Post-Operative Pain & Hypersensitivity PDF

Post-operative pain and hypersensitivity Dr. Fatma Hussein  Outline: Causes of pain: 1. Thermal stimuli 2. Osmotic stimuli 3. Mechanical stimuli a) Fracture restoration b) Cracked tooth c) Faulty occlusal and proximal contact relationship d)...

Post-operative pain and hypersensitivity Dr. Fatma Hussein  Outline: Causes of pain: 1. Thermal stimuli 2. Osmotic stimuli 3. Mechanical stimuli a) Fracture restoration b) Cracked tooth c) Faulty occlusal and proximal contact relationship d) Pulp degeneration: e) Gingival irritation by operative procedure 4. Electrical stimuli Galvanism 5. Other causes of pain: a) Pain due to local anesthetic problems b) Barodontalgia c) Hypersensitivity d) Disinfecting drugs e) Contamination of zinc containing amalgam Treatment of postoperative pain Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is felt whenever a noxious stimulus just exceeds the pain perception threshold. Hypersensitivity is an exaggerated sharp transient or temporary sensation of discomfort due to non-noxious low intensity stimuli. Take Note Hypersensitivity doesn't denote or related to tissue damage. But it could continue up to tissue damage and pain Pain is unpleasant sensation which mostly warns that there is a degree of tissue damage. Pain arises from the pulp in three ways: 1. In case of pulp exposure: by direct effect of the irritants on the naked nerve endings present below the odontoblasts in the plexus of Raschaw present in the pulp tissues. 2. In case of exposure to external stimuli e.g. trauma or caries by the effect of the irritants on the terminal filaments of the nerve endings inside the dentinal tubules. 3. In case of direct exposure of the sound teeth to external stimulus by exposure of the sound tooth to extremely cold or hot temperature below or above the thermal tolerance zone (TTZ). Dentin hypersensitivity is a common clinical condition that is difficult to treat because the treatment outcome is not consistently successful. Definition: Dentin hypersensitivity is characterized by short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other form of dental defect or pathology Characteristic and Prevalence: 1. Short , sharp pain. 2. Most in cervical. 3. Most in premolars and canines. 4. Most in females. Etiology: Dentin hypersensitivity is a multifactorial condition However There is a definite morphological and structural change of dentin in the affected area. These areas contain a larger number of patent dentinal tubules with a larger tubular diameter than the normal unaffected areas. I. Direct Innervation Theory This theory postulates that: direct mechanical stimulation of exposed nerve endings at the dentino-enamel junction (DEJ) is responsible for dentinal hypersensitivity. The major shortcoming of this theory is that there is insufficient evidence to prove that the outer dentin that is most prone to be sensitive is well innervated. II. Odontoblast Receptor Theory This theory proposes that the odontoblasts themselves act as neural receptors and relay the signal to the nerve terminal. The major shortcoming of this theory is that there is no evidence to demonstrate synapses between odontoblasts and nerve terminals III.Hydrodynamic Theory This is the most accepted theory to explain the mechanism behind dentin hypersensitivity. The hydrodynamic theory suggests that dentin hypersensitivity is due to the hydrodynamic fluid movements occurring across exposed dentin with open tubules which in turn mechanically activates the nerves present at the inner ends of the dentin tubules or in the outer layers of the pulp. The causes for dentinal exposure could be the result of one of the following processes: 1. Anatomical characteristics of the cement-enamel junction (CEJ) 2. Loss of the enamel covering the crown of the tooth 3. Denudation of the root surface due to loss of cementum and overlying periodontal tissues. The intensity of pain varies from mild discomfort to severe sensitivity. The pain is typically rapid in onset, sharp in character and is of short duration Causes of pain: 1.Thermal stimuli:  The site of neural excitation for the thermal stimulus is at the DEJ.  Clinical significance and postoperative pain due to thermal stimuli: metallic restorations conduct thermal changes to underlying dentin and pulp. Pain is felt during the few days after restorations. Treatment: application of sufficient thickness of base material in deep cavities under metallic restorations 2.Osmotic stimuli:  When osmotic agents as concentrated sugar or salt adhere to margins of leaky restoration or contact dentin they affect a flow of dentinal tubules.  Clinical significance and postoperative pain due to osmotic stimuli:  within the leaky restoration (microleakage), the polymerization shrinkage of composite and dissolution of luting cement under cast restoration will admit fluids causing movement of fluid due to the osmotic pressure. This is the main cause of leakage and postoperative pain.  Treatment: treatment of the cause of failure as old failed restoration is removed and a new filling with perfect (well sealed margins is constructed. 3.Mechanical stimuli:  Fluid movement in dentinal tubules due to mechanical stresses or moving instruments such as burs or hand instruments will elicit pain.  Clinical significance and postoperative pain due to mechanical stimulus: a)Fracture restoration: o Fracture line usually opens up during mastication and admits oral fluids, irritants and oral microbes this will lead to movement of dentinal fluids that cause pain and hypersensitivity. o It will be treated by treatment the cause of failure as removal of the old faulty restoration and the cavity will be restored with a new filling. a)Cracked tooth: o Weakened tooth due to caries or due to overcutting during cavity preparation are subjected to fracture leading to crake formation “craked tooth syndrome”. o Clinical significant and postoperative pain of cracked tooth is the patient chief complain is pain when taking citrus fruits and foods and when releasing pressure. o In case of sever pain endodontic treatment is indicted  a)Faulty occlusal and proximal contact relationship: Clinical significant and postoperative pain due to faulty occlusal and proximal contact relationship: o High Occlusal contact will result in sensitivity of the tooth to biting pressure, sensitivity to hot and cold, some mobility may develop with damage to supporting structure especially in cases of traumatic occlusion, in case of amalgam restoration with high marginal ridge fracture of the restoration will occur even before correction. o Open Proximal contact may result in food impaction and subsequent gingival inflammation resulting in considerable patient discomfort. Treatment by detection and correction of the cause of failure. Removal and replacing of the restoration a)Pulp degeneration: o Clinical significant and postoperative pain due to pulp exposure: a deep carious lesion and large and deep restoration may cause pulp to devitalize due to traumatic thermal and chemical stresses many years later. o Direct pulp trauma to exposed pulp may initiate an immediate hyperemia with subsequent pulp death. The patient suffers in sever conditions sharp radiating pain particularly at night and during supine position. o Treatment: the pulp of the affected tooth must be removed and root canal treatment is indicated.  a)Gingival irritation by operative procedure: o There are some operative procedures which may affect gingival tissues mechanically or chemically. o Clinical significant and postoperative pain due to gingival irritation by operative procedures such as overhanging restorations, overcontoured interproximal restorations, overcontoured and undercontoured restorations will apply a pressure to the gingiva and if left for a long time without correction, a chronic inflammation will be contributed. o Cementing media left in the gingival crevices and application of retraction cord may irritate the gingival tissues. Treatment: remake of the faulty restoration, employ a smart (delicate) technique in cementation of the restoration and in application of retraction cord Electrical stimuli:  Electrical stimuli reach the pulp almost instantaneously unlike other stimuli  Galvanism: o If two dissimilar metals are placed in a mouth they will act as electromotive force and electric current is suddenly short circuited most probably through one of the two restorations causing pain.  o The electromotive force value will depend on:  Difference in electrode potential for dissimilar metals in direct ratio.  The electric resistance of dentin and soft tissues.  Whether the pulp is healthy or in state of hyperalgesia due to inflammation which increase in pulp sensitivity.  The current density. o If two teeth kept in contact or if they come in contact for a second time, the electric cell polarizes and current intensity falls below pain perception threshold and pain will eventually cease. o Treatment: painting the other surface of one of the restoration by separating agent such as varnish or dentin bonding agent.  5.Other causes of pain: a)Pain due to local anesthetic problems:  Clinical significant and postoperative pain due to local anesthetic problem:  Soreness from trauma at the site of injection.  Hematoma as a result of trauma and subsequent extravasation of blood into surrounding tissues.  Infection at the injection site.  Treatment: application of warmth in case of soft tissue pain and swelling after injection of the anesthetic solution.  b)Barodontalgia:  This refers to pain occurring in a tooth in association with reduced pressure (in riding airplane in high altitude).  This can be explained on the basis that the presence of air voids under an old faulty restoration or may be due to gases in infected non vital pulp.  Treatment: remove the old restoration and refill it with suitable restoration. The non vital tooth was endodontically treated and restored with suitable restoration.  c)Hypersensitivity:  It is characterized by a short sharp pain that arises from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical.  Causes: a) Dentin exposure occurs as result of gingival recession or enamel loss. b) Dentinal tubules are to be opened by either abrasive or erosive agent following dentin exposure. c) Stimuli increase the flow rate of the fluid in tubules which in turn excites nerve terminal. d) Trauma during cavity preparation may contribute to temporary pulpitis. e) Over extension of cervical finishing line may be responsible for the loss of cementum. f) Short margins may contribute to hypersensitivity especially with hot, cold and tooth brush bristles. g) Cutting at high speed shows a destruction of odontoblastic layer with all the cellular and vascular changes of acute inflammation (low speed with continous stream of water shows no detectable sings of injury). h) Applying an air jet even for relatively short period can produce pathological effect on the pulp. i) Vibration causes unpleasant sensation to the patient. Most patient can tolerate vibration of 150-200 cycle per second (if above 560 CPS it is not tolerated).  Treatment: may be either o Preventing the increase in tubular fluid flow (blocking the tubules). o Reducing the excitability of intradental nerves. o Blocking the nerve activity in peripheral nerves or central nervous system. o Tubular occlusion (desensitization) is another methods of treatment. o There are two types of tubular occlusion (desensitization): a) Endogenous (naturally): either by deposition of surface layer composed of salivary minerals or smear layer or by intratubular dentin deposition as well as by tertiary dentin deposition. b)Exogenous desensitization: such as Creating surface barrier using toothpaste constituents. Varnished, bonding agent, glass ionomer and resin composite. Increasing the viscosity of the tubular fluid through increasing its macromolecular protein content. Desensitizing agents such as potassium ions could block the nerve function and reduce intradental nerve excitability by raising the local extracellular potassium ion concentration.  Conservative mechanism to reduce the hypersensitivity: this can be performed by: o Removing any causative or predisposing factor. o Increasing the flow rate and buffer capacity of the saliva. o Treating the gingival diseases and thus reduce the incidence of gingival recession. o Increases salivary Ph by using carbonated tooth paste.  d)Disinfecting drugs:  Disinfecting drugs as strong antiseptic in deep cavities produce postoperative pain. e)Contamination of zinc containing amalgam:  Contamination of zinc containing amalgam with moisture during trituration or condensation leads to what is called delayed expansion of value higher than 400 microns after 3.5 days.  This expansion may create pressure on the pulp resulting postoperative pain. Treatment of postoperative pain: In addition to the previously mentioned treatment for each postoperative problems, the treatment of such cases generally can be summarized in the following: 1. the use of the different types of commercially available analgesics such as asprine, codeine and paracetamols is suitable. 2. the application of warmth in case of soft tissue pain and swelling after injection of the anesthetic solution. 3. in case of cavity preparation, covering with well-sealed, non irritating and temporary sedative cement has a very good effect on post operative pain. 4. prevention is better than curing, so avoid once of causing damage to both of the soft and hard tissue will reduce or eliminate post operative pain.