CONTENTS I. Introduction.3 II. Definition..3 III. Nerve physiology..3 1. Neurons 2. Structure of nerve fiber 3. Classification of neurons 4.

Nerve impulse 5. Synapse 6. Neurotransmitters 7. The sensory System . The !eceptors IV. P in....!" 1. !eceptors 2. Stimuli for pain 3. Characteristic of pain 4. "ain reaction 5. "ain path#ay 6. !eferre$ pain 7. %isceral pain . Tri&eminal system '. Theories of pain V. # n ge$ent of dent l p in..3% o o o o (ntro$uction an$ classification of pain )*amination an$ assessment of patient #ith +ro,facial pain -etermination of $ia&nosis .ana&ement of $ental pain o o o o o Types of treatment

Somatic pain of "ulpal ori&in Somatic pain from $ental supportin& tissue / "ain $isor$ers that mimic o$ontala&ia 0typical pain $isor$ers that mimic o$ontala&ia -ru& therapy "ain mana&ement principles Non opioi$ anal&esics +pioi$ anal&esics !ole of corticosteroi$s Ne# $evelopments in pain mana&ement

VI. Conclusion....&" VII. 'eferences...&&

(ntro$uction "ain is one of the most commonly e*perience$ symptoms in $entistry an$1 as such is a ma2or concern to the $entist. "ain is not a simple sensation but rather a comple* neurobehavi oural event involvin& at least t#o components. 3irst is an in$ivi$ual4s $iscernment or perception of the stimulation of speciali5e$ nerve en$in&s $esi&ne$ to transmit information concernin& potential or actual tissue $ama&e .6nociception7 Secon$ is the in$ivi$ual4s reaction to this perceive$ sensation 6pain behavior7. "ain is a protective mechanism for the bo$y8 pain &ives information about states of the bo$y1 but unli9e other sensations1 not about the nature of the stimulus. Definition The $efinition &iven by (0S" 6(nternational 0ssociation for the stu$y of pain7, :0n unpleasant sensory an$ emotional e*perience associate$ #ith actual or potential tissue $ama&e1 or $escribe$ in terms of such $ama&e;. "ain is al#ays sub2ective. )ach in$ivi$ual learns the application of the #or$ throu&h e*perience relate$ to in2ury in life. (f is un<uestionably a sensation in a part of bo$y1 but it is also al#ays unpleasant an$ therefore also an emotional e*perience. Nerve physiology !. Neurons( Nerve cells calle$ neurons are responsible for con$uctin& nerve impulse from one part of bo$y to another. They are the structural an$ functional unit of the nervous system. Structure of a Neuron/ Consist of three $istinct portions 1. Cell bo$y 2. -en$rites an$ 3. 0*on 1. Cell bo$y 6soma or peri9aryon7 , contains1 a #ell,$efine$ nucleus an$ nucleolus surroun$e$ by a &ran$er cytoplasm. =ithin the cytoplasm are typical or&anelles such as lysosomes1 mitochon$ria an$ >ol&i comple*es. 0lso in cytoplasm are locate$ structures Characteristics of neurons8 chromatophilic substance an$ neurofibrils.

Chromatophilic substance 6Nissl bo$ies7 is an or$erly arran&ement of &ranular 6rou&h7 en$oplasmic reticulum #hose function is protein synthesis. Neurofibrils are lon&1 thin fibrils compose$ of in support an$ transportation of nutrients mature neurons $o not contain a mitotic apparatus. 2. Neurons have t#o 9in$s of cytoplasmic process/ -en$rites 6$en$ro ?tree7 are usually hi&hly branche$1 thic9 e*tensions of the cytoplasm of cell bo$y. There function is to con$uct nerve impulses to#ar$s the cell bo$y. 3. 0*on/ is usually a sin&le lon& thin process that is hi&hly speciali5e$ an$ con$ucts nerve impulse a#ay from the cell bo$y to another neuron. (t usually ori&inates from the cell bo$y as a small conical elevation calle$ a*on hilloc9. (ts cytoplasm is calle$ a*oplasm an$ is surroun$e$ by a plasma membrane 9no#n as the a*olemma. 0*on vary in len&th from a fe# millimeter in brain to a meter or more in spinal cor$ an$ toes. The $istal en$s of a*on terminals are e*pan$e$ into bulb li9e structures calle$ synaptic en$ bulbs.

). Structure of $yelin ted nerve fi*re( The term nerve fibre may be applie$ to any process pro2ectin& from the cell bo$y. .ore commonly it refers to an a*on. 0 nerve fibre may be myelinate$ 6or me$ullate$7 or non,myelinate$ 6non,me$ullate$7. Myelin sheath is a multilayere$1 #hite phospholipi$ se&mente$ coverin&. 0*ons #ith such a coverin& is calle$ myelinate$1 #here as those #ithout it unmyelinate$. The function of the myelin sheath is to increase the spee$ of nerve impulse con$uction an$ to insulate an$ maintain the a*on. .yelin is responsible for color of #hite matter in the nerves1 brain an$ spinal cor$.

The

myelin

sheath

of

a*on

is

pro$uce$

by

flattene$

cells1

calle$

Neurolemmocytes. 6sch#ann cells7 locate$ alon& the a*ons. The peripheral nucleate$ cytoplasmic layer of neurolemmocyte is calle$ the neurolemma 6sheath of Sch#ann7.

@et#een the se&ments of myelin sheath are unmyelinate$ &aps calle$ neurofibral no$es. 6 Nodes of ranvier7. 0t no$e of ranvier1 there is no myelin sheath an$ the neurilemma is in $irect contact #ith a*is cylin$er. The central core of the a*on is calle$ a*oplasm8 #hich is pasty in nature. The a*oplasm is ensheathe$ by a membrane calle$ a*olemma.

Non $yelin ted nerve fi*res+ 0s there is no myelin sheath the $iameter of these nerves are very small1 an$ there is no no$e of ranvier. 3. Cl ssific tion of neurons( 1. Structural classification/ @ase$ on number of processes e*ten$in& from the cell bo$y. 1. .ultipolar neurons A several $en$rites an$ one a*on 2. @ipolar A one $en$rite an$ one a*on 3. Bnipolar 6pseu$ounipolar7, has only one process e*ten$in& from the cell bo$y1 #hich $ivi$e$ into a central branch1 #hich function as an a*on1 an$ a peripheral branch1 #hich functions as a $en$rite. 2. 3unctional classification/ @ase$ on the $irection in #hich they transmit impulses. 1. Sensory 6afferent7 A transmit impulse from receptor in s9in1 sense or&ans1 muscles1 2oints1 viscera to brain an$ spinal cor$. They are usually unipolar. 2. .otor 6efferent7 neurons A convey impulses from the brain an$ spiral cor$ to effectors1 #hich may be either muscle or &lan$s. 3. +ther neurons calle$ association neurons carry impulses from sensory to motor neurons an$ are locate$ in brain an$ spinal cor$. )&1.stellate cells. The processes of afferent an$ efferent neurons are arran&e$ into bun$les calle$ Nerves1 if outsi$e the CNS or fiber tracts if insi$e the CNS. The functional components of nerves are nerve fibres1 #hich may be &roupe$ accor$in& to follo#in& scheme. 1. >eneral somatic afferent fibres 2. >eneral somatic efferent fibres 3. >eneral visceral afferent fibres 4. >eneral visceral efferent fibres 6autonomic7 , Convey impulse from CNS to help control contractions of smooth an$ car$iac muscle an$ rate of secretion of salivary &lan$s. ". Nerve i$pulse The stri9in& features of neurons is their hi&hly $evelope$ ability to &enerate an$ con$uct electrical messa&es calle$ nerve impulse. .embrane potentials A (n a restin& neuron 6one that is not con$uctin&7 there is a $ifference in electrical char&es on either si$e of membrane. This $ifference is partly the result of une<ual $istribution of potassium 69C7 ions an$ so$ium ions 6NaC7 on either si$e of membrane. )ven #hen a nerve cell is not con$uctin& an impulse1 it is active1 transportin& ions across its membrane. Na C ions are actively

transporte$ out1 an$ 9C transporte$ in. The membrane system by #hich Na C an$ 9C actively transporte$ simultaneously is calle$ the sodium potassium pump.

ions are

The so$ium,potassium pump not only actively transports Na C an$ 9C ions1 but also establishes concentration &ra$ient for ions. The result is that there is $ifference in char&e on either si$e of membrane1 net positive outsi$e an$ net ne&ative insi$e. This $ifference in char&e on either si$e of membrane of restin& neuron is the resting membrane potential (RMP), such a membrane is sai$ to be polarized. )lectrical measurements of a polari5e$ membrane in$icate a volta&e of about A 7D m%. )*citability The ability of nerve cells to respon$ to stimuli an$ convert them into nerve impulses is calle$ e*citability. 0 stimulus is any con$ition in the environment capable of alterin& the restin& membrane potential. (f an e*citatory stimulus is of a$e<uate stren&th1 calle$ a threshold stimulus1 is applie$ to a polari5e$ membrane1 the membrane4s permeability to Na C ions &reatly increases at the point of stimulation. The so$ium channels open an$ permit the inflo# of Na C ions by $iffusion. 0s more NaC ions enter the membrane then leave1 the restin& membrane potential be&ins to chan&e. 0t first1 the potential insi$e the membrane shift from E7D to 5ero1 then to a positive value. This process is calle$ epolarization. -epolari5ation be&ins at E6' m% an$ from this point on the membrane is sai$ to be $epolari5e$. Throu&hout $epolari5ation the Na C ions continue to rush insi$e until the !." is reverse$. +nce the events of $epolari5ation have occurre$1 #e say that a nerve impulse 6nerve action potential7 is initiate$.

0n action potential is a rapi$ chan&e in membrane potential that involves a $epolari5ation follo#e$ by repolari5ation. The nerve impulse that is &enerate$ at any one point on membrane usually e*cites 6$epolari5es7 a$2acent portions of the membrane1 causin& the impulse to be propa&ate$. @y the time the nerve impulse has travele$ from one point to the ne*t1 the previous point becomes Repolarized, its restin& potential is restore$. The repolari5ation perio$ returns the cell to its restin& membrane potential A7D m%. 'efr ctory Period( =hen a nerve fibre is pro$ucin& an action potential1 the fibre becomes refractory to a secon$ stimulus. The first phase of this refractory perio$ is calle$ !bsolute Refractory period1 i.e. no matter ho# stron& is the stimulus1 the fibre $oes not respon$. -urin& the later phase1 only a very stron& stimulus can pro$uce a response1 6i.e. the threshol$ is no# hi&her than normal7 this phase is calle$ Relative refractory period.

,ll or None principle( 0 sin&le nerve cell1 transmits an action potential accor$in& to the all,or,none principle. 0ny stimulus stron& enou&h to initiate a nerve impulse is referre$ to as "hreshold (liminal) #timulus. (f a stimulus stron& enou&h to initiate a nerve action potential1 the impulse is con$ucte$ alon& the entire neuron at a constant an$ ma*imum stren&th. 0ny stimulus #ea9er than a threshol$ stimulus is terme$ a subthreshold stimulus. Such a stimulus1 if occurrin& only is incapable of initiatin& a nerve impulse. (f ho#ever1 a secon$ stimulus or a series of subthreshol$ stimuli is <uic9ly applie$ to the neuron1 the cumulative effect may be sufficient to initiate an impulse. This phenomenon is calle$ $summation%. S lt tory Conduction( The step by step $epolari5ation of each a$2acent area of the a*on or $en$rite plasma membrane1 is seen in unmyelinate$ fibres1 the con$uction calle$ Fcontinuous4. The myelin sheath surroun$in& a fibre $oes not con$uct electric current. The myelin sheath is interrupte$ at various intervals calle$ no$es of ranvier. 0t no$es1 membrane $epolari5ation can occur an$ nerve action potentials can be &enerate$ an$ con$ucte$ #hen a nerve impulse is con$ucte$ alon& a myelinate$ fiber1 (t moves from one no$e to another by ionic current flo# throu&h the surroun$in& e*tracellular flui$. Thus the impulse 2umps from no$e to no$e. This type of con$uction seen in myelinate$ fibers is calle$ #altatory conduction.

Speed of nerve conduction Nerve fibers havin& a &reater $iameter an$ those #ith a myelin sheath1 con$uct faster1 than those #ith small ones. @ase$ on their velocity of con$uctions >asser an$ )rlan&er ma$e a classification in 1'2D as belo#. Class of nerve 3ibre 0I HI 0 0J HJ 0KHK 0LHL @ C -iameter 6in Gm7 thic9 or thin 22,128 thic9est Meavily myelinate$ 12,68 thinner than I myelinate$ 6,38 still more thin sli&htly myelinate$ 5,28 still thinner N2 8 myelinate$ 1.5, D.38 Non,myelinate$ )*tremely thin 3D,12 1D,3 2,D.5 6slo#est7 3D,15 .otor nerves to intrafusal muscle if the spin$le 0fferent for thermal senses "re&an&lionic fibres of 0NS 0fferent for pain 8 post,&an&lionic sympathetic 7D,3D %elocity of con$uction 6mHsec7 12D,7D .otor nerve 6somatic7 an$ proprioceptive 6sensory7 0fferent for touch ($entity of nerves 6#here foun$7

&. Syn pse (mpulses are con$ucte$ bet#een one neuron to another across a synapse A a 2unction bet#een t#o neurons. The synapse is essential for homoestasis because of its ability to transmit certain impulse an$ inhibit other. =ithin a synapse is a minute space1 fille$ #ith e*tracellular flui$1 about 2D nm across1 calle$ synaptic cleft. 0 presynaptic neuron is locate$ before a synapse. 0 post synaptic nerve is locate$ after a synapse. (n the presynaptic bulb&'nob there are small vesicles1 each about 5Dnm $iameter1 containin& a chemical substance1 #hich acts as a synaptic transmitter calle$ a*o$en$ritic1 a*osomatic an$ a*oa*onic

Synaptic transmission Can be e*citatory or inhibitory transmitter,receptor interaction. 0n e(citatory receptor interaction is one that can lo#er the post synaptic neuron4s membrane potential so that a ne# nerve impulse can be &enerate$ across the synapse. 0s a result of combination of the chemical transmitter #ith the receptor1 the post synaptic membrane is partially $epolari5e$1 i.e. there is a $rop of potential across the membrane. This chan&e from !." level in the $irection of threshol$ level is calle$ )"S". 6)*citatory post,synaptic potential7 )nhibitory transmitter receptor interaction * (s one that can inhibit nerve impulse &eneration at a synapse. The inhibitory transmitter receptor interactions ma9e the post synaptic neuron4s !." more ne&ative. This is referre$ to as hyperpolari5ation. The alteration of the post synaptic membrane in #hich the restin& membrane potential is ma$e more ne&ative is calle$ the inhibitory post synaptic potential 6("S"7.

"re,synaptic inhibition. This occurs before a nerve impulse reaches a synapse. (n this process1 a synaptic en$ bulb of an inhibitory neuron synapses #ith the synaptic en$ bulb of a presynaptic neuron at an e*citatory synapse. =hen inhibitory neuron releases neurotransmitter it $epresses the release of

e*citatory transmitter by presynaptic neuron. This1 in turn $ecreases stimulation of the post synaptic neuron. "resynaptic inhibition occurs in many sensory path#ays of nervous system an$ provi$es a means by #hich responses of post,synaptic neuron can be re&ulate$. -. Neurotr ns$itters+ are chemicals secrete$ by the nerve terminals, 1. 0NS,fibers 6sympathetic an$ parasympathetic7 )&. 0cetylcholine. 2. Special neuronal tracts in the brain. 6).&./ Nora$rener&icHcholiner&icH serotininer&icHhistaminera&icH>0@0er&ic fibers7 3. Somatic 3ibres 6e.&. neuromuscular 2unction7 4. )NS 6)nteric nervous fibres7 an$ so on. .. The sensory Syste$( The sensory system brin&s information from the periphery to the CNS. The CNS re<uires a continual flo# of information to maintain homeostasis an$ initiate appropriate responses to chan&es in the internal an$ e*ternal environments. +ur ability to sense stimuli is vital to our survival. Conventionally the sensory system is $ivi$e$ into 1. >eneral Senses 2. Special senses.

/. The 'eceptors( 0 receptor or sense or&an may be vie#e$ as a speciali5e$ nervous tissue that is e*tremely sensitive to certain type of chan&es in internal or e*ternal con$itions. 3rom the

10

receptors emer&e1 the afferent sensory nerve #hich eventually reaches the CNS. Thus receptor is the first structure in the sensory path. !eceptors are also calle$ as +nd organ. Cl ssific tion( Types 1. !eceptors of special senses, e.&. eye A ro$s an$ cones. 2. !eceptors of somatic an$ visceral. 1. Touch 1 pressure , 6i7 .er9el4s $isc 6ii7 .eissners corpuscle 6iii7 "acinian corpuscle 6iv7 !uffini en$ or&an 6v7 Mair en$ or&an 6vi7 3ree nerve en$in&. 2. "ain, 3ree nerve en$in& 3. Col$,col$ receptors. 4. Meat,free nerve en$in& 5. "roprioception an$ 9inesthesia, muscle spin$les8 cristae an$ maculae of vestibular apparatus. 6. (nteroception, 6a7 Chemoreceptor 6i7 Caroti$ bo$y chemoreceptor , bloo$ +2 H C+2 tension1 pM. chemoreceptor, $etection C+2 6@rain Stem7. 6b7 @aroreceptors/ 17 Caroti$ Sinus 6@loo$ "ressures7 27 0fferent arteriole of renal artery. 37 Oeft %entricular mechanoreceptors. 47 !eceptors of Merin& @reuer refle*. 3. Can be classifie$ as/ 6i7 .echanoreceptors 6ii7 Thermoreceptors 6iii7 "ain receptors 6iv7 Chemo receptors. IV. P,IN "ain is in$ispensable for normal life. (t provi$es us #ith information about tissue $ama&in& 6no*ious7 stimuli an$ helps us to protect ourselves from &reater $ama&e. 1. !eceptors for pain A 0re calle$ nociceptors, are simply free nerve en$in&s1 the branchin& en$s of the $en$rites of certain neurons. They are foun$ in practically every tissue of the bo$y. +ther cutaneous receptors for touch1 pressure1 heat an$ col$ #hen stimulate$ e*cessively may cause pain. 2. Stimulus for pain, 6ii7 Central

11

Stimulus may be "hysical or chemical nature. Physical stimuli, pain is pro$uce$ in the s9in by many 9in$s of physical stimuli1 thermal1 mechanical an$ electrical stimuli8 Chemical stimuli, it is possible that physical pain stimuli act via chemical me$iators. The physical in2ury causes the release of certain chemical factors #hich are responsible for the lastin& pain an$ hyperal&esia. Nature of chemical factors ,hich produce pain / .any substances can arouse pain #hen applie$ to s9in or mucous membrane or #hen infecte$ into the bo$y. They can be e*trinsic alo&enic substances or (ntrinsic alo&enic Substances. +(trinsic alogenic substances inclu$e stron& irritants such as aci$s an$ al9alies1 or&anic solvents1 #ar &ases an$ li<ui$s #hich penetrate s9in an$ mucous membrane. 0lso inclu$e$ are plant an$ animal stin&s an$ venoms. )ntrinsic alogenic substances are the substances $erive$ from livin& bo$y1 cells an$ flui$s. (t has been sho#n that many substances normally present insi$e bo$y cells can cause pain #hen release$ into e*tracellular flui$. ).&. #hen bloo$ platelets $isinte&rate they release 5MT 6Serotonin7 #hich pro$uces pain. )rythrocytes have hi&h 9C an$ 0T"1 #hich can evo9e mar9e$ pain #hen the cell is lyse$. Oeucocytes have hi&h cationic protein in their lysosomes1 #hich pro$uce pain. .ast cells contain histamine #hich in hi&h concentration pro$uces pain. +ther substances inclu$e, acetylcholine. "lasma 9inins/ The plasma an$ )C3 contains a protein system from #hich very active pain pro$ucin& plasma 9inins can be forme$ e.&. @ra$y9inin #hich is a nanopepti$e an$ 9alli$in #hich is a $ecapepti$e. They have actions li9e , cause vaso$ilatation1 increase vascular permeability an$ pain. "ain pro$uce$ by @ra$y9inin is enhance$ by 5.MT. Stu$ies have reveale$ that bra$y9inin is a physiolo&ical me$iator of pain an$ patient receptors are selectively locali5e$1 to thin C unmyelinate$ FC4 fibers1 alon& #ith other several sites. (t is interestin& to note that .yelinate$ 0L fibers1 sho#e$ no response to application of bra$y9inin. 0llen . Oepins9i et al in a in vivo stu$y have foun$ $etecte$ level of bra$y9inin in pulp tissue $ia&nose$ #ith irreversible pulpitis #hen the patient ha$ reporte$ pain in the past1 compare$ #ith patients #ho #ere in pain 2ust before their visit to to en$o$ontist. Marol$ >oo$ies et al in have $evelope$ the use of reverse phase 1 hi&h performance li<ui$ chromato&raphy 6M"OC7 to i$entify an$ <uantify bra$y9inin 1 substance p1 an$ neuro9inin 0 containe$ in $ental pulp 6Pournal of )n$o$ontics 1''78 23647/21D,2D47 "rosta&lan$in4s 6">4s7

12

0re capable of pro$ucin& pain #hen present in hi&h concentration 6e.&./ 1DQmol l ,17 but lo#er concentration pro$uce hyperal&esia. ">4s are forme$ from arachi$onic aci$1 an$ since anti, inflammatory $ru&s such as aspirin inhibit "> synthesis #hich may account for relief of pain. ">4s cause $e&ranulation of mast cells #hich in turn release Mistamine. The histamine then function as a chemotactic factor to #hich eosinophils respon$. )osinophils &ranules1 contain eosinophilic cation protein 6)C"7 that has a &reat neuroto*ic potential an$ is capable of $ama&in& sensin& nerve en$in&s resultin& in $ischar&e of neuropepti$es such as substance P an$ calcitonin gene related peptide.

3. Ch r cteristics of P in -. "hreshold and intensity (f the intensity of stimulus is belo# the threshol$ 6subthreshol$71 pain is not felt. 0s the intensity increases more an$ more pain is felt. .. !daptation "ain receptors sho# no a$aptation an$ so the pain continues as lon& as the receptors continue to be stimulate$. This non,a$aptin& nature of pain receptors 9eep the person apprise$ of a $ama&in& stimulus. /. 0ocalization of pain "ain sensation is some #hat poorly locali5e$. "ain is accurately locali5e$ in s9in1 but accuracy is lost as the source of pain sin9s $eeper into bo$y. (t may be sai$ that pain is primarily locali5e$ to the se&ment correspon$in& to the stimulate$ nerves1 an$ that accuracy of locali5ation is superimpose$ on this se&mental pattern. True visceral an$ $eep somatic pain is sometimes felt at the site of primary stimulation an$ may or may not be associate$ #ish pain1 #hich is referre$. 1. +motional accompaniment "ain is commonly accompanie$ by emotions. These emotions are unpleasant. 5. (nfluence of rate of $ama&e on intensity of pain. (f the rate of tissue in2ury is hi&h1 intensity of pain also is hi&h an$ vice versa. 6. T#o types of pain Can be 6i7 3ast "ain 6ii7 Slo# "ain 0fter receivin& a nociceptive stimulus1 either 0L or C type fiber or both may be stimulate$. !2 delta fibers are some#hat thic9 an$ finely myelinate$ #ith a faster rate of con$uction1 but C fibers are very thin an$ non,myelinate$ #ith a much slo#er rate of con$uction. C type of fibers ho#ever outnumber 0,$elta fibers. Bsually the pain $ue to C fibres stimulation is particularly unpleasant an$ outlasts the perio$ of stimulation.

13

3ast pain is also $escribe$ by many alternative names1 such as sharp pain1 pric9in& pain1 acute pain an$ it is not felt in most of $eeper tissues of bo$y. Slo# pain &oes by multiple a$$itional names burnin& pain1 achin& pain1 throbbin& pain nauseous pain an$ chronic pain. (t can occur both in s9in an$ in almost any $eep tissue or or&an. ". 'e ctions of p in 1. @ehavioral Cryin&1 moanin& screamin&1 ra&e1 pain1 frustration1 mental irritation an$ $epression can $evelop. 2. .uscular/ Spasm of the s9eletal muscles in the affecte$ re&ion $evelops. ).&. spasm of muscles aroun$ a fracture$ bone. 3. Chan&es in autonomic nervous system. Somatic pain is accompanie$ usually by si&ns of sympathetic overactivity. ).&./ rise in @"1 tachycar$ia1 pupillary $ilatation. Conversely in visceral pain there is fall in @"1 nauseatin& feelin&1 syncope. 4. !efle* response &. P in P th0 y 3iel$s $ivi$e$ the processin& of pain from stimulation of primary afferent nociceptors to the sub2ective e*perience of pain in 4 steps / a. Trans$uction b. Transmission c. .o$ulation an$ $. "erception 1.Trans$uction/ is the activation of the primary afferent nociceptor. "rimary afferent nociceptors can be activate$ by various stimuli both intrinsic an$ e*trinsic. "rimary afferent nociceptors can be activate$ by intense thermal an$ mechanical stimuli1 no*ious chemicals an$ no*ious col$. They are also activate$ by stimulation from en$o&enous al&esic chemical substances 6inflammatory me$iators7 pro$uce$ by bo$y in response to tissue in2ury. -ama&e$ tissue or bloo$ cells releases the polypepti$e bra$y9inin1 R C1 histamine1 serotonin an$ arachi$onic aci$. 0rachi$onic aci$ is processe$ by t#o $ifferent en5yme systems to pro$uce prosta&lan$ins an$ leu9otrienes1 #hich alon& #ith bra$y9inin1 act as inflammatory me$iators. The presence of such an on&oin& inflammatory state courses physiologic sensitization of the primary afferent nociceptors. Sensiti5e$ nociceptors $isplays on&oin& $ischar&e1 a lo#ere$ activation threshol$ to normally non painful stimuli an$ an e*a&&erate$ response to no*ious stimuli. 6"rimary Myperal&esia7.

14

(n a$$ition to sen$in& nociceptive impulses to synapse in $orsal horn of spinal cor$1 activation of cutaneous C fibers cause their cell bo$ies to synthesis the neuropepti$es1 substance " an$ calcitonin &ene relate$ pepti$e 6C>!"7. These neuropepti$es are then anti$romically transporte$ alon& a*on branches to periphery1 #here they in$uce further plasma e*travasation an$ increase inflammation 6pro$uce flare7 aroun$ in2ury site1 referre$ to as neurogenic inflammation or a(on refle( 2. Transmission !efers to the process by #hich peripheral nociceptive information is relaye$ to the central nervous system. The primary afferent nociceptors synapses #ith a secon$ or$er pain transmittin& neuron in the $orsal horn of the spinal cor$ #here a ne# action potential hea$s to#ar$s hi&her brain structures. Du l p in p th0 ys in spin l cord nd *r in ste$ +n enterin& the spinal cor$1 the pain si&nals ta9e t#o $ifferent path#ays to brain1 throu&h the Neospinothalamic tract an$ the "aleospinothalamic tract.

15

"he Neospinothalamic tract for fast pain The Ffast4 type 0L pain fibers transmit mainly the mechanical an$ thermal pain. They terminate mainly in lamina ( of $orsal horns1 an$ there e*cite the secon$ or$er neurons of the Neospinothalamic tract. These &ive rise to lon& fibers that cr si$e of the cor$ throu&h the anterior commissure an$ then pass up#ar$s to brain in the anterolateral columns. 0 fe# fibers of the Neospinothalamic tract terminate in the reticular area of brain stem1 but most pass all the #ay to thalamus1 terminatin& in the ventrobasal comple*1 alon& #ith cross imme$iately to the opposite $orsal column me$ial lemniscus tract. 3rom these areas of the si&nals are transmitte$ to other basal areas of brain an$ to the somatic sensory corte*.

16

"he Paleospinothalamic path,ay for transmitting slo, chronic pain. Transmits pain mainly carrie$ in the peripheral slo# sufferin& type C pain fibers. The C,fibers terminate almost entirely in the laminas (( an$ ((( of $orsal horns1 #hich to&ether is calle$ substantia gelationsa1 the lateral most $orsal root fiber. .ost of the si&nals then pass throu&h one or more a$$itional short fiber enterin& mainly lamina %1 also in $orsal horn. Mere the last neuron in the series &ive rise to lon& a*ons1 that mostly 2oin the fibers from the fast path#ay1 passin& throu&h the anterior commissure to opposite si$e of the cor$1 then up#ar$s to brain in same anterolateral path#ay. Termination/ only one,tenth to one forth of the fibers pass all the #ay to thalamus. (nstea$ they terminate principally in one of three $ifferent areas/ 1. Reticular nuclei of medulla1 pons an$ mesencephalon. 2. "ectal area of mesencephalon 3. Periac3ueductal gray re&ion surroun$in& the a<ue$uct of sylvius. These lo#er re&ions of brain appear to be very important in the appreciation of sufferin& type of pain. neurons #ithin $orsal horns themselves before

17

3rom the reticular area of the brain stems1 multiple short A fiber neurons relay the pain si&nals up#ar$s into the intralaminar nuclei of the thalamus an$ also into certain portions of hypothalamus. "he neurotransmitters The sensory fibers 60L S C7 transmit information by releasin& e*citatory amino aci$s1 such as &lutamate or neuropepti$es 6e.&./ substance " or Calcitonin &ene relate$ pepti$e 6C>!"7 #ubstance P is the probable neurotransmitter of type C nerve en$in&s. (t is slo# to buil$ up at synapse an$ also slo# to be $estroye$. 0fter the pain is over1 the substance " probably persists for many more secon$s or perhaps minutes. This may e*plain at least partially the persistence of slo# type of pain even after the painful stimuli is remove$. 6Note/ (n animal stu$ies the a$ministration of receptor anta&onists to &lutamate 6in particular7 an$ anta&onists to substance " an$ C>!" 6to lesser e*tent7 has been sho#n to bloc9 hyperal&esia.7 )vi$ence &athere$ in animal stu$ies stron&ly implicates anta&onists to the &lutamate N, methyl -,aspartate 6N.-07 receptor as bein& effective in re$ucin& hyperal&esia. These compoun$s are li9ely to serve as prototype for future classes of anal&esic $ru&s. 3. .o$ulation/

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!efers to mechanisms by #hich the transmission of no*ious information to the brain is re$uce$. The en$o&enous pain inhibitin& system consists of 3 ma2or components an$ other accessory components. 1. The Periac3ueductal gray area of the mesencephalon an$ upper pons surroun$in& the a<ue$uct of sylvius. Neurons from this area sen$ si&nals to 1 2. The Raphe magnus nucleus1 a thin mi$line nucleus locate$ in the lo#er pons an$ upper me$ulla. 3rom here si&nals are transmitte$ $o#n the $orsolateral columns in the spinal cor$. 3. 0 pain2inhibiting comple( locate$ in the $orsal horns of the spinal cor$. 0t this point the anal&esia si&nals can bloc9 the pain before it is relaye$ on to the brain. Several $ifferent transmitter substances are involve$ in pain inhibition system1 especially )n9ephalin an$ serotonin. .any nerve fibers $erive$ from both periventricular nuclei an$ the "0> area secrete )n9ephalin at their en$in&s. The en$in&s of fibers of raphe ma&nus nucleus terminate in $orsal horns of the spinal cor$1 secrete serotonin at their en$in&s. The serotonin in turn acts on still another set of local cor$ neurons that are believe$ to secrete en9ephalin. )n9ephalin is believe$ to cause presynaptic inhibition of both incomin& type C an$ type 0L pain fibers1 #here they synapse in $orsal horns. Thus1 the pain inhibitin& system can bloc9 pain si&nals at the initial entry point of the spinal cor$. 0n en$o&enous opioi$ system for pain mo$ulation also e*ists. )n$o&enous opioi$ pepti$es are naturally occurrin& pain $ampenin& neurotransmitters an$ neuron mo$ulators that are implicate$ in pain suppression an$ mo$ulation e.&./ J,en$orphin1 met,en9ephalin1 leu,en9ephalin an$ $ynorphin. They re$uce nociceptive transmission by preventin& the release of e*citatory neurotransmitter substance " from primary afferent nerve terminal. There are receptors calle$ opio$ receptors in brain 6e.&. "0>7 an$ S>!. These receptors are of 4 9in$s i.e.1 R1 G11 1 #hich can combine #ith en$o&enous opio$ pepti$es1 e*o&enous opio$ al9aloi$s 6morphine7 an$ also #ith anta&onists of opium. 4. "erception( the final step in the sub2ective e*perience of pain is perception. =hen nociceptive impulse reaches the corte*1 perception occurs. (t is at this point that sufferin& may occur. #uffering refers to the manner in #hich the patient respon$s to pain. Mo# an$ #here the brain perceives pain is still un$er investi&ation. "art of the $ifficulty lies in fact that pain e*perience has at least t#o components/ 6i7 6ii7 The sensory $iscriminatory $imension The affective 6emotional7 $imension.

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The effective $imension of pain is ma$e up of feelin&s of unpleasantness an$ emotions associate$ #ith future implications relate$ to pain. 0lthou&h ma&netic resonance ima&in& 6.!(7 stu$ies have $emonstrate$ the involvement of thalamus an$ multiple cortical areas in perception of pain1 it is clear form the intersub2ect variability in the activation of any one of these areas that affective reactions an$ possibly motor responses are also involve$. +f si&nificance is the fact that #ith hi&h level of mo$ulation1 or #ith $ama&e in the pain transmission system. (t is possible to have nociception #ithout pain perception. Conversely1 #ith certain types of $ama&e to the nervous system1 there may be an overreaction to pain stimuli or pain stimuli or pain perception #ithout nociception.

-. 'eferred p in( "ain arisin& from $eep tissue muscles li&aments1 2oints an$ viscera is often perceive$ at a site $istant from the actual nociceptive source. This pain is calle$ !eferre$ pain. .echanism of referre$ pain/ T#o most popular theories to e*plain referre$ pain are 6i7 6ii7 Conver&ence,pro2ection theory Conver&ence, facilitation theory.

(i) Convergence2pro4ection theory* "rimary afferent nociception from both visceral an$ cutaneous neurons often conver&e onto the same secon$ or$er pain transmission neuron in the spinal cor$. The brain1 havin& more a#areness of cutaneous than visceral structures throu&h the past e*perience1 interprets the pain as comin& from the re&ions sub serve$ by the cutaneous afferent fibers.

(ii) Convergence2 facilitation theory* This theory is similar to conver&ence,pro2ection1 e*cept that the nociceptive input from the $eeper structures causes the restin& activity of secon$ or$er pain transmission neuron in

20

spinal cor$ to increase or be :facilitate$;. The restin& activity is normally create$ by impulses from the cutaneous afferents. :3acilitation; from the $eeper nociceptive impulses causes the pain to be perceive$ in the area that creates the normal restin& bac9&roun$. .. Viscer l P in/ 0 viscous is insensitive to most sensory stimuli. Mo#ever1 pain sensation can1 un$er some con$itions arise from viscera. Characteristics/ i7 ii7 iii7 iv7 0s a rule1 the visceral pain is Freferre$4 +ften accompanie$ by vomitin& an$ fall in @" -ru&s re<uire$ to alleviate visceral pain are often sharply $ifferent from those re<uire$ to alleviate the somatic pain. "ain of a hollo# viscus is often felt as colic1 that is1 it comes an$ &oes to reappear a&ain. Causes/ ).&. a. (schemia e.&. Car$iac pain. b. +bstruction of hollo# viscera A e.&. obstruction of se&ment of lar&e intestine. c. (nflammation, inflame$ appen$i*. $. +ver$istension of hollo# viscus. e. Severe vaso$ilatation, e.&. hea$ache $ue to meanin&ful vaso$ilatation. Ph nto$ li$* p in( 0 9in$ of pain fre<uently e*perience$ by patients #ho have ha$ a limb amputate$ is calle$ Fphantom limb pain4. They still e*perience sensations such as itchin&1 pressure1 tin&lin& or pain in e*tremity as if limb #ere still there. This probably occurs because the remainin& pro*imal portions of sensory nerves that previously receive$ impulse from limb are bein& stimulate$ by the trauma of amputation an$ brain interprets these stimuli from cut nerves1 as if comin& from non e*istin& limb. /. Trige$in l Syste$( The primary afferent nociceptors from the ma*illary an$ man$ibular1 branches of tri&eminal nerve synapse in the nucleus caudalis of brain stem 6at level of pons7. The nucleus cau$alis is the cau$al portion of the tri&eminal spinal tract nucleus an$ correspon$s to the substantia gelatinosa of the rest of spinal $orsal horn. 6Nucleus cau$alis is the sensory nucleus of Tri&eminal nerve7

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3rom here the nociceptive input is transmitte$ to the hi&her centers via tri&eminal lemniscus1 to "ostero,ventral nucleus of the thalamus S via connectin& neurons to contralateral si$e of corte* of brain. +f si&nificance is the arran&ement of tri&eminal nerve fibers #ithin this nucleus an$ the fact that the nucleus $escen$s as lo# as the 3,S 4 cervical vertebral 6C,31 47 in the spiral Cor$. 3ibers from all three tri&eminal branches are foun$ at all levels of nucleus cau$alis arran&e$ #ith the man$ibular $ivision hi&hest S ophthalmic $ivision lo#est. (n a$$ition1 they are arran&e$ in such a manner that fibers closest to mi$line of face synapse in most cephala$ portion of the tract. The more lateral the ori&in of fibres of face1 the more cau$al the synapse in the nucleus. Bn$erstan$in& this laminate$ arran&ement helps to e*plain #hy a ma*illary molar toothache may be perceive$ as pain in man$ibular molar on same si$e 6!eferre$7 but not in an incisor.

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@ecause the tri&eminal nucleus $escen$s to C3,4 level in spinal cor$1 primary afferent nociceptors from $eep cervical structures synapse on same secon$ or$er pain transmission neurons that subserve the fifth cranial nerve1 this serves as a basis for un$erstan$in& #hy cervical pain $isor$er may be perceive$ as pain in hea$ S face1 particularly in forehea$ S temple. 1. Theories of p in The precise mechanism for transmission of pain an$ the afferent efferent path#ay itself are not completely un$erstoo$ an$ therefore sub2ect to postulation. T#o ol$ but popular an$ one recent theory #ill be $iscusse$ -. "he specificity theory 0$vance$ by von 3rey in 1 '41 states that $ifferent sensory fibers me$iates $ifferent sensory mo$alities such as pain1 heat1 col$ touch S pressure. The receptors for pain are specific an$ mostly unmyelinate$ free nerve en$in&s. =hen stimulate$1 these fibers transmit impulses alon& specific path#ays. .. "he pattern theory (n 1 '4 >ol$schei$er #as the first to propose that stimulus intensity an$ central summation are the critical $eterminants of pain. The theory proposes that pain is &enerate$ by nonspecific receptors. (t is assume$ that all nerve fiber en$in&s are ali9e an$ that the pattern for pain is pro$uce$ by a more intense stimulation than for the other sensations. The summation of the pain impulses pro$uce a pattern that the brain receives S reco&ni5es.

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/. 5ate control theory The specific S pattern theories have been challen&e$ by evi$ence from .el5ac9 S =all 61'657 #ho intro$uce$ the >ate control theory of pain transmission. The actual mechanism is sub2ect of controversy 17 0*ons of large diameter afferent neurons 60I1 0J1 0K7 enter the Spinal Cor$ throu&h $orsal root. The "rincipal branch of lar&e, $iameter a*on enter $orsal horn1 synapsin& #ith "2cell 6calle$ Transmission cells1 locate$ a$2acent to substantia &elatinosa7. 0 collateral of some fiber enter the S> an$ another ascen$ to hi&her center. 27 Similarly 0*on of small,$iameter afferent neurons 6C an$ 0L7 also enters the $orsal horn of spinal cor$ to synapse #ith T,cells. They also sen$ collateral to S>. 37 The S> cells sen$ branches to synapse #ith incomin& a*on 6afferent7 fiber enterin& T cell pool. @ranches from S> cells $o not contact the T cells $irectly but rather the terminal area of 0 an$ C a*ons. The only activity that can be performe$ by cells of S> is to sen$ inhibition impulses to T,cell1 preventin& them from firin& impulse.

24

25

47 Oar&e $iameter fibers can only e*cite the S> cells1 #hich inturn sen$ out inhibitory impulses to T,cells 6"resynaptic inhibition7. Since T cells are unable to transmit an impulse1 the &ate is close$ to pain. 57 .essa&es 6impulses7 from the branches of smaller 0L an$ C fibres can only inhibit the S> cells1 stoppin& them from sen$in& inhibitory impulses to T cells. This action opens the &ate to pain. Since T cells are not receivin& inhibitory impulses from S> cells1 they are free to sen$ a painful response #hen activate$ by the smaller #hen activate$ by the smaller C an$ 0L fibers. Thus the small fibers 0L an$ C fibers1 open the &ate to pain by inhibitin& S> Cells8 lar&er 0I1 0J1 0K fibers close the &ate by e*citin& the S> cells. (t is postulate$ that the &ate control mechanism may be further mo$ulate$ by intrinsic brain mechanism 6"eriac<ue$uctal &ray1 reticular formation1 thalamus7 an$ throu&h emotional1 motivate$1 peripheral1 psychic1 an$ visual stimuli. 3inal response #ill $epen$ on the balance or net result of the initial input from all three system8 lar&e $iameter fibers1 small $iameter fibers an$ central control.

V .# n ge$ent of Dent l P in Introduction +rofacial pain is the presentin& symptom of a broa$ spectrum of $iseases. 0s a symptom1 it may be $ue to $isease of +rofacial structures inclu$in& teeth1 &enerali5e$ musculos9eletal or rheumatic $isease1 peripheral or central nervous system $isease1 or psycholo&ical abnormality8 or the pain may be referre$ from other sources. 6).&./ Cervical muscles or intracranial patholo&ies7. 3rom a $ia&nostic perspective1 the presence of absence of pain an$ its characteristics provi$es si&nificant an$ reliable $ia&nostic information. 3rom a practical perspective1 most patients &au&e the compliance of their $entist by ho# #ell the pain of $ental proce$ures is controlle$ an$ ho# effectively con$itions that cause pain are treate$. Therefore pain is central $ia&nostic an$ therapeutic issue in the practice of $entistry. -efinition of "ain The international 0ssociation of stu$y of pain 6(0S"7 $efine$ pain as :0n unpleasant sensory an$ emotional e*perience associate$ #ith actual or potential tissue $ama&e or $escribe$ in terms of such $ama&e. Cl ssific tion of orof ci l p in (. Somatic pain

26

!esults from no*ious stimulation of normal neural structures that innervate the bo$y tissues. 1. superficial A ).&. / Cutaneous an$ muco&in&ival pain 2. -eep A visceral pain A).&./ "ulpal $ental pain ((. .uculos9eletal A e.&. / T.P pain1 .uscle pain Neuro&enic pain (s &enerate$ #ithin the nervous system an$ is cause$ by an abnormality of the neural structure that innervates the bo$y tissue. 0 A "aro*ysysmal "ain ).&./ ($iopathic Neural&ia Symptomatic neural&ia @, -ifferentiation "ain A !esults from interference #ith the transmission of afferent impulses by primary sensory neurons. ).&./ , traumatic neuroma1 "ost traumatic pain. (((. "sycho&enic "ain Mas $iffuse an$ va&ue $istribution1 no apparent cause or physical evi$ence of inflammation. ).&./ Chronic face pain Chronic structural pain "sycho&enic pain Conversion hysteria "sychohoic hallucinations E2 $in tion nd ssess$ent of p tient 0ith Oro+f ci l p in 0n accurate $ia&nosis of pain an$ effective treatment re<uire an un$erstan$in& of the patient4s sub2ective perception of the $iscomfort. 0 systemic approach for collectin& $ia&nostic information is nee$e$ to minimi5e$ ris9 of missin& critical information. Mistory1 physical e*amination an$ behavior assessment serve as the basis for $ia&nosis. Mistory )valuation of pain must inten$ all the stan$ar$ component of a me$ical intervie#. Chief complaint1 history of presentin& illness past me$ical history1 me$ications1 revie# of system an$ family an$ social history. Mistory of presentin& illness M+"( shoul$ inclu$e a $etaile$ $escription of pain an$ its location. Pain characteristics intensity <uality location

27

onset associate$ events at onset $uration an$ timin& of pain course of symptoms since onset activities or e*periences that increase pain or $ecrease pain 0ssociate$ symptoms 6).&./ altere$ sensation1 s#ellin&7 "revious treatment an$ their effects.

0 %isual 0nalo& Scale 6%0S7 or numeric scale can be use$ to assess intensity an$ a <uestionnaire such as the ."T 6.c>ill pain <uestionnaire7 can capture the multi$imensional e*perience of pain. -etails of previous in2uries1 sur&eries an$ ra$iation therapy shoul$ be obtaine$. 6isual analog scale 0 visual analo& scale is a line that represents a continuous of a particular e*perience such as pain. The most common form use$ pain is a 1D cm line1 #hether hori5ontal or vertical1 #ith perpen$icular stops at the en$s. The en$s are anchore$ by :No pain;an$ :=orst pain ima&inable;. "atients are as9e$ to place a slash mar9 some#here alon& the line to in$icate intensity of their current pain complaints. No pain UUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUUU =orst pain ima&inable

Mc5ill pain 3uestionnaire (MP7) ."T is a verbal pain scale that uses a vast array of #or$s commonly use$ to $escribe a pain e*perience."atients use $ifferent #or$s to $escribe the affective component of their pain. To facilitate the use of these #or$s in a systemic #ay. .el5ac9 an$ Tor&erson set about cate&ori5in& many of these verbal $escriptors into classes an$ subclasses $esi&ne$ to $escribe these $ifferent aspects of the pain e*perience. The #or$s are liste$ in 2D $ifferent cate&ories. They are arran&e$ in or$er of ima&ine$ from least intense to most intense an$ are &roupe$ accor$in& to $istinctly $ifferent <ualities of pain. "atients are as9e$ to circle only one #or$ in each cate&ory that applies to them. The first 1D cate&ories represent $ifferent sensory $escriptors. The ne*t five cate&ories are effective or emotional $escriptors1 cate&ory 16 is evaluative1 6i.e. intensity7 an$ last four cate&ories are &roupe$ as miscellaneous. Chan&es in a patient4s pain e*perience can be monitore$ by a$ministerin& the <uestionnaire at various time points $urin& treatment an$ follo#,up. Sample of Mc5ill pain 3uestionnaire

28

"ast me$ical history an$ revie# of systems Melps to provi$e an insi&ht into the &eneral health of the patient an$ may provi$e clues re&ar$in& the present pain complaint. "atients use of me$ication shoul$ be recor$e$. "ain may be a presentin& feature or an on&oin& complaint in systemic $isease. The $ia&nostician shoul$ as9 supplemental <uestions in the follo#in& areas of concern. 1. Current me$ical con$itions. 2. Mistory of si&nificant illness or serious in2ury 3. "rior hospitali5ation 4. )motional an$ psycholo&ical history 5. Current me$ications 6. Mabit 6).&./ alcohols 1 tobacco1 $ru&s7 7. 0ny other noticeable sin&s or symptoms that may in$icate an un$ia&nose$ health problems. -ental history ,(s most important aspect of $ia&nosis. Specific information re&ar$in& the a&e of previous $ental #or91 as #ell as symptoms before an$ after the #or9 #as $one1 shoul$ be sou&ht from the patient. 3amily1 social an$ occupational history

29

Traumatic events or emotional $istress prior to the onset of pain1 a history of other close family members #ith chronic illness or pain1 an$ any chan&e in #or9 shoul$ be e*plore$ because these can be si&nificant stressors. Clinical e*amination +(tra oral 0ll patients shoul$ be e*amine$ for abnormal asymmetries1 s#ellin&1 chan&e in s9in color1 $rainin& sinus tracts1 or si&ns of trauma. )*tra oral e*amination inclu$es visual e*amination an$ $i&ital palpation of the face1 lips an$ nec9. )*tra oral s#ellin&s may in$icate serious sprea$in& of intraoral $isease process. "ainful an$ enlar&e$ lymph no$es are of particular importance1 because they in$icate sprea$ of infection an$ the possibility of mali&nant $isease. The e*tent an$ manner of 2a# openin& can provi$e information re&ar$in& sprea$ of infection an$ possible myofascial pain $ysfunction. )ntraoral e(amination , inclu$es a visual inspection of har$ an$ soft tissues of the oral cavity. 0n intraoral e*amination of oro,pharyn*1 chee9s alveolar mucosa1 &in&ival1 har$ an$ soft plate1 ton&ue an$ floor of mouth to i$entity possible areas of information1 abrasion ulceration1 neoplasm1 or other abnormality To prevent missin& any subtle lesions1 soft tissues an$ teeth of the area to be e*amine$ shoul$ be ma$e free of saliva. -ental e*amination , has t#o components 1. "hysical inspection 2. -ia&nostic tests Physical inspection Shoul$ inclu$e observation of perio$ontal health tissue color an$ tissue te*ture. 0ny restorations1 caries1 tooth $iscoloration1 erosion1 fractures1 s#ellin& an$ sinus tract shoul$ be note$. 0ny sin&s of perio$ontal $isease must be consi$ere$ in the $ifferential $ia&nosis. iagnosis tests* )nable the practitioner to/ i. ii. -efine the pain by evo9in& repro$ucible symptoms that1 characteri5e the chief complaint. Compare normal responses to abnormal responses #hich may be in$icative of pathosis. -ia&nostic tests inclu$e the pulpal sensitivity tests, hot an$ col$ thermal testin&1 as #ell as electric pulp testin&.

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.echanical tests inclu$e the tooth percussion an$ tissue palpation. Transillumination an$ ma&nification1 test cavity preparation an$ anesthetic tests are a$$itional means of confirmin& a $ia&nosis !a$io&raphic e*amination !a$io&raphic vie# #ill contribute to the location an$ i$entification of patient problem. Chan&es in pulp chambers compare$1 often constitute a recor$s of past pulpal insults1 caries1 secon$ary $entin un$er restorations1 very lar&e or narro# pulp chamber compare$ #ith a$2acent teeth1 $eep bases1 calcification an$ con$ensin& osteitis can all in$icate chronic inflammatory chan&es in the pulpal tissue. "eriapical films1 bite#in& an$ other supplemental films li9e panore* may be use$ for ra$io&raphic e*amination. -eterminin& the $ia&nosis The final phase of the $ia&nostic se<uence re<uire a systematic analysis of all pertinent $ata accumulate$ from the patients history as #ell as clinical1 $ental an$ ra$io&raphic evaluations. The first consi$eration #hen $eterminin& a $ia&nosis is #hether the patient chief complaint is repro$ucible. Bnless the symptoms can be $uplicate$1 a $ia&nosis shoul$ not be ma$e. "ulpal pain can be cause$ by caries1 fractures1 trauma an$ recent restorative treatment an$ less obvious cause such as $evelopmental anomalies or ortho$ontic tooth moment. =hen a correct $ia&nosis has been ma$e the cause of pain must be clearly un$erstoo$8 the $ia&nosis must be consistent #ith etiolo&y. Tre t$ent of p in "ain is the source of most chief complaints1 #hich implies the e*pectation of e*pe$ient treatment an$ relief. "ain mana&ement can be approache$ in several $ifferent #ays. Curative or definitive treatment A provi$es relief by eliminatin& the cause. (t is consi$ere$ the optimal approach if a $efinitive $ia&nosis of the problems can be ma$e an$ an effective treatment for the con$ition is available. Palliative treatment A 0lleviate pain an$ other $istressin& symptoms #ithout curin& the con$ition. (t is the appropriate approach to provi$e relief #hen no curative treatment is available for the con$ition. (t is also useful in con2u&ation #ith curative treatment to provi$e relief until curative treatment eliminates the pain. #ymptomatic treatment A 0ttempts to eliminate symptoms as they $evelop #ithout specifie$ consi$eration of their ori&in. (t is an unsuitable approach 1 because 1 control of pain may allo# the pro&ression of potentially harmful un$ia&nose$ $iseases. .ost complaints $irecte$ to the $entist are relate$ to somatic pain of inflammatory ori&in1 #hich is usually controlle$ by curative $ental proce$ures.

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So$ tic p in of Pulp l origin Toothache or o$ontala&ia results in most instances from inflammatory stimulation of neural fibers of either the $ental pulp or supportive alveolar tissues. "ulp pain or pulpal&ia is by far the most commonly e*perience$ pain in an$ near the oral cavity an$ may be classifie$ accor$in& to $e&ree of severity an$ the patholo&ic process present. 1. Myperreactive pulpal&ia a7 -entinal Mypersensitivity b7 Myperemia 2. 0cute pulpal&ia a7 (ncipient b7 .o$erate c7 0$vance$ 3. Chronic pulpal&ia 4. Myperplasic pulpitis 5. Necrotic pulp 6. (nternal resorption 7. Traumatic occlusion . (ncomplete fracture 17 Myperreactive pulpal&ia / Characteri5e$ by short1 sharp1 shoc9 that is :pain; best $escribe$ as a sensation of su$$en shoc9. The sensation is as sharp as it is su$$en an$ elicite$ by some e*citin& factor. (t is never spontaneous. "ain is of short $uration1 lastin& only sli&htly lon&er than the time $urin& #hich the irritatin& element is in contact #ith the tooth. Myperreactive pulpal&ia can be $ivi$e$ into/ "reatment @est treatment for hypersensitivity or hyperemia is prevention. 0pplication of the resin a$hesive or placement of an insultin& base un$er metallic restorations #ill materially re$uce most hypersensitivity. !ecent metho$s/ "hysical metho$s, are reminerali5ation of the $entinal tubuli from the : calcium,phosphate protein comple*; in saliva an$Hor from the formation of irritation $entin from the pulp ChemicalHmechanical obstruction/ Bse of materials li9e calcium hy$ro*i$e1 formalin an$ silver nitrate. 0&ents that have prove$ successful are potassium o*alate1 strontium chlori$e1 so$ium an$ stannous fluori$e an$ resins. 0nother approach1 usin& potassium nitrate1 bloc9s sensory nerve activity at the "ulpal en$s of the tubules by alterin& the e*citability of the nerves Mypersensitivity an$ Myperemia.

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27 0cute pulpal&ia True pulpal&ia be&ins #ith the $evelopment of pulp inflammation or pulpitis. (t may be $ue to increase$ intrapulp tissue pressure. "reatment* (n incipient cases of acute pulpal&ia1 removal of caries1 follo#e$ by calcium hy$ro*i$e application an$ se$ative cement for fe# $ays. 3or mo$erate cases1 pulpectomy an$ )n$o$ontic treatment may be re<uire$ if the tooth can an$ shoul$ be save$1 or e*traction for hopeless tooth. 37 Chronic pulpal&ia "ain is of lon& stan$in& nature. "ain is <uite $iffuse1 an$ the patient may hasve $ifficulty in locatin& the source. Chronic pulpala&ia is li9ely to cause referre$ pain. "reatment* "ulp e*tirpation an$ en$o$ontic therapy may be re<uire$. 47 Myperplasic pulpitis 6pulp polyp7 The e*pose$ tissue of hyperplasic pulp is practically free of symptoms unless stimulate$ $irectly. -ifferential $ia&nosis is concerne$ #ith only one problem1 namely that of $iscernin& #hether the polyp is &in&ival or pulpal ori&in. "reatment* 3or tooth #ith hyperplasic pulpitis1 if possible root canal shoul$ be carrie$ out1 or if the pro&nosis is poor1 e*traction is in$icate$. 57 Necrotic pulp There are no true symptoms of complete pulp necrosis1 sine the pulp #ith its sensory nerves1 is totally $estroye$. +ften1 ho#ever1 if only partial necrosis has occurre$1 an$ the patient has some va&ue1 mil$ $iscomfort1 as in chronic pulpal&ia. "reatment* )n$o$ontic therapy. 67 (nternal resorption , is an insi$ious process #hen the afflicte$ pulp is completely free of symptoms. +n the other han$1 this con$ition has been 9no#n to mimic mo$erate acute pulpal&ia in pain intensity. "reatment* "ulpectomy is the only treatment for resorption follo#e$ by +bturation #ith thermplastici5e$ &uttta percha. 77 Traumatic occlusion 0 tooth traumati5e$ by bru*ism or because of a restoration is in Myperocclusion often respon$s much li9e the tooth #ith mil$ pulpal&ia. "reatment*

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(nvolves relievin& the point of occlusal trauma by 2u$icious &rin$in& to reshape the involve$ tooth an$ its opponent. 7 (ncomplete fracture or split tooth The symptoms ran&e from those of a constant une*plaine$ hypersensitive pulp to constant une*plaine$ toothache. The most fre<uent complaint is that of a tooth painful to bite on1 #ith an occasional mil$ ache. "reatment* (f (ncomplete fracture is suspecte$1 but the pulp is not involve$1 full cro#n shoul$ be prepare$. (f an incomplete fracture has entere$ the pulp 1 then root canal treatment shoul$ be $one first1 follo#e$ by full covera&e to prevent a total fracture. So$ tic p in fro$ dent l supporting tissue ( "erira$icular pain A may be almost as e*cruciatin& as pulp pain an$ often continue for lon&er perio$ of time. 17 Symptomatic apical perio$ontitis/ This acute form of perira$icular pain can be most e*cruciatin& an$ sometimes lasts for $ays. The tooth is painful to touch1 an$ even contactin& the tooth in closure may brin& a floo$ of tears. The pain has been $escribe$ as constant1 &na#in&1 throbbin& an$ poun$in&. There is no overt s#ellin& involve$1 2ust &rossly painful tooth elevate$ in its soc9et. "reatment* To relive pain1 an imme$iate in2ection of a lon& lastin& local anesthetic shoul$ be &iven 6@upivacaine #ith epinephrine7 +cclusal corrections shoul$ be $one to free the tooth completely from contact in closure in any e*cursion Typically1 symptomatic apical perio$ontitis follo#s initial )n$o$ontic treatment 0 rubber $am is place$1 an$ temporary fillin& remove$ carefully1 Bsin& paper points1 the chamber an$ canal shoul$ be cleare$ of any li<ui$ contents My$rocortisone1 combine$ #ith neomycin1 is recommen$e$ as an anti, inflammatoryHantibacterial me$icament The canal is floo$e$ #ith li<ui$ suspension an$ then the flui$ is tease$ out #ith a sterile file 0 loose cotton pellet is then place$ in chamber an$ a thin temporary fillin& place$ #ithout un$ue pressure The patient shoul$ also be carrie$ on systemic antibiotics an$ on anti,inflammatory $ru&s.

27 0cute apical abscess The pain of acute apical abscess1 is similar to acute apical perio$ontitis1 but some#hat lo#er in intensity. "reatment*

34

-raina&e is establishe$ throu&h the root canal 1 if abscess is in its by incision if abscess is fluctuant

initial sta&e1 or

trephination may also be performe$ to establish $raina&e an$ relieve pressure occlusion is relieve$ an$ a re&imen of systemic antibiotics an$ either hot or col$ rinses prescribe$ $epen$in& on the sta&e of $evelopment of abscess .il$ anal&esics such as acetaminophen for pain or opio$s or steroi$s if pain is severe.

)n$o$ontic therapy or e*traction1 is complete$ after the acute symptoms have subsi$e$. 37 Chronic apical perio$ontitis (s sel$om painful an$ its mana&ement usually involves en$o$ontic therapy for affecte$ teeth. 47 Chronic apical abscess (s &enerally free of symptoms. There may be sta&es in the lonf& history of such lesion1 #hen a $rainin& fistula closes an$ mil$ s#ellin& an$ $iscomfort ensue. "reatment* (f the involve$ tooth can be save$1 it may be retaine$ by en$o$ontic therapy. "erira$icular sur&ery is sometimes in$icate$ for these patholo&ic lesions. P in disorders th t $i$ic odont l gi "ain problems mimic9in& $ental problems can be separate$ into t#o ma2or cate&ories/ a7 Typical pain $isor$ers, those in #hich patho&enesis are 9no#n. b7 0typical pain $isor$ers, have no establishe$ etiopatho&enesis. Typical pain $isor$ers 17 Neural&ias/

i) "rigeminal neuralgia ( "ic ouloureu() * 3acial pain $isor$er #ith specific clinical features. The pain involves one or more of tri&eminal nerve $ivisions. "recise cause un9no#n1 empiric evi$ence su&&ests that the symptoms evolve as a conse<uence of vascular compression of &asserian &an&lion. The character an$ $uration of symptoms are uni<ue1 an$ a specific anatomic tri&&er point can be i$entifie$. "ain is severe an$ lancinatin&1 shootin& into bone an$ teeth. Treatment mo$alities are varie$ an$ inclu$e me$ical intervention an$ various sur&ical interventions.

35

Carbama5epine1 the stan$ar$ me$ical therapy for tri&eminal neural&ia1 is <uite effective. Sur&ical mo$alities available are peripheral neurotomy1 rhi5otomy1 alcohol in2ections1 &lycerol in2ections1 cryotherapy1 ra$iofre<uency lesionin& an$ laser therapy. .ost #i$ely accepte$ are the/ sur&ical $ecompression an$ transcutaneous &an&lionic neurolysis. (ii) Post2herpetic neuralgia* "rimary infection #ith varicella 5oster causes chic9en po*1 a $isease that affects '5V of population $urin& early chil$hoo$. (n its secon$ary or recurrent form1 the $isease is referee$ as herpes 5oster or shin&les. (n the hea$ an$ nec9 area1 it is tri&eminal &an&lion that harbors the latent virus. The painful lesions of shin&les cause a $eep borin& ache1 involvin& not only the superficial mucosal an$ cutaneous tissue but also the ma*illary an$ man$ibular bones. @efore the onset of vesicular eruption1 it is common for the patient to e*perience pro$romal pain1 obscurin& the $ia&nosis. "reatment* a variety of techni<ues use$ to mana&e pain1 inclu$in& transcutaneous electrical nerve stimulus1 antisei5ure $ru&s1 anal&esics an$ topical preparations. 2. Cluster hea$ache 6Slu$ers neural&ia7 Cluster hea$aches $erive their name from their temporal pattern. They ten$ to occur in :clusters1; a series of one to ei&ht 2D, to 1 D,minute attac9s per $ay lastin& for several #ee9s or months1 follo#e$ by remissions of months or years. These hea$aches are foun$ five to ei&ht times more fre<uently in men than in #omen1 particularly in men a&e$ 2D to 5D years #ho smo9e. The pain is a severe1 unilateral1 continuous1 intense ache or burnin& that often occurs at ni&ht. .ovements that increase bloo$ flo# to the hea$ may result in throbbin&. The most common sites are either aroun$ or behin$ the eye ra$iatin& to the forehea$ an$ temple or aroun$ an$ behin$ the eye ra$iatin& infraorbitally into the ma*illa an$ occasionally into the teeth1 rarely to the lo#er 2a# an$ nec9. @ecause of the oral symptoms1 serious $ia&nostic errors are committe$ by $entists. "reatment inclu$es/ i7 ii7 iii7 iv7 vasoactive $ru&s, calcium channel bloc9ers pre$nisone hyperbaric o*y&en therapy %asoactive antimi&rane $ru&s.

3. +titis me$ia The mi$$le ear infection symptoms ra$iate from ear over the posterior aspects of ma*illa an$ man$ible. The $efinitive $ia&nosis is ma$e by usin& an otoscope to e*amine the tympanic membrane.

36

"reatment consist of antibiotic therapy usually penicillin #ith p,lactase inhibitor or clin$amycin. +nce $ia&nosis is establishe$1 referral to an otolaryn&olo&ist is recommen$e$. 4. Sino&enic pain 0cute .a*illary Sinusitis / @ecause the roots of the ma*illary teeth e*ten$ to the sinus floor1 it is a*iomatic that acute infectious processes involvin& the sinus mucous membrane #ill simulate $ental pain. .ost forms of sinusitis are aller&ic an$ are characteri5e$ by $ull pain complaints in the malar re&ion an$ ma*illary alveolus. =hen ma*illary sinusitis is the conse<uence of an acute pyo&enic bacterial infection1 the symptoms are usually acute. The pain may be stabbin&1 #ith severe achin& pressure an$ throbbin&. "ain is fre<uently referre$ up#ar$1 un$er the orbit1 an$ $o#n#ar$1 over the ma*illary posterior teeth. 6(mportantly1 pain is not referre$ to a sin&le tooth but is perceive$ in all teeth in the <ua$rant. "ercussion sensitivity of the molar teeth is a common fin$in&1 an$ #hen the hea$ is place$ belo# the 9nees1 the pain is often e*acerbate$.7 Transillumination is a $ia&nostic ai$ that is easy to perform. @ecause ma*illary root apices are separate from the antral floor by a fe# millimeters of bone. Mence it is essential to assess each ma*illary tooth in patient #ith acute ma*illary sinusitis1 because treatment #ithout mana&ement of the $ental source #ill only result in recurrence of symptoms. 0ntibiotic therapy an$ in$uce$ sinus $ischar&e recommen$e$. !eferral to otolaryn&olo&ist is recommen$e$. 57 Car$iac 2a# pain %ascular occlusive $isease is one of the most common afflictions. The accumulation of atherosclerotic pla<ue in coronary vessels 6in association #ith vasospasm7 #ill lea$ to an&ina pectoris. The most common manifestation of coronary vascular occlusion1 particularly in its acute manifestation1 is substernal pair #ith reffere$ pain rotatin& over the left shoul$er an$ $o#n the arm. +ccasionally an&ina pectoris is manifeste$ as left shoul$er an$ arm pain #ithout a substernal component. )ven less fre<uent is referral of pain up the nec9 into the left an&le of the man$ible. (n these instances the referre$ pain may mimic o$ontal&ia. =hen a patient reports left posterior man$ibular pain an$ there is no obvious o$onto&enic source of infection1 referre$ car$io&enic pain shoul$ be consi$ere$. (mportantly1 the patient shoul$ be <uestione$ about the onset of the symptoms. (f they occur after e*ercise or other e*ertion1 then coronary vascular $isease shoul$ be consi$ere$. +nce suspecte$1 referral to physician is recommen$e$. 67 Sialolithiasis

37

)tiolo&y is un9no#n. -es<uamate$ epithelial cells from the ma2or salivary $ucts may accumulate an$ form comple*es #ith salivary mucin to form ni$us for calcification. Salivary stone evolves by se<uential concretion of calcium phosphate salts1 much li9e the &ro#th rin&s of a tree. +nce the stone reaches a critical si5e1 the salivary $uct becomes occlu$e$ an$ symptoms $evelop. Sialolithiasis is si&nificantly more fre<uent in the subman$ibular $uct8 therefore pain associate$ #ith subman$ibular stones is more prone to mimic en$o$ontic pain in the posterior aspect of the man$ible. The occlu$e$ $uct often lea$s to s#ellin& of the subman$ibular area. Mence it may mimic lympha$enitis associate$ #ith an en$o$ontic infection of a posterior man$ibular tooth. Treatment consists of physical attempts to remove the stone by manipulatin& it #ith out the orifice. Oar&er stones #ill re<uire a sur&ical cut $o#n to the $uct. 77 0bnormal 2oint function 6(nternal $eran&ement7 (nternal $eran&ement of the T.P is often associate$ #ith locali5e$ 2oint area pain complaints. (nternal $eran&ements of the T.P inclu$e meniscus $isplacement1 formation of intraarticular a$hesions1 an$ various forms of arthritis. The chief fin$in&s associate$ #ith internal $eran&ement inclu$e limitation of 2a# openin&1 $eviation on openin&1 2oint clic9in& or crepitus1 an$ pain $irectly locali5e$ to the 2oint re&ion in front of the tra&us of the ear. The pain associate$ #ith internal $eran&ement is &enerally a borin& ache1 but it may be more acute #hen e*acerbate$ by #i$e openin& of the man$ible or che#in&. "ain is often referre$ into the temple1 chee9 an$ posterior $ental areas of ma*illa an$ man$ible. (n such instances the patient may perceive a 2oint problem as a $ental problem or as a temple area hea$ache. 7 .yal&ia .yal&ic pain $isor$ers involvin& the masticatory musculature can be perceive$ as $ental pain. These $isor$ers appear to be the conse<uence of sustaine$ muscle contraction usually associate$ #ith 2a# clenchin& an$ bru*ism. .yal&ic pain is constant1 variable in intensity1 usually $ull1 achin& an$ it involves multiple muscle areas. (n &eneral most patients complain of symptoms over the man$ible an$ temple. "alpation of masticatory muscles #ill often reveal the presence of locali5e$ ten$er areas. Treatment is by physical therapy. '7 .yofascial pain , are characteri5e$ by continuous1 $ull pain of variable intensity1 #ith locali5e$ ten$erness in one or more muscles. )ssential to the $ia&nosis of myofascial pain is $iscovery of locali5e$ hypersensitive areas 6i.e.1 tri&&er points7 Tri&&er points foun$ in superficial aspect of masseter muscles have consistent referral patterns to the ma*illary an$ man$ibular teeth/ tooth ache is the main problem

38

Temporalis muscle tri&&er point can refer pain to ma*illary posterior an$ anterior teeth/ hea$ache an$ toothache are common associate$ complaints. +nce tri&&er point has been locate$ an$ a .yofascial $isor$er $ia&nose$1 treatment can be institute$. .ost common techni<ues for eliminatin& tri&&er point inclu$e/ i7 ii7 iii7 "hysical therapy Spray an$ stretch therapy Tri&&er point in2ections.

,typic l p in disorders th t $i$ic odont l gi / +f all the facial pain syn$romes1 the &roup that most often simulates en$o$ontic or o$onto&enic pain is :atypical facial pain;. (nclu$e$ in this are variety of $isor$ers inclu$in& phantom tooth pain1 N(C+, neural&ia in$ucin& cavitatory osteonecrosis. C!"S, comple* re&ional pain syn$rome an$ causal&ia. 0typical facial pain represents a pain syn$rome that $oes not conform to specific or&anic $isease an$ $oes not represent another #ell $efine$ form of pain $isor$er. 1. "hantom tooth pain The term phantom tooth pain is use$ to $escribe pain that persists in teeth or the area of a specific tooth after the pulp has been e*tirpate$. "hantom tooth pain is estimate$ to occur in less than 3V of patients un$er&oin& root canal therapy. (t has been su&&este$ that sur&ical e*tirpation of the pulp results in $ama&e to nerve fibers at the ape* of the teeth an$ shoul$ be consi$ere$ a traumatic neural&ia. 0nother possible mechanism is formation of a small traumatic neuroma in the apical perio$ontium. 0lthou&h psycholo&ical factors have been su&&este$ to be important in phantom tooth pain1 there is not a &reat $eal of evi$ence 6on the basis of psychometric testin&7 that psychopatholo&ic mechanisms are ma2or factors. Mo#ever it is su&&este$ that phantom tooth pain is a $eafferentation pain. 2. N(C+, neural&ia in$ucin& cavitatory osteonecrosis, Neural&ia,in$ucin& cavitational osteonecrosis 6N(C+7 is an atypical orofacial pain locali5e$ to e$entulous foci1 #hich can sometimes be alleviate$ #ith a subperiosteal in2ection of local anesthetic. (n such instances it has been propose$ that small resi$ual inflammatory1 foci e*ist #ithin en$osteum an$ the focal necrosis occurs #ith neural $ama&e. (n selecte$ cases sur&ical curetta&e has alleviate$ associate$ pain. Tissue curette$ from these cavities often sho#s minor patholo&ic chan&es1 such as fibrosis an$ mil$ inflammation. 3. C!"S, comple* re&ional pain syn$rome

39

Comple* re&ional pain refers to pain complaints that have lasted longer than the normal healing period and have increased in comple(ity. -epen$in& on the cause of the pain complaint1 this $ia&nosis coul$ be ma$e in .4 to 6 #ee9s. 0 variety of factors can contribute to the perpetuation of pain complaints1 inclu$in& a lac9 of healin&1 inappropriate therapy1 misse$ $ia&nosis1 increase in psycholo&ic involvement1 an$ secon$ary &ain. 4. Causal&ia Causal&ia pain can involve the 2a#s1 hea$1 an$ nec9. =hen present1 it may be confuse$ #ith o$ontala&ia. Causal&ic pain is often associate$ #ith trauma1 2a# fracture1 or laceration an$ it may evolve after sur&ery. (t has been hypothesi5e$ that in causal&ia1 nociceptor fibers become retracte$ in association #ith autonomic fiber. "atients have a ten$ency to rub an$ scratch the involve$ area1 pro$ucin& #hat are 9no#n as trophic foci8 the s9in can become encruste$ an$ 9eratotic. The pain is characteristically paro*ysmal an$ burnin&1 an$ it may be both superficial an$ $eep. =hen the pre$ominant complaint is a $eep component1 it may be confuse$ #ith toothache. To arrive at a $efinitive $ia&nosis of causal&ia1 historical trauma events an$ clinical features must be i$entifie$. =hen symptoms of orofacial pain are mil$1 the pain shoul$ be mana&e$ #ith anal&esics an$ reassurance. .any patients #ith atypical facial pain respon$ favorably to tricyclic anti$epressants1 an$ particularly amitriptyline. (n more severe cases1 the therapy use$ for tri&eminal neural&ia may be in$icte$. V . Drug ther py 1."ain mana&ement principles Treatment of mil$ to mo$erate pain shoul$ be&in #ith non,narcotic anal&esic. (f these $ru&s alon& are ineffective1 interme$iate potency opio$s such as co$eine or its $erivatives are combine$. Treatment of acute pain is $irecte$ to#ar$s the location1 ori&in an$ cause of pain. opiates are often employe$1 but NS0(-4S are also staples of acute pain therapy because they can limit pain1 s#ellin& an$ erythema. other a&ents a$ministere$ for acute pain inclu$e muscle rela*ants an$ in2ectable local anesthetics. 3or server or chromic pain1 anal&esic shoul$ be &iven at re&ular intervals in a$e<uate $ose anal&esic a$2uvant such as tricyclic anti$epressant is a$$e$ to the $ru& re&imen. +ther a$2unct inclu$e anticonvulsant1 antiarrythmics1 antihistamine or phenothia5ines.

40

). Non opiod n lgesics( Non,steroi$al anti,inflammatory $ru&s 6NS0(-S 7 this &roup $ru&s are use$ to treat mil$ to mo$erate acute or chronic pain from trauma1 sur&ery or inflammatory con$itions. 0cetaminophen1 althou&h not an NS0(- because it lac9s anti, inflammatory properties1 is the most commonly non,prescription pain reliever. NS0(-S $iffer from opioi$ anal&esics in that they are antipyretics an$ $o not in$uce physical or psycholo&ical $epen$ence NS0(-S #or9 primarily at the site of in2ury by inhibitin& the en5yme cyclo,o*y&enase 6co*71 #hich is re<uire$ for the synthesis of prosta&lan$ins1 substances that sensiti5e peripheral sensory nerves an$ contribute to e*perience of pain. "atients may vary in their response to NS0(-S pro$uce an anal&esic effect after several $ays $ifferent NS0((t is (na$visable to prescribe t#o $ifferent NS0(- at the same time1 rather 1 one NS0(shoul$ be use$ an$ its $ose an$ timin& a$2uste$ for ma*imum anal&esic effect. Combinations of NS0(- increase the ris9 of si$e effects @ecause of e*tensive si$e effects profiles1 lon& term use of NS0(- must be carefully #ei&hte$ a&ainst the clinical response of each patient for #hom they are prescribe$. The most serious a$verse reactions involvin& the >(T 1 inclu$e $yspepsia at one e*treme to potentially serious blee$in& ulcers at the other +ther a$verse events attribute$ to NS0(-S are 9i$ney $ysfunction or failure1 $ermatolo&ic reactions such as rash1 $ro#siness or $i55iness1 e*cessive blee$in& or bruisin& because of inhibition of prate$ activity an$ increase$ ris9 of an asthamatic episo$e =hile all NS0(- pose a ris9 of a blee$in&1 ibuprofen an$ $iclofenac are consi$ere$ to pose a lo#er ris9 an$ 9etoprofen an$ piro*icam consi$ere$ to pose a hi&h ris9. =ith any NS0(- the ris9 increase #hen hi&h $oses are prescribe$.

41

NS0(- are available that selectively inhibit only one of isoforms of Co*1 namely Co*,2. The inhibition of Co*,2 seems to the relate$ to the anti,inflammatory an$ anal&esic effect1 #hereas the inhibition of co*,1 is thou&ht to be responsible for many of the si$e effects.

The co*,2 inhibitor coleco*ib an$ rofeco*ib pose less ris9 of >( blee$in& an$ $o not inhibit platelet a&&re&ation. NS0(- have a si&nificant number of $ru& interactions. The most troublesome of these are e*acerbation of blee$in& $isor$ers in patient ta9in& anticoa&ulants such as #arfarin1 an$ anta&onism of a&ents use$ in treatment of hi&h bloo$ pressure.

3.Opioid n lgesics The lar&est &roup of opioi$s that are use$ for anal&esia consist of morphine li9e a&onists. opioi$s inclu$e$ bath natural an$ synthetic a&ents. They are uni<ue in their ability to re$uce mo$erate to severe pain #ithout pro$ucin& loss if consciousness. There are three classes of opio$s 1. The phenanthrenes A )&/ morphine1 co$eine1 o*yco$one 2. The phenylpiperi$ine $erivatives A )&/ .eperi$ine1 fentanyl 3. -ipheyl heptane $erivative e&/ methan$one an$ propo*yphene. !e<uire$ $oses of opioi$s vary accor$in& to patients prior e*posure1 severity of pain1 hepatic or renal function1 an$ rate of a$ministration .ost clinically available opioi$s activate the Q opioi$ receptor. This opioi$ receptor is locate$ at several important site in brain an$ is activation inhibits the transmission of nociceptive si&nals

42

0lthou&h opio$ are effective as anal&esics for mo$erate to server pain there use is &enerally limite$ by their a$verse effects.

+pio$ inclu$e numbers si$e effects inclu$in& nausea1 emesis1 $i55iness1 $ro#siness an$ the potential for respiratory $epression an$ constipation. Chronic use is associate$ #ith tolerance an$ $epen$ence. 0nal&esic $oses of representative opio$s -ru& Co$eine +*yco$eine My$roco$one "ro*yphene (% .eperi$ine Trama$ol 1D 146 'D 5D -ose e<uivalent to co$eine 66D m&7 6D 5,6

!ole of corticosteroi$s The cause of postoperative pain or flare,up after en$o$ontic treatment can be attribute$ to inflammation or infection or both occurrin& in the perira$icular tissue. The act of establishin& patency an$ subse<uently $ebri$in& an$ shapin& the root canal system $irectly irritates the perira$icular tissues an$ ina$vertently intro$uces bacteria. @acterial pro$ucts1 necrotic pulpal tissue1 or caustic irri&atin& solution throu&h apical foramen >lulocorticosteroi$s are 9no#n to re$uce the acute inflammatory response. They inhibit the formation of arachi$onic aci$ from neutrophil an$ macropha&e cell membrane phospholipi$s/ thus bloc9in& the cyclo*y&enase an$ lipo*y&enase path#ays an$ respective synthesis of prosta&lan$in an$ leu9otriens. 0nti$epressants Tricyclic anti$epressants1 #hich inhibit the reupta9e an$ stora&e of the neuro&enic amines serotonin an$ norepinephrine1 have anal&esic properties relate$ to their ability to increase pain tolerance. The anti$epressants inclu$e several classes of a&ents1 #hich can be or&ani5e$ into three cate&ories/ tricyclic anti$epressants1 monoamine o*i$ase inhibitors1 an$ ne#er heterocyclic compoun$s.

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Clinical effects inclu$e improvement in moo$ an$ sleep1 an*iety re$uction1 an$ a $ecrease$ perception of pain. The tricyclic a&ents are commonly employe$ in the mana&ement of neuro&enic pain con$itions. The tricyclic anti$epressants are available as either tertiary or secon$ary amine structures8 the former a&ents pro$uce more fre<uent an$ more intense si$e effects than the latter. .onoamine o*i$ase inhibitors have been use$ infre<uently for treatment of painful con$itions such as mi&raine an$ are reserve$ for patients refractory to the tricyclic anti$epressants. .ost commonly employe$ anti$epresse$ for painful con$itions is amitriptyline in $oses of 25,15D m&H$ay. 0nticonvulsants The mechanism of action of carbama5epine an$ valproate is suppression spontaneous neuronal firin&. Oancinatin& or @ufferin& pains are best treate$ these a&ents1 an$ they are prescribe$ for tri&eminal neural&ia1 cranial nerve $isor$ers1 $eafferentation pains 6e.&.1 phantom tooth pain71 an$ other neural&ic syn$romes. Typical a$ult $oses of carbama5epine are 2DD to 4DD m& to four times $aily1 an$ valproate is usually $ose$ as 25D to 75D m& t#o to three times $aily. 0 sustaine$,release carbama5epine pro$uct that allo#s t#ice,$ $osin& is also available. "lasma levels shoul$ be monitore$ because si$e effect may inclu$e ata*ia1 $iplopia1 nausea1 an$ emesis. 0ntiarrhythmics an$ Oocal 0nesthetics Oi$ocaine is also &iven for neuropathic syn$romes1 an$ similar to all local anesthetics1 enters the central an$ peripheral nervous systems after a$ministration. .e*iletine has been use$ in li$ocaine,responsive patients re<uirin& lon&er,actin& substitute because both a&ents re$uce neuronal firin&. -ose, 1D m&H9&H$ay. 0$2untive me$ications/ @en5o$iapenes such as $ia5epam are useful foe s9eletal muscle rela*ation an$ an*iolysis in the treatment of acute pain1 an$ clona5epam has been use$ in the mana&ement of neuropathic an$ atypical facial pain. 0ntihistaminics , such as hy$ra5ine an$ prometha5ine have been use$ to au&ment se$ation an$ re$uce itchin& associate$ #ith opioi$s a$ministration. They may have some anal&esic activity by virtue of re$uction of histamine release in areas of inflammation. Ne0 develop$ents in p in $ n ge$ent N methyl2 2aspartate (NM !) is an e*citatory amino aci$ that #as $iscovere$ to pro$uces hyperal&esia of CNS ori&in. >lutamate may also play a similar role in activatin& pain system.

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!esearch into N.-0 receptor anta&onist offer an e*citin& hint at the future of pharmacolo&ic a&ents for pain mana&ement. Retamine1 a commercially available anesthetic is one such N.-0 anta&onist1 but is available only parentally an$ pro$uces a$verse reactions such as $ysphoria an$ hallucinations. e(trorphan, the $emethylate$ metabolite of $e*tromethorphan 6a cou&h suppressant7 is another a&ent un$er&oin& investi&ation. Calcium channel bloc'ers use$ in the treatment of hypertension may also potentiate morphine anal&esia by mo$ulation of calcium availability to the cell. These $ru&s are $evoi$ of any anal&esic activity #hen &iven alone. +pioi$ pepti$es such as en'ephalin analogues sho# promise as therapeutic a&ents because they $iffer from opioi$s in several #ays. +ne a$vanta&e the pepti$es may have over their opioi$ counterparts is $e&ra$ation to constituent amino an$s instea$ of active an$ possible to*ic metabolites.

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VI. Conclusion "ain is mainly a protective mechanism for the bo$y8 it occurs #henever any tissues are bein& $ama&e$1 an$ it causes the in$ivi$ual to react to remove the pain stimulus. This basic nervous an$ $efense function is applicable to the $ental pulp. 0 conscious reco&nition of irritants to the tooth &ives the patient an opportunity to have the problem correcte$ before irreversible effects can occur. (n evaluatin& pulpal an$ periapical pain1 other $isor$ers must be consi$ere$ in the $ifferential $ia&nosis. "ain mana&ement has pro&resse$ a &reat $eal scientifically throu&hout the last century1 in part as a result of the intro$uction of more effective pharmacolo&ic a&ents an$ $evelopment of better un$erstan$in& of the molecular biolo&ic principles that &overn their use.

VII. 'eference 1. >uyton an$ Mall. Te*tboo9 of .e$ical physiolo&y A 1Dth )$ition 2. >eral$ P Tortora an$ Nicholas ".0na&nosta9os. "rinciples of 0natomy an$ "hysiolo&y, 6th )$ition 3. Cyril 0.Reele1 )ric Neil 1an$ Norman Poels. Samson =ri&ht4s 0pplie$ physiolo&y, 13th )$ition 4. "ath#ays of pulps A
th

e$ition1 Stephen Cohen1 !ichar$.C.@urns

5. (n&le an$ @a9lan$. )n$o$ontics 5,th e$ition 6. 3ran9lin S. #eine , )n$o$ontic Therapy 5th e$ition. 7. Oocal anesthesia, .onheim4s

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. Oori 0 !eisner,Reller. "harmacotherapeutics in the mana&ement of +rofacial pain. -ent Clin N 0m 6-CN07 1''78 41627/ 25',27 '. >reenber& an$ >lic9. @ur9et4s +ral me$icine -ia&nosis an$ Treatment. 1D th )$ition 1D. 0llen . Oepins9i1 Renneth . .Mar&reaves1 Marol$ ). >oo$ies an$ =alter !. @o#les. @ra$y9inin levels in -ental pulp by microanalysis. P )n$o$on 2DDD8 266127/744,747 11. Marol$ >oo$ies an$ Runi9o Sae9i. ($entification of @ra$y9inin1 Substance " an$ Neuro9inin 0 in Muman $ental pulp. P en$o$on 1''7823647/2D1,2D4

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