1. Differential diagnosis of the pain in orofacial system
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.
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 characteristic of pulpal pain as that the patient is unable to localize the affected tooth.
The ability of the pulp to recover from injury depends upon its blood supply, not the nerve supply, which must be borne in brain when vitality (sensibility) testing is carried out
Although numerous classifications of pulpal disease exist, only limited number of clinical diagnostic situations require identification before affective treatment can be given.

5. 1. Dental pain Expressive pain Non-expressive pain
Dentine hypersensitivity
Chronic Pulpitis
Pulpitis
Neuritis from inclusion teeth
Periodontitis
Dental rip
Chronic apical Periodontitis
Dentitio difficilis
Retentio dentis
Synalgia
Sekundárne neuralgie

6. 2. Non-dental pain, located near the teeth
Expressive pain
Non-expressive pain
Affection near the tooth and its neighbours
Pregnancy
Affection of a distant bodies
aerodontalgia
Primary neuralgia
Systemic diseases

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 pain less than <30 seconds, but similar to control tooth
Sweets:
Sensitive (if caries, crack, or exposed dentin) with mild pain less than<30 seconds (similar to control tooth)
Biting Pressure:
None (unless tooth is cracked)

10. Diagnosis Reversible Pulpitis
If there is a discrepancy between the patient’s main complaint, 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 prolonged pain (>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 spontaneous pain

14. Diagnosis Irreversible 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)
# 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 not engage 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. (always conduct 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:
Biting Pressure:
Usually moderate to severe pain (not symptom of necrotic pulp, but rather periapical inflammation)
Moderate to severe spontaneous pain (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.
Periapical radiolucency is strong but not conclusive evidence that pulp is necrotic.

23. Treatment of Necrotic Pulp
Minimum immediate 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)
# 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 in Acute 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 fracture exists)
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 show a radiolucent lesion; some thickening of the periodontal ligament is common

32. Immediate Treatment of Acute 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 of Acute 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 of Acute 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 of Acute Apical Abscess (necrotic pulp)
Minimum immediate 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 of Acute 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. Chronic Apical Periodontitis
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.

41. Chronic apical periodontitis
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 of Chronic 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 of Chronic 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 pulpitis Symptoms: 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. Dentine hypersensitivity
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.

51. Signs: usually no response to vitality testing, unless one
canal of a multirooted tooth is still vital.
Rtg: Periapical lession- granuloma, cyst
Acute periapical abscess
Symptoms: Severe pain which will disturb sleep. Tooth is
exquisitely tender to touch.
Sings: Affected tooth is usually extruded, mobile. May be
associated with a localized or diffuse swelling. Vitality
testing may be misleading as pus may conduct stimulus to
apical tissues.

52. Chronic periapical abscess
Often symptomless. Possibly associated with persistent
sinus. Presentation may be: coincidental or acute
exacerbation.
Lateral periodontal abscess
Symptoms: similar to periapical abscess with acute pain
and tenderness, and often an associated bad taste.
Sings: Tooth is usually mobile, with associated localized
or diffuse swelling of the adjacent periodontium.
A deep periodontal pocket is usually associated,
which will exude pus on probing.
RTG: vertical or horizontal bone loss,(vitality testing ) is
usually positive, unless there is an associated perio-
endo lesion.

53. Non-dental pain
When no signs of dental or periradicular pathology can be detected then non-dental causes must be considered. Other causes of pain that can present as toothache include:
temporomandibular pain-dysfunction/facial arthromyalgia
sinusitis
psychological disorders (atypicalodontalgia)
tumours

54. Temporomandibular pain – dysfunction/facial arthromyalgia
The prblem being addressed is pain in the preauricular area and muscles of mastication with trismus, with or without evidence of internal derangement of the meniscus.
Clinical features: pain, clicking, locking, crepitus and trismus are the clasical signs and symptoms. Some patients may be clinically depressed but most are not. Pain is elicited by palpation over the muscles of mastication or the preauricular region.

55. Sinusitis
Antral pathology: often mimics symptoms attributable to maxillary teeth. Diagnosis is by exclusion of dental pathology, nasal discharge or stiffiness, tenderness over the cheeks, and pain worse on moving the head.
X-rays may reveal antral opacity, fluid level or fractures. Other X-rays: DPT (dental panoramic tomogram) for cysts, and roots and CT scans for tumours, pansinusitis, and blowout fractures.

56. Facial pain – pain not directly related to the teeth and jaws.
Trigeminal neuralgia-it is present as a shooking electric shock type of pain of rapid onset and short duration, which is often stimulated by touching a trigger point in the distribution of the trigeminal nerve. In the early stages of the disease there may be a period of prodromal pain not conforming to the classical description and it may be difficult to arrive at a diagnosis. Patients often have multiple extractions in a attempt to relieve the symptoms.

57. Atypical facial pain
This constitutes a large proportion of patients presenting with facial pain.
Classicaly, their symptoms are unrelated to anatomical
distribution of nerves or any known pathological
process, and these patients have often been through
a number of specialist disciplines in an attempt to
establish a diagnosis and gain relief. This diagnosis
tends to be used as a catch-all for a large group of
patients, with the connecting underlying supposition
that the pain is of psychogenic origin.

58. Pointers to a psychogenic etiology include imprecise localization, often bilateral pain or all over the place. Pain is described as being continuous for long periods with no change, and none of the usual relieving or exacerbating factors apply.
Most analgesics are said to be unhelpful.
Oral dysaesthesia or burning mouth syndrome is an unpleasant abnormal sensation affecting the oral mucosa in the absence of clinically evident disease. Five times more common in women aged years than other groups. Related to atypical facial pain.