical trauma
  2. Anoxia
  3. Low temperature
  4. Chemical irritants
  5. Neurolactic agent (alcohol,phenol)
  6. Chemical agents (local anesthetics)

History

  • The history of local anesthesia started
  • In 1859, when cocaine was isolated by “Niemann”.

niemann

  • In 1884, the ophthalmologist Koller used cocaine for topical anesthesia in ophthalmological surgery.
  • In 1884, regional anesthesia in the oral cavity was first performed by surgeon Halsted, for removing wisdom tooth without pain.

halsted

  • In 1905, Einhorn reported the synthesis of procaine, which was first ester type local anesthetic agent. Procaine was most commonly used local anesthetic for more than four decades.

Einhorn

  • In 1943, Lofgren synthesized lidocaine, which was first “modern” local anesthetic agent.  Lidocaine was marketed in 1948 & is upto now most commonly used local anesthetic in dentistry worldwide.
  • Other amide local anesthetics were introduced into clinical use:
  1. Mepivacaine 1957,
  2. Prilocaine 1960,
  3. Bupivacaine 1963.
  • In 1969, Articaine was synthesized by the chemist “Muschaweek” and was approved in 1975 as local anesthetic agent in Germany.

DEFINITION

  • Local anesthesia has been defined as loss of sensation in circumscribed area of body caused by depression of excitation in nerve endings or an inhibition of conduction process in peripheral nerves.(Stanley F. Malamed)

OR

  • Local anesthetic are the drugs have a little or no irritating effects when injected into the tissues and that will temporarily interrupt conduction when absorbed into the nerves(Monheims)

OR

  • Local anesthesia has been defined as direct administration of anesthetic agent to tissue to include the absence of sensation in small area of body (Mosby’s dictionary)

CLASSIFICATION

I. Based on bioavailability

  • Natural – eg. cocaine.
  • Synthetic nitrogenous compound –  eg. procaine, benzocaine, lignocaine & bupivacane
  • Non Nitrogenous compounds – benzyl alcohol
  • Miscellaneous – clove oil , phenol.

II. According to structure:

  1. Esters  :

Benzoic acid esters:

    • Benzocaine
    • Cocaine

Para-amino benzoic esters:

    • Tetracaine
    • Chlorprocaine
    • Procaine
    • Propoxycaine

amino esters and amino amides

2. Amides :

  • Articaine
  • Bupivacaine
  • Etidocaine
  • Lidocaine
  • Mepivacaine
  • Prilocaine

3. Quinolones : Centbucridine

III. According to duration of action :

1) Ultra Short acting anesthetic – less than 30 min

  • Procaine without a vasoconstrictor
  • 2 chloroprocaine without vasoconstrictor
  • 2% lidocaine without a vasoconstrictor

2) Shot acting local anesthetic – 45 to 75 min

  • 2% lidocaine with 1:100000 epinephreine
  • 2% mepivacaine with 1: 20000 lavonordefrin
  • 4% prilocaine when used to nerve block

3) Medium acting anesthetics 90 – 150min

  • 4% prilocaine with 1:200000 epinephrive
  • 2% lidocaine and 2% mepivacaine with a vasoconstrictor
  • May produce pulpal anesthesia of this duration

4) Longer acting anesthestic – 180 min or longer 

  • 0.5% bupivacaine with 1: 200000 epinephrine
  • 0.5% or 1.5% etidocaine with 1:200000 epinephrine

IV. According to mechanism of action

  • Class A : Agents acting at receptor site on external surface of nerve membrane

    eg: Biotoxins

  • Class B : Agents acting at receptor sites on internal surface of nerve membrane

    eg: scorpion venom

  • Class C : Agents acting by receptor independent physio-chemical mechanism

    eg: Benzocaine

  • Class D :Agents acting in combination of receptor dependent-independent mechanism                     eg: Lidocaine, Mepivacaine, PrilocaineV. ACCORDING TO  MODE OF ACTION:
    • TOPICAL
    • INJECTABLE

VIACCORDING TO ORIGIN (Vinod Kapoor 2nd Edition)

Natural :- Cocaine 

  • Synthetic nitrogenous compounds 

a) Amino esters of para amino benzoic acid :- Procaine

b) Alkyl esters of Paba (Benzocaine)

c) Amino esters of Meta amino Benzoic acid (MABA) Unacaine

d) Amino –amides (xylocaine) (Bupivacaine)

  • Systemic non nitrogenous compounds (Benzyl alcohol)
  • Miscellaneous drugs (Clove oil/Phenon) 

local anesthesia color coding

 

COMPOSITION

  1. Lidocaine hydrochloride (20mg/ml) –  Local anesthetic agent
  2. Adrenaline bitarterate (epinephrine) (0.012mg) –  vasoconstrictor
  3. Methylparaben (1mg) –  Preservative
  4. Thymol –  Fungicide
  5. Sodium metabisulphate (0.5mg) –  Reducing agent
  6. Sodium chloride (6mg) –  Isotonic solution
  7. Ringer’s lactate solution : Vehicle
  8. Distilled water :  Diluting agent
  9. sodium hydroxide :  ph adjuster

1) Lidocaine hydrochloride

In 1940, the first modern local anesthetic agent was lidocaine, It developed as a derivative of xylidine which belongs to amide class. It is hypo allergenic. Sets on quickly produces a desired anesthesia effect for several hours.

lidocain hydrochloride

Mechanism of action

Lidocaine stabilizes the neuronal membrane by inhibiting ionic fluxes, required for initiation and conduction of nerve impulses, thereby effecting local anesthetic action.

Hemodyanamics:

Excessive blood levels may cause change in output, total peripheral resistance and mean arterial pressure. These changes may be attributable to a direct depressant effect of local anesthetic agent on various components of CVS. The net effect is normally a modest hypotension when there commended dosages are not exceeded.

Pharmacokinetics & metabolism lidocanine is absorbed following topical administration to mucous membrance, its rate and extent of absorption being dependent upon concentrated and total dose administered. The specific site of application and duration of exposure. In general, the rate of absorption of local anesthetic agent is following topical application occur most rapidly after intrathecal administration. Lidocaine is also well absorbed from GIT, but little intact drug appears in circulation because of biotransformation in liver.

The plasma binding of lidocaine is dependant upon drug concentration and fraction bound decreases with increasing concentration. At concentration of 1 to 4 mcg of free base /ml ,60 to 80 % if lidocaine is protein bound. Binding is also dependent upon plasma concentration of alpha and glycoprotein.

Lidocaine crosses blood brain barriers and placental barriers presumably by passive diffusion.

Lidocaine is metabolized rapidly by liver and its metabolites and unchanged drug are excreated by kidney biotransformation include oxidative dealkylation, a major pathway of biotransformation yields the metabolites monoethylglycinxylidine and glycinexylidine. The pharmacological and toxicological action of these metabolites are similar to but less potent than those of lidocaine, Approximately 90% lidocaine administered is excreted in the form of various  metabolites and less than 10% excreted unchanged .

The primary metabolite in urine is a conjugate of 4-hydroxy,2,6-fimryhylaniline. The elimination of halflife of lignocaine as IV Bolus injection is typically 1.5 to 2 hrs. the half life may be prolonged few fold more in patient with life dysfunction. Renal dysfunction does not lignocaine kinetic but may increases the accumulation of metabolites. Factor such as acidosis and uses of CNS stimulants depressant affect CNS level of lignocaine required to produce overt systemic effects.

2) Adrenaline bitarterate (epinephrine) 

Adrenaline bitarterate is a hormone neurotransmitter. It increases the heart rate constrict the blood vessels, dilates air passage and participate in fight of flight response of the sympathetic nervous system. Chemically epieprine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenyalanine and tyrosine.

Adrenaline was first synthesized by “Friedrich Stolz” and “Henry Drysdale dakin” in the laboratory.

Epinephrine added to injectable form of a number of local anesthetics, such as bupivacaine a lignocaine, as a vasoconstrictor to retard the absorption and therefore prolong the action of the anesthetic agent. Some of the adverse effects of local anesthetic use, such as apprehension, tachycardia or tumour may be caused by epinephrine (Cannon W.B., 1129) American journal of physiology.

adrenaline

ACTION 

The addition of vasoconstrictor (Adrenaline) to a local anesthetic agent causes constriction of blood vessels and thereby controls tissue perfusion. The net effects caused by addition of vasoconstrictors to local anesthetic agents are :

  1. It decreases the blood flow to the site of injection, because of vasoconstriction.
  2. It decreases the rate of absorption of local anesthetic agent into cardiovascular system.
  3. It lowers the plasma level of local anesthetic agent (Cannall et al, 1975) and Wildsmith et al, 1977), thereby decreasing the risk of systemic toxicity of local anesthetic agent.
  4. Higher volumes of local anesthetic agent remain in and around the nerve for longer periods; thereby increasing the duration of action of most local anesthetic agents (Brown, 1968).
  5. It decreases bleeding at the site of injection because of decreased perfusion. This is useful when increased bleeding is expected during a surgical procedure (Carpenter et al, 1989; and Myers and Heckman, 1989).

3) Methylparaben

Many of  the local anesthetic solution containing  methyl paraben which is used as a known local anesthetic. Methylparaben had been associated with few allergic reaction therefore care full consideration must be given to this compound. When true allergic reaction has been manifested following the use of local anesthetic solution containing methylparaben.

It has got phenol like action, it acts by denaturation of protein and its antimetabolites present in a low conc. of 0.1 to 0.3% in local anesthetic solution.

Methylparaben, also methyl paraben, one of the parabens, is a preservative with the chemical formula CH3 (C6H4(OH)COO). It is the methyl ester of p-hydroxybenzoic acid.

Methylparaben

Methylparaben is an anti-fungal agent often used in a variety of cosmetics and personal care products. It is also used as a food preservative. Methylparaben is commonly used as a fungicide in Drosophila food media. Usage of methylparaben is known to slow Drosophila growth rate in the larval and pupal stages.

Methylparaben is produced naturally and found in several fruits, primarily blueberries, along with other parabens. There is no evidence that methylparaben or propylparabens are harmful at concentrations typically used in body care or cosmetics. Methyl and propylparabens are considered GRAS (generally regarded as safe) for food and cosmetic antibacterial preservation. Methylparaben is readily metabolized by common soil bacteria, making it completely biodegradable.

Methylparaben is readily absorbed from the gastrointestinal tract or through the skin. It is hydrolyzed to p-hydroxybenzoic acid and rapidly excreted without accumulation in the body.Acute toxicity studies has shown that methylparaben is practically non-toxic by both oral and parenteral administration. In a population with normal skin, methylparaben is practically non-irritating and non-sensitizing; however, allergic reactions to ingested parabens have been reported. Studies indicate that methylparaben applied on the skin may react with UVB leading to increased skin aging and DNA damage.

4) Thymol

Thymol (also known as 2-isopropyl-5-methylphenol), (IPMP) is a natural monoterpene phenol derivative of cymene, C10H14O, isomeric with carvacrol, found in oil of thyme, and extracted as a white crystalline substance of a pleasant aromatic odor and strong antiseptic properties.

Thymol is part of a naturally occurring class of compounds known as biocides, with strong antimicrobial, antifungal effects. Thymol is only slightly soluble in water at neutral pH, but it is extremely soluble in alcohols and other organic solvents. It is also soluble in strongly alkaline aqueous solutions due to deprotonation of the phenol.

Thymol

Thymol resembles phenol in its action, but owing to its insolubility in fluids of the body it is absorbed much more slowly. it is also less irritant to wounds, while its germicidal action is greater than that of phenol. In alcoholic solution it penetrates skin and produces local anesthesia. Compound Glycerin of Thymol is used to treat mouth ulcer. One of the active ingredients of this preparation is thymol. Thymol is also used as an antiseptic, local anesthetic, cooling agent, and as a preservative.  It acts as a local irritant and anesthetic to the skin and mucous membranes.

Thymol was in originally introduced as a disinfectant in lieu of carbolic acid having the advantage of a more pleasant odor. Thymol is employed in many of the antiseptic mixtures intended for use upon mucous cavity, especially in gargles, mouth washes, and other oral preparations and as a local anesthetic in toothache.

DISTRIBUTION 

  • Highly perfused organs have higher blood levels of anesthetic than less highly perfused organs.
  • Skeletal muscles contains greatest percentage of local anesthetics as constitute biggest mass of tissue in body.
  • All LA’s can cross blood brain barrier and placenta.
  • Plasma concentration of local anesthetic in target organs depends on :-
    • Rate at which drug is absorbed into CVS
    • Rate of drug distribution from blood to tissues
    • Drug elimination through metabolic or excretory pathways.
    • Elimination Half life of lidocaine is 1.6 hours.

METABOLISM (BIOTRANSFORMATION)

Ester local Anesthetics

  • Hydrolyzed in the plasma by enzyme Pseudocholinesterase .
  • Site – Plasma.
  • Rate of hydrolysis – Varies and inversely proportional to toxicity.
  • Action of biotransformation products.
  • Allergic reaction – PABA responsible for causing allergic reactions.
  • Atypical Pseudocholinesterases – Causes inability to hydrolyze ester local anesthetics and other chemically related drugs (Succinyl choline)

metabolism of local anesthesia

metabolism of L.A

AMIDE LOCAL ANESTHETICS 

  • Primary site – liver
  • Rate of biotransformation – influenced by liver function and hepatic perfusion.
  • Poor liver function – unable to biotransform amide local anesthetics at a normal rate.
  • Action of biotransformation products
    • Monoethylglycinexylidide
    • Glycinexylidide
    • Methemoglobinemia – in patients receiving large doses of prilocaine.
    • Produced not by prilocaine but by its primary metabolite orthotoluidine.
    • Sedative effect – Produced by two metabolites of lidocaine.

EXCERTION 

  • Primary site – kidneys
  • Esters – Appear in small concentration as parent compound in urine since hydrolyzed completely in plasma.
  • Amides – Present in urine as parent compound in a greater percentage because of their more complex process of biotransformation.
  • Renal disease – Relative contraindication to local anesthetic administration.
  • Increase blood levels and potential for toxicity of local anesthetic compounds esp. cocaine.

amino esters and amino amides

IDEAL PROPERTIES 

Physical properties

1. Non-flammable, non-explosive at room temperature

2. Stable in light.

3. Liquid and vapourisable at room temperature i.e. low latent heat of vaporization.

5. Stable with soda lime, as well as plastics and metals

6. Environmentally friendly – no ozone depletion

7. Cheap and easy to manufacture

Biological properties 

  1. Pleasant to inhale, non-irritant, induces bronchodilatation
  2. Low blood: gas solubility – i.e. fast onset
  3. High oil: water solubility – i.e. high potency
  4. Minimal effects on other systems – e.g. cardiovascular, respiratory, hepatic, renal or endocrine
  5. No biotransformation – should be excreted ideally via the lungs, unchanged
  6. Non-toxic to operating theatre personnel

The use of reversible local anesthetic chemical agents is the most common method to achieve pain control in dental practice. Some ideal properties of local anesthetics are as follows:

  • Specific action
  • Reversible action
  • Rapid onset of action
  • Suitable duration of action
  • Active whether applied topically or injected
  • Nonirritant
  • Causes no permanent damage
  • No systemic toxicity
  • High therapeutic ratio
  • Chemically stable and a long shelf life
  • Ability to combine with other agents without loss of properties
  • Sterilizable without loss of properties
  • Non-allerenic
  • Non-addictive

Where do Local Anesthesia Act ?­

where does local anesthesia work

L.A can interfere with excitation process in nerve membrane in one or more of the following ways:­

  1. Altering the basic resting potential of nerve membrane.
  2. Altering the threshold potential
  3. Decrease rate of depolarization
  4. Increase prolonging rate repolarization.

Theories of Local Anesthesia

  1. Acetylcholine theory        acetylcholine theory
  2. Calcium gate theory calcium gate theory
  3. Surface charge theory surface charge theory
  4. Membrane expansion membrane expansion theory
  5. Specific receptor theory specific receptor theory

INDICATIONS OF LOCAL ANESTHESIA

Local anesthesia can be used by itself or it can be combined with other types of anesthesia such as spinal or epidural anesthesia.

This is done to reduce the stress associated with surgery, and to provide pain relief after surgery.

More commonly, it is used for pain caused by hemorrhoids, fissure, insect bite, and minor burns. It is applied topically.

It is also indicated for vaginal, rectal and otological examination, cystoscopy, catheterization, urethral operations, and endotracheal intubation.

Indications of local anesthesia in various field of dentistry

ORAL SURGERY

  1. To make needle insertion painless
  2. Extraction of teeth and fractured roots
  3. Odentectomy
  4. Treatment of alveolgia
  5. Alvelectomy
  6. Apicectomy
  7. Incision and drainage of localized abscess
  8. Removal of cyst ;residual infection, hpertrophic scar and neoplastic growth , ranula and salivary calculi
  9. In the treatment of tic doulorex by producing prolonged anesthesia  with a combination of local anesthetic agent and alcohol injection ,for blocking the involved nerve
  10. A therapeutic test to localize the source of vague pain about the face.

IN CONSERVATIVE DENTISTRY

The following operative and restorative procedures

  1. Cavity preparation
  2. Crown and bridge abutment preparation
  3. Pulpotomy or pulpectomy

IN PERIODONTOLOGY 

  1. Surgical treatment of periodontal tissue
  2. Deep scaling and prophylaxis treatment
  3. Mucogingival surgical procedures

IN PROSTHODONTICS

  1. Giving denture patients relief from sore spots which are painful even though denture have been relieved

IN ORTHODONTIA

1. Separation of teeth

IN RADIOLOGY 

1To prevent gagging and retching caused by the contact of the film with palatal tissues and posterior part of the oral cavity .These tissues or the areas are anesthetized before placing the film in these cases usually surface anesthesia is used.

CONTRAINDICATIONS OF LOCAL ANESTHESIA

These can be divided into two groups:

1 Absolute contraindications

2 Relative contraindications

Absolute contraindications

History of allergy to local anesthetic agents

Local anesthetic agents belonging to the same chemical group should not be used. However, local anesthetic agents in the different chemical group can be used .In case, a patient gives history of allergy to an amide local anesthetic agent, an ester local anesthetic agent can be used.

RELATIVE CONTRAINDICATIONS:

1. Fear and apprehension

2. Presence of acute inflammation or suppurative infection at the site of insertion of the needle

3. infants or small children

4. mentally retarded patients

5. restricted mouth opening

6. patient with significant medical diseases :, cardiovascular diseases , hepatic dysfunction, renal dysfunction ,clinical hyperthyroidism

a. patient with significant cardiovascular diseases ;all local anesthetic solution containing high concentration of vasoconstrictors ,such as epinephrine as in gingival retraction  cord should be avoided .local anesthetic agents containing higher dilution of epinephrine ,such as 1.10000000 or 3%  mepivacaine or 4 % prilocaine can be used

b. patient with hepatic dysfunction : all local anesthetics agents belonging to amide group undergo biotransformation in the liver

c.  patient with significant renal dysfunction: all amides and esters should be avoided  however these can be used judiciously .

d.  patient with clinical hyperthyroidism: high conc. of vasoconstrictor as in epinephrine should be avoided .local anesthetic agents containing higher dilutions of epinephrine such as 1.1000 or 1 ;200000 or 3% mepivacaine or 4 % prilocaine can be used

7. Major surgical procedures

8. presence of certain anamolies or developmental defects

9. presence of congenital methemoglobinemia

10. presence of atypical plasma cholinesterase

ADVANTAGES 

1. Patient remains awake and cooperative

2. little distortion of normal physiology ,therefore can be used in poor risk patients

3. Low incidence of morbidity

4. additional trained personally not required

5. Technique not difficult to master

6. Percentage of failure is small

7. no additional expenses to the patient

8. patient need not miss the previous meal .in fact ,should have one ,patient should not come on empty stomach

DISADVANTAGES

                   No true disadvantages to the use of regional analgesia, when the patient is mentally prepared and when there are no contraindications .in every instance ,when satisfactory anesthesia can be achieved and the patient is cooperative ,regional analgesia is the method  of choice.

MECHANISM OF ACTION OF LOCAL ANESTHESIA

All local anesthetics are membrane stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors). Though many other drugs also have membrane stabilizing properties, not all are used as local anesthetics (propranolol, for example). Local anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Local anesthetic drugs bind more readily to sodium channels in activated state, thus onset of neuronal blockade is faster in neurons that are rapidly firing. This is referred to as state dependent blockade.

Local anesthetics are weak bases and are usually formulated as the hydrochloride salt to render them water-soluble. At the chemical’s pKa the protonated (ionized) and unprotonated (unionized) forms of the molecule exist in equilibrium but only the unprotonated molecule diffuses readily across cell membranes. Once inside the cell the local anesthetic will be in equilibrium, with the formation of the protonated (ionized form), which does not readily pass back out of the cell. This is referred to as “ion-trapping”. In the protonated form, the molecule binds to the local anesthetic binding site on the inside of the ion channel near the cytoplasmic end.

MECHANISM OF LOCAL ANESTHESIA

Acidosis such as caused by inflammation at a wound partly reduces the action of local anesthetics. This is partly because most of the anesthetic is ionized and therefore unable to cross the cell membrane to reach its cytoplasmic-facing site of action on the sodium channel.

All nerve fibers are sensitive to local anesthetics, but generally, those with a smaller diameter tend to be more sensitive than larger fibers. Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying nociceptive impulses), non-myelinated axons, then large myelinated axons. Thus, a differential block can be achieved (i.e. pain sensation is blocked more readily than other sensory modalities).

HOW DOES LA WORKS ?

Displacement of Ca++ from sodium channel receptor site

Binding of LA molecule to this site

Blockade of sodium channel

Decrease in sodium conductance

Failure to achieve threshold potential level lack of development of

propagated action potential

COMPLICATION OF LOCAL ANESTHESIA

A) Complications arising from drugs or chemicals used for local anesthesia

1. Soft tissues injurySOFT TISSUE INJURY FROM L.A

2. Sloughing of tissues ( Tissues ischemia and necrosis)

B) Complications arising from injection techniques

I. Breakage of anesthetic cartridge

2. Breakage of needle NEEDLE BREAKAGE

3.. Needle-stick injuries

4. Hematoma HEMATOMA FORMATION

5. Failure to obtain local anesthesia

C) Complications arising from both

1. Pain on injection

2. Burning on injection

3. Infection

4. Trismus  TRISMUS

5. Edema EDEMA

6. Mucosal Blanching

7. Persistent aesthesia or anesthesia

8. Persistent or prolonged pain pain

9. Post-injection herpetic lesions or post-anesthetic intraoral lesions

10. Bizarre neurological complications

a) Facial nerve paresis or paralysis facial nerve paralysis

b) Visual disturbances

1. Diploma or double vision

many fingers seen on single hand isolated on white
many fingers seen on single hand isolated on white

2. Amaurosis or temporary blindness

3. Permanent blindness.

Local anesthetics complication are broadly classified in two parts.

A) localized complication

B) Systemic complication  localized complication:-

The localized adverse effects :-

• The local adverse effects of anesthetic agents include

• neurovascular manifestations such as prolonged anesthesia (numbness) and paresthesia ( tingling, feeling of “pins and needles”. or strange sensations ). These are symptoms of localized nerve impairment or nerve damage.

 Causes of localized symptoms include:

1. Neurotoxicity due to allergic reaction,

2. Excessive fluid pressure in a confined space,

3. Severing of nerve fibers or support tissue with the needle/catheter,

4. Injection-site hematoma that puts pressure on the nerve, or

5. Injection-site infection that produce inflammatory pressure on the nerve and/or necrosis.

Systemic complication :-

General systemic adverse effects are due to the pharmacological effects of the anesthetic agents used. The conduction of electric impulses follows a similar mechanism in peripheral nerves, the central nervous system, and the heart. The effects of local anesthetics are therefore not specific for the signal conduction in peripheral nerves.

A) Neurological complication of local anesthesia:- 

  • Local anesthetics may cause adverse effects either by action on the nerves  and muscles or neurotoxicity following systemic absorption.
  • Injection injury of neural structures may result from the procedure.
  • Seizures are a frequent adverse effect of local anesthetics, and principal of management are those applicable to drug- induced seizures.
  • Careful selection of the anesthetic agent and meticulous procedure for local anesthesia are important preventive measures.

Clinical manifestations

CNS excitation manifested by:

  • Restlessness
  • Tremors
  • Light-headedness
  • Syncope – Tinnitus
  • Nausea and vomiting
  • Slurring of speech
  • Irrational conversation

Seizures that may be followed by CNS depression.

CNS depression manifested by:

  • Drowsiness
  • Respiratory arrest – Coma respiratory arrest

• Complications related to peripheral and cranial nerves: –

  1. Irritation of spinal nerve roots
  2. Complications of leakage of cerebrospinal fluid
  3. Cauda equine syndrome
  4. Paraplegia due to toxic or ischemic myelopathy
  5. Meningitis
  6. Epidural hematoma

Effect on muscles:

  1. myonecrosis following local injection into muscles

Neurophthalmologic complications:

  1. Reduction of visual acuity following retro bulbar anesthesia
  2. Homer syndrome
  3. Extra ocular muscle palsies
  4. Neurologic manifestations of systemic toxicity of local anesthetics: Numbness of the tongue and perioral region

Cardiovascular system

The conductive system of the heart is quite sensitive to the action of local r anesthetic. Cardiovascular manifestation are usually depressant and are  characterized by bradycardia, hypotension, and cardiovascular collapse, which  may lead to cardiac arrest.

Allergic

Allergic reactions are characterized by cutaneous lesions, urticaria, edema or anaphylactoid reactions. Allergic reactions may occur as a result of sensitivity either to local anesthetic agents or to the methylparaben used as a preservative in the multiple does vials. Allergic reactions as a result of sensitivity to lidocaine are extremely rare and, if they occur, should be managed by conventional means. The detection of sensitivity by skin testing is of doubtful value.

 Hypersensitivity/allergy

Adverse reactions to local anesthetics (especially the esters) are not uncommon, but true allergy is very rare Allergic reactions to the esters is usually due to a sensitivity to their metabolite, para-aminobenzoic acid (PABA), and does not result in cross-allergy to amides. Therefore, amides can be used as alternatives in those patients. Nonallergic reactions may resemble allergy in their manifestations. In some cases, skin tests and provocative challenge may be  necessary to establish a diagnosis of allergy. There are also cases of allergy to paraben derivatives, which are often added as preservatives to local anesthetic solutions.

OCCULAR COMPLICATIONS ASSOCIATED WITH LOCAL  ANESTHESIA ADMINISTRATION IN DENTISTRY

  1.  Amourosis
  2. Mydriasis mydriasis
  3. Ptosis         ptosis
  4. Diplopiamany fingers seen on single hand isolated on white

Venous

This theory suggests that after inadvertent administration into the inferior alveolar vein following an inferior alveolar nerve block, the pressurized injection and diffusion will allow the flow of anesthetic into the pterygold venous plexus and consequently into the cavernous sinus through emissary veins that traverse the bony foramina. Once the anesthetic is positioned within the cavernous sinus, the abducens nerve would be more vulnerable to the effect of the anesthetic because of its immediacy within the sinus

Myofascial planes

Often considered a cause of anesthetic failure, myofascial plane orientation may create a path of least resistance where the anesthetic solution flows away from the nerve and toward the orbital area. Studies radiopaque dyes combined with local anesthetics have demonstrated that an injection can be made within the direct area of nerve without producing an effect, whereas in supplementary illustrations, the solution was administered more than 2 cm away but still generated excellent anesthesia. In the formal case, the anesthetic spreads over the path of least resistance away from the nerve; in the latter case, it is directed toward the nerve.

Sympathetic ganglion anesthesia

Campbell and the conjunctive a case with a Horner-like syndrome with ptosis, vascular dilatation of the conjunctiva miosis, horseness in vocalization, and  wide-spread rash over the ipsilateral upper body. In their report, it was suggested that the local anesthetic administration resulted in a stellate ganglion block, which may explain the patient’s hoarseness of voice. Proposed Causes of Occular Complications with maxillary injections

Diffusion

As opposed to mandibular injections for which the injection site is further   away from the orbit, maxillary injections have an increased opportunity of diffusion carrying the local anesthetic solution into the orbital area. It is  oik proposed that simple diffusion from the pterygomaxillary fossa to the orbit (through defects in the bone or via the vascular, lymphatic and venous networks that link these spaces results in ocular consequences.

Arterial

Inadvertent intra-arterial injection into the superior alveolar artery, with retrograde flow to the internal maxillary artery and then to the middle meningeal artery, serves as the basis for this theory. A middle meningeal branch occasionally penetrates the superior orbital fissure and anastomoses with the lacrimal branch of the ophthalmic artery the risk of an ocular complication occurring as proposed by this theory would be increased when the solution is injected rapidly and under pressure.

This hypothesis proposes an inadvertent venous injection in to the pterygoid venous plexus to explain a possible cause of ocular complication.   The theory proposes that the anesthetic solution would reach the orbit through the canvernous sinus, which recives drainage from the pterygoid venous plexus via the inferior and superior ophthalmic veins, which could communicate with the various musculature associated with the eye.

 

PREDISPOSING FACTORS :

The factors which can precipitate vasodepressor syncope may be divided into two group:

1. Psychogenic factors, and

2. Non-psychogenic factors

Psychogenic factors

  • Fright and anxiety
  • Emotional stress
  • Receipt of unwelcomeness
  • Pain of sudden and unexpected nature
  • Sight of blood or of surgical or other dental instruments, such as local anesthetic syringe, injection needle etc.

In dental surgery set-up the psycologenic factors are the most common precipitating factors. These factors lead to fight-or-flight response; and in the absence of muscular activity, manifest as loss of consciousness, termed as vasodepressor syncope.

Non-psychogenic Factors

  • Sitting in upright position or standing for prolonged period. It leads to 4.4 pooling of blood in periphery thereby decreasing cerebral blood flow.
  • Hunger or starvation.
  • Exhaustion.
  • Poor physical condition boo
  • Hot, humid and crowded environment.
  • The above mentioned condition and contribute to a situation resulting in syncope.
  • Injection of a local anesthetic agent with or without a vasoconstrictor in to an it artery.

 Clinical Manifestations

The clinical manifestations develop rapidly. However the actual loss of mtr consciousness occurs after a period of time. The clinical features of vasodepressor syncope may be grouped into three definite phases:

i) Presyncope

ii) Syncope

iii) Postsyncope

ADVERSE DRUG REACTIONS

Local anesthetic agents are relatively safe and free of side effects provided they are administered in an appropriate dosage and in an appropriate anatomical location. The ester group of drugs is more toxic than the amide group. The adverse drug reactions include:

1) Allergic reactions,

2) Anaphylactic reactions,

3) Toxic reactions (overdose),

4) idiosyncratic reactions.

The causes, signs and symptoms, prevention of these reactions are mentioned. The management procedures are common to all the reactions.

These include the following:

1. Stop the dental procedure.

2. Place the patient in supine position (legs slightly elevated).

3. Call medical assistance.

4. Institute the prelim nary medical care.

5. Keep the airway patent.

6. Administer

7. Monitor the vital signs.

8. Transfer the patient to a general hospital in the vicinity having ICU facility.