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Orofacial pain

Differential diagnosis of the pain in orofacial system. Pain of dental origin and nondental origine pain. Orofacial pain. Orofacial pain is the pain in the area of face and its adjacent structures.

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Orofacial pain

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  1. Differential diagnosis of the pain in orofacial system.Pain of dental origin and nondental origine pain.

  2. Orofacial pain • Orofacial pain is the pain in the area of face and its adjacent structures. • The pain is expressing itself in various clinical syndroms which are arising by the influence of various mechanisms and they involve multidiscilpinary approach to diagnostics and the treatment itself.

  3. Dental pain may be classified as follows: • Pulpal pain • Periapical/periradicular pain Non-dental pain Dental pain can be very difficult to diagnose. • Pulpal pain The pulp may be subject to a wide variety of insult, (bacterial, thermal, chemical, traumatic) the effects of which are cumulative and can ultimately lead to inflamation in the pulp (pulpitis) and pain.

  4. A characteristicofpulpalpainasthatthepatientisunable to localizetheaffectedtooth. Theabilityofthepulp to recoverfrominjurydependsuponitsbloodsupply, notthe nerve supply, whichmustbeborne in brainwhenvitality (sensibility) testingiscarriedout • Althoughnumerousclassificationsofpulpaldiseaseexist, onlylimitednumberofclinicaldiagnosticsituationsrequireidentificationbeforeaffectivetreatmentcanbegiven.

  5. 1. Dental pain

  6. 2. Non-dental pain, located near the teeth

  7. PULPAL DISEASE Classified as: • Reversible pulpitis • Irreversible pulpitis • Necrotic pulp

  8. Reversible Pulpitis • Condition should return to normal with removal of the cause. • Common causes: • Caries, recent restorative procedures, faulty restorations, trauma, exposed dentinal tubules, periodontal scaling. • Pulpal recovery will occur if reparative cells in the pulp are adequate.

  9. Symptoms of Reversible Pulpitis • Thermal: • Hypersensitive with mild painlessthan <30 seconds, but similar to control tooth • Sweets: • Sensitive (if caries, crack, or exposed dentin) with mild painlessthan<30 seconds (similar to control tooth) • Biting Pressure: • None (unless tooth is cracked)

  10. DiagnosisReversible Pulpitis • If there is a discrepancy between the patient’s maincomplaint, symptoms, and clinical examination – obtain more information or data interpretation. • Remember: both a preoperative pulpal and periapical diagnosis are made before treatment is initiated (if reversible pulpitis is only condition, the periapical area should be normal). • If the tooth is percussion sensitive – consider bruxism or hyperocclusion.

  11. Treatment of Reversible Pulpitis • Remove irritant if present (caries; fracture; exposed dentinal tubules). • If no pulp exposure: CaOH, restore, monitor • If pulp exposure: • Carious: initiate RCT • Mechanical: >1 mm: initiate RCT <1 mm crown planned: initiate RCT <1 mm: direct cap or RCT • If recent operative or trauma – postpone additional treatment and monitor.

  12. Irreversible Pulpitis • Pulpal inflamation and degeneration not expected to improve. • A physiologically older pulp has less ability to recover due to decrease in vascularity and reparative cells. • As inflammation spreads apically, cellular organization begins to break down. • Localized pressure slows venous return, resulting in buildup of toxins and lower pH that causes widespread cellular destruction.

  13. Symptoms of Irreversible Pulpitis • Thermal: • Hypersensitive with moderate to severe prolongedpain (>30 seconds) as compared to the control • Sweets: • Moderately to severely sensitive (if caries, crack, or exposed dentin) • Biting Pressure: • Usually sensitive in later stages (periapical symptom) • Moderate to severe spontaneouspain

  14. DiagnosisIrreversible Pulpitis • Hypersensitive to hot or cold that is prolonged. • A history of spontaneous pain. • Vital or partially vital pulp.

  15. Treatment of Irreversible Pulpitis Minimum immediate treatment (if not extraction) • Pulpotomy: • Remove all decay (essential) • Large canals: passively broach 75% of tooth length • Small canals: spoon excavate orifice while removing pulpal tissue from chamber. • Copious irrigation with sodium hypochlorite (1%). • Dry chamber with cotton pledget • Place Ca(OH)² into large and over small canals • Place dry cotton pellet in chamber, cover with cavit, temporarily restore with Ketac-fill; completely relieve occlusion if have acute apical peridontitis

  16. Treatment of Irreversible Pulpitis Ideal immediate treatment • Pulpectomy(complete removal of pulpal tissue) • Determine the ideal working length (WL) • Fully instrument canals with master apical file • At least # 25 file for small canals (and anterior teeth) • # 35 - 40 file for larger canals • Alternate working files with #8 or 10 patency file • Copious irrigation with sodium hypochlorite (1%) • Dry chamber with cotton pledget • Place dry cotton pellet over canals, cover with cavit, temporarily restore with Ketac-fill; completely relieve occlusion if have acute periapical peridontitis.

  17. Irreversible Pulpitis(more treatment considerations) • Any residual decay can result in an inadequate seal, contamination of canal space, and inter-appointment flare-ups. • Inflammation can be judged by the amount of hemorrhage from the remaining pulp stump. If bleeding continues, re-broach or file for residual pulpal tags with copious irrigation. • To decrease risk of instrument separation within the canal space, do notengage the canal walls with broach.

  18. Irreversible Pulpitis(additional considerations) • Do not leave teeth open between appointments – causes contamination of the canals and difficulty closing them later. • Incomplete tooth fractures involving the pulp will show symptoms of irreversible pulpitis. Periodontal probing of associated pocket will indicate depth of fracture. If depth of pocket (fracture) extends below the attachment level, the prognosis is guarded to poor.

  19. Necrotic Pulp • Results from continued degeneration of an acutely inflamed pulp. • Involves a progressed breakdown of cellular organization and no reparative potential. • Commonly have apical radiolucent lesion. (alwaysconduct proper pulp testing to rule out a non-pulpal origin). • With multi-rooted teeth, one root may contain partially vital pulp, whereas other roots may be nonvital (necrotic).

  20. Maxillary first molar with large amalgam restoration and periapical radiolucencies around all three roots. The tooth was unresponsive to electrical and thermal testing.

  21. Symptoms of Necrotic Pulp • Thermal: • No response • Sweets: • No response • Biting Pressure: • Usually moderate to severe pain(not symptom of necrotic pulp, but rather periapical inflammation) • Moderate to severe spontaneouspain(usually dull and throbbing; associated with periapical area)

  22. Diagnosis of Necrotic Pulp • Distinguishing features: • No response to cold. • No response to pulpal test. • Caveats • Decreased sensitivity to cold/ept may be from of insulating effects of additional dentin. • Fluid in canal space conducting electrical current can give false-positive. • Periapicalradiolucency is strong but not conclusive evidence that pulp is necrotic.

  23. Treatment of Necrotic Pulp Minimumimmediate treatment (if not extraction) • Partial instrumentation of canals: • Remove all decay, evaluate restorability • Determine working length of all canals • Large canals: up to #40 file, 4mm short of WL • Small canals: up to #25 file, 4mm short of WL • Alternate working file with #8 or 10 patency file • Copious irrigation with sodium hypochlorite (1%) • Dry chamber with cotton pledget • Place Ca(OH)² into all canals • Place dry cotton pellet in chamber, cover with cavit, temporarily restore with Ketac-fill; completely relieve occlusion if have acute apical periodontitis.

  24. Treatment of Necrotic Pulp Ideal immediate treatment • Complete instrumentation of canals: • Determine the ideal working length • Fully instrument canals with master apical file • At least # 25 file for small canals (and anterior teeth) • # 35 - 40 file for larger canals • Alternate with #8 or 10 patency file • Copious irrigation with sodium hypochlorite (1%) • Place dry cotton pellet over canals, cover with cavit, temporarily restore with Ketac-fill; completely relieve occlusion if have acute apical periodontitis.

  25. Necrotic Pulp(additional considerations) • Antibiotic coverage • Usually not required unless patient has progressive swelling or fever. • Pain Management • Always determine allergy, contraindication, and interaction with present medications • Clock regulate NSAID (ibuprofen) for 3 days • Narcotic for approximately 3 days, if needed • Occlusal Reduction • Reduction in all cases with acute apical periodontitis (remember that length measurements may change)

  26. PERIAPICAL DISEASE Classified as: • Acute Apical Periodonitis • Acute Apical Abscess • Chronic Apical Periodontitis (Suppurative Apical Periodontitis with sinus tract) • Condensing Osteitis

  27. Treatment of Periapical Disease Pulpal status always dictates treatment of periapical disease

  28. Acute Apical Periodontitis • Mild to severe inflammation that surrounds or is closely associated with the apex of a tooth. • Results from: • Irreversible inflammation or necrotic pulp. • Trauma or bruxism of normal or reversibly inflamed pulpitic conditions. • Consider vertical fractures, periodontal abscess, and non-odontogenic pain.

  29. Clinical Findings inAcute Apical Periodontitis • Visual • Check for decay, fracture lines, swelling, sinus tracts, orientation of tooth, and hyperocclusion • Palpation • Sensitive (usually on buccal surface) • Percussion • Moderate to severe (initially use index finger to reduce patient discomfort) • Mobility • Slight to no mobility (if moderate mobility exists, check for possible periodontal condition before continuing)

  30. Acute Apical Periodontitis, con’t. • Perio Probing • WNL(unless concomitant periodontal disease or vertical fractureexists) • Thermal (pulpal symptom) • Response (not prolonged) – consider traumatic occlussion • If response prolonged – consider irreversible pulpitis • No response – consider necrotic pulp • EPT (pulpal test) • Response – pulp is vital (reversible or irreversible) • No response – pulp is necrotic

  31. Acute Apical Periodontitis, con’t. • Translumination • Not used unless fractured is suspected • Selective Anesthesia • Not necessary, offending tooth easily located • Test cavity • Not necessary • Radiographic • Periapical image does not showa radiolucent lesion; some thickening of the periodontal ligament is common

  32. Immediate Treatment ofAcute Periapical Periodontitis If from irreversible pulpitis: • Pulpotomy or extraction. If from necrotic pulp: • Root canal therapy initiated or extraction. If from hyperocclusion: When the pulp is normal or reversibly inflamed, adjusting the occlusion provides immediate relief. Always consider cracked tooth, irreversible pulpitis, or necrotic pulp if discomfort persists. If from bruxism: A biteguard may be indicated.

  33. Acute Apical Abscess • Acute inflammation of the periapical tissue characterized by localized accumulation of pus at the apex of a tooth. • A painful condition that results from an advanced necrotic pulp. • Patients usually relate previous painful episode from irreversible or necrotic pulp. • Swelling, tooth mobility, and fever are seen in advanced cases.

  34. Symptoms ofAcute Apical Abscess • Spontaneous dull, throbbing, persistent pain; exacerbated by lying down. • Percussion: • Extremely sensitive • Mobility: • Horizontal / vertical; often in hyperocclusion • Palpation: • Sensitive; vestibular or facial swelling likely • Thermal: • No response

  35. Clinical Findings ofAcute Apical Abscess Visual: • Check for decay, fracture lines, swelling, sinus tracts, orientation of tooth, hyperocclusion Palpation: • sensitive; intraoral or extraoral swelling present Percussion: • Moderate to severe (initially use index finger) Mobility: • Slight to none; may be compressible Perio probing: • WNL (unless have perio disease or vertical fracture)

  36. Acute Apical Abscess, con’t. Thermal: • No response (pulp is necrotic) EPT: • No response (false-positive from fluid in canal) Translumination: • Not used unless fractured is suspected Selective Anesthesia: • Not necessary, offending tooth easily located Test cavity: • Not necessary unless vitality is suspected

  37. Acute Apical Abscess, con’t. Radiographic: • Thickening of the periodontal ligament is common; may not show a frank lesion If tests indicate pulp vitality: (red flag!) • Review diagnostic information (repeat diagnostic tests) • Rule out lateral periodontal abscess • Review medical history for previous malignant lesions or other conditions (hyperparathyroidism) that may explain contradictory information • Do not begin treatment until this discrepancy has been resolved

  38. Treatment ofAcute Apical Abscess(necrotic pulp) Minimumimmediate treatment (if not extraction) • Partial instrumentation of canals: • Remove all decay, evaluate restorability • Determine working length of all canals • Achieve apical patency all canals with #10 file, look for drainage and allow to continue until it stops • Large canals: up to #40 file, 4mm short of WL • Smaller canals: up to #25 file, 4mm short of WL • Alternate with #8 or 10 patency file • Copious irrigation with sodium hypochlorite (1%) • Dry chamber with cotton pledget continued on next slide

  39. Treatment ofAcute Apical Abscess, con’t. • Place Ca(OH)² into all canals • Place dry cotton pellet in chamber, cover with cavit, temporarily restore with Ketac-fill, and completely relieve tooth from occlusion. • Incision and drainage may be required • Prescribe antibiotics and analgesics Continued pain and swelling are common postoperative problems – so prepare the patient for several days of discomfort.

  40. Results from prolonged inflammation that has eroded the cortical plate making a periapical lesion visible on the radiograph. Caused by a necrotic pulp, the lesion contains granulation tissue consisting of fibroblasts and collagen (with macrophages and lymphocytes). Must rule out central giant cell granuloma, traumatic bone cyst, and cemental dysplasia. Usually asymptomatic, but in acute phase may cause a dull, throbbing pain. Chronic Apical Periodontitis

  41. Chronic apical periodontitis. Extensive tissue destruction in the periapical region of a mandibular first molar occurred as a result of pulpal necrosis. Lack of symptoms together with presence of a radiographic lesion is diagnostic.

  42. Chronic Apical Periodontitis, con’t. • Most common pitfall is assuming that the presence of a periapical lesion automatically indicates a necrotic pulp. If tests indicate pulp vitality: (red flag!) • Review diagnostic information (repeat diagnostic tests) • Rule out lateral periodontal abscess, central giant cell granuloma, traumatic bone cyst, and cemental dysplasia. • Review medical history for previous malignant lesions or other conditions (hyperparathyroidism) that may explain contradictory information • Do not begin treatment until this discrepancy has been resolved

  43. Treatment ofChronic Apical Periodontitis(necrotic pulp) • If asymptomatic, no immediate treatment needed; schedule for root canal therapy • If in acute suppurative phase, immediate treatment same as with acute apical abscess, i.e., • Partial instrumentation of canals: • Remove all decay, evaluate restorability • Determine working lengths of all canals • Achieve apical patency all canals with #10 file, look for drainage and allow to continue until it stops • Large canals: up to #35 file, 4mm short of WL • Smaller canals: up to #25 file, 4mm short of WL • Alternate with #8 or 10 patency file

  44. Treatment ofChronic Apical Periodontitis, con’t. • Copious irrigation with sodium hypochlorite (1%) • Dry chamber with cotton pledget • Place Ca(OH)² into all canals • Place dry cotton pellet in chamber, cover with cavit, temporarily restore with Ketac-fill, and completely relieve tooth from occlusion. • Incision and drainage may be required • Prescribe antibiotics and analgesics Continued pain and swelling are common postoperative problems – so prepare the patient for several days of discomfort.

  45. Condensing Osteitis • Increased trabecular bone in response to persistent irritant diffusing from the root canal into the periradicular tissue. • May be either asymptomatic(pulpal necrosis) or associated with pain(pulpitis). • Therefore, may or may not respond to diagnostic tests, i.e., thermal, electric, palpation, percussion. • Root canal treatment, when indicated, may result in complete resolution.

  46. Inflammation followed by necrosis in the pulp of the first molar has resulted in the diffuse radiopacity of the periradicular tissue.

  47. Reversible pulpitisSymptoms: Fleeting sensitivity/pain to hot, cold or sweet with inmmediate onset.Pain is usually sharp and may be difficult to locate. Quickly subsides after removal of the stimulus. Signs: Exaggerated response to pulp testing. Carious cavity/leaking restoration Ireversible pulpitis Symptoms: Spontaneous pain which may last several hours, be worse at night, and is often pulsatile in nature. Pain is elicited by hot and cold at first, but in later stages heat is more significant and cold may actually ease symptoms.

  48. A characteristic feature is that the pain remains after the removal of the stimulus. Localization of pain may be difficult intially, but as the inflammation spreads to the periapical tissues the tooth will become more sensitive to pressure. • Signs: Application of heat elicits pain. • Dentine hypersensitivity This is pain arising from exposed dentine in response to a thermal, tactile, or osmotic stimulus. It is thought to be due to dentinal fluid movement stimulating pulpal pain receptors.

  49. Cracked tooth syndrome Symptoms: Sharp pain on biting-short duration. Signs: Tooth often has a large restoration.Crack may not be apparent at first but transillumination and possibly removal of the restoration may aid visualization. Positive response to vitality (sensibility) testing and pain can normally be alicited by getting the patient to bite with the affected tooth on a cotton-wol roll or tooth sleuth. May be associated with bruxing habit.

  50. Periapical/periradicular pain Progression of irreversible pulpitis ultimately leads to death of the pulp (pulpal necrosis). At this stage the patient may experience relief from pain and thus may not seek attention. Characteristically the patient can precisely identify the affected tooth, as the periodontal ligament, which is well supplied with proprioreceptive nerve endings, is inflamed. Pulpal necrosis with periapical periodontitis Symptoms:Variable, but patients generally describe a dull ache exacerbated by biting on the tooth.

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