this seminar consists of details regarding odontogenic pain,varius types, dentine hypersensitivity, pulpitis, apical pain, cracked tooth,periapical periodontitis, acute periapical abscess, granulomas, cysts ,traumatic periodontitis, periodontal abscess, perio-endo, endo-perio lesions, acute alveolar osteitis, acute pericoronitis relevance to endodontics

1. ODONTOGENIC
PAIN
Presented by:
Dr. Ritu Gupta
MDS I Year
Dept of Conservative
Dentistry and Endodontics
PDA, Bhopal(M.P)

2. CONTENTS
• Introduction
• Types
• Dentine hypersensitivity
• Pulpitis
• Apical pain
• Cracked tooth
• Periapical periodontitis
• Acute periapical abscess
• Periapical
granulomas/cysts
• Traumatic periodontitis
• Periodontal abscess
• Perio-endo/endo-perio
lesions
• Acute alveolar osteitis
• Acute pericoronitis
• Conclusion
• Bibliography

3. INTRODUCTION
• Odontogenic pain (Dental pain)
refers to pain initiating from the
teeth or their supporting
structures, the mucosa, gingivae,
maxilla, mandible or periodontal
membrane.
• For an effective diagnosis and
treatment, the clinician should
have a thorough knowledge of the
various pain complaints pertaining
to the orofacial region and the
different options available for their
optimal management

4. • For managing odontogenic pain, The “3-D’s”
principle—diagnosis, dental treatment, and drugs—
should be used.
• The first and foremost step is to determine the
condition causing the pain and then to discover that
what caused that condition.
• Removal of the cause usually leads to rapid recovery
and should be done by an appropriate dental
treatment.
• Medications should only be used to complement the
dental treatment .

5. TYPES OF ODONTOGENIC PAIN
Origin Possible causes
Pulpal pain Dentine hypersensitivity
Reversible pulpitis
Irreversible pulpitis
Cracked tooth syndrome
Periodontal pain Periapical periodontitis
Periapical abscess
Periapical granuloma and cyst
Traumatic periodontitis
Periodontal (lateral) abscess
Perio-endo, endo-perio, and combined
lesions

6. DENTINE HYPERSENSITIVITY
• Dentine sensitivity is a
common form of odontogenic
pain and is described as a
short, sharp pain from
exposed dentin in response to
thermal , tactile , osmotic ,
evaporative or chemical
stimuli and that cannot be
ascribed to any other pathosis
or any form of dental defect
Rotstein I, Ingle JI. Ingle’s Endodontics. 7/e. Raleigh (North Carolina) : PMPH USA Ltd ; 2019

7. • RISK FACTORS
1. Caries
2. anatomical defects
3. gingival recession
4. erosion
5. abrasion
6. Attrition
7. Bleaching
8. Periodontal treatment

8. PREVALENCE
• The prevalence of dental pain and its
characteristics were recorded using
standard measures of pain (WHO criteria).
• In a study of 1,052 individuals the
prevalence of reported toothache in
school children in the last six months was
33.6%
• analysis showed a significant association
of both the prevalence and severity of
dental pain with lower social class, later
birth order, failure at school and
attendance at the dentist only when in
trouble.
Goes PSA, Watt RG Hardy R, Sheiham A. The prevalence and severity of dental pain in 14-15 year old Brazilian
schoolchildren Community Dental Health 2007; 24 (4) 217-224

9. • INCIDENCE
1. some studies reports the
incidence of dentin
hypersensitivity peaks in the
third and fourth decades
2. The decrease in dentin
hypersensitivity after fourth
decade may be due to the
formation of tertiary dentin or
loss of pulp vitality
Canadian Advisory Board on Dentin Hypersensitivity.
Consensus-based recommendations for the diagnosis and
management of dentin hypersensitivity. J Cand Dent
Assoc. 2013;69:221–226.

10. Mechanisms to explain dentin hypersensitivity
• Schematic representation of the three main theories explaining the dentin
sensitivity. The nerve theory postulates the direct stimulation of dentinal
tubules and pulpar nerve terminals; the hydrodynamic theory assumes
stimulation of dental nerves by dentinal fluid; and the odontoblastic theory
postulates direct stimulation of odontoblast, and is based on the expression of
several ion channels by these cells.

11. • MANAGEMENT
1. Reduction in dentinal fluid flow
• Agents such as sodium fluoride, stannous fluoride,
strontium chloride, potassium oxalate, calcium
phosphate, calcium carbonate, and bioactive
glasses reduce fluid flow by plugging dentinal
tubules.
• Dentin adhesive sealers, including fluoride
varnishes, oxalic acid and resin, glass ionomer
cements, composites, and dentin bonding agents,
occlude the tubules, resulting in attenuation of
dentin hypersensitivity.

12. 2. Reduction in dentinal neuron activity
• Neural modulating agents such as potassium
nitrate are thought to act by depolarizing the
nerves and preventing repolarization
3. Making enamel-dentin more resistant to
demineralization
• application of fluoride-containing medicaments
prevents demineralization

13. PULPITIS
• Inflammation of the pulp (and periapical
tissues) is commonly associated with pain
constituting ~90% of emergency visits with
tooth pain as the chief complaint.
• This pain is attributed to activation of
pulpal or periapical nociceptors.
• Causes:
1. Insult of the tooth due to caries
2. iatrogenic insult
• Type of pain : short sharp ‘neuralgic’ pain
with extreme sensitivity to cold and sweet
flavours
Hasselgren G, Calev D. Endodontics emergency treatment sound and
simplified. NY State Dent J. 1994;60:31–33.

15. • A study comparing the quality of pain in patient with
odontalgia (n = 359) to those with craniofacial pain
referred from cardiac origin (n = 115) showed that the
quality descriptors, have high validity (P = 0.53) for
differentiating between odontogenic and cardiac pain
• The pain descriptors "pressure" and "burning" were
statistically associated with pain from cardiac origin,
while "throbbing" and "aching" indicated an
odontogenic cause.
• other signs of acute cardiac disease rather than dental
pathology, i.e., pain provocation/aggravation by
physical activity, pain relief at rest, and bilateralism.
Kreiner M, Falace D, Michelis V, Okeson JP, Isberg A. Quality difference in craniofacial pain of
cardiac vs. dental origin. J Dent Res. 2010;89:965–969.

16. • It was previously thought that the sensation of
throbbing was caused by the rhythmic activation of
pain sensory neurons in close approximation to blood
vessels.
• An elegant study on the relationship between
throbbing pain and arterial pulsations in odontogenic
pain patients showed that the throbbing rate (44
bpm ± 3 standard error of mean [SEM]) was much
slower than the arterial pulsation rate (73 bpm ± 2
SEM) and, that there was no synchronicity between
the two rhythms (P < 0.001)
• Therefore, it appears that the physiological
mechanisms underlying these two rhythmic events
are distinct.
Mirza AF, Mo J, Holt JL, et al. Is there a relationship between throbbing pain and arterial pulsations? J
Neurosci. 2012;22: 7572–7576.

17. Toothache, a signal for cardiac arrest!!
• Toothache remains one of the discreet
symptoms but, researchers say that
Craniofacial pain is the sole symptom of
Cardiac Ischemia (a condition of
insufficient blood flow to the heart
muscle) or Acute Myocardial Infarction
and is almost 10 times more common in
females than in males.
• Craniofacial pain symptoms mixed with
the classic cardiac symptoms include
pain felt at throat, left mandible (lower
jawbone), right mandible, ears, jaw
joints and teeth
https://www.deccanherald.com/content/362517/toothache-signal-cardiac-arrest.html

18. • Thermal hyperalgesia is considered a
hallmark of symptomatic irreversible pulpitis
pain.
• Several studies have examined the expression
of thermoreceptors and ion channels in the
dental pulp in order to better understand the
mechanisms underlying thermal hyperalgesia
in pulpitis.

19. • studies on TRP receptors show that
Preclinical studies and ex vivo studies clearly show that these
receptors are functional and that they are sensitized in the
presence of infection and inflammatory mediators.
Odontoblasts express TRPV 1-3, TRPAA 1, TRPM 8
Pulp fibroblasts express TRPA 1, TRPM 2, TRPM 8
Axons innervating dental pulp express TRPA 1, TRPM 2, TRPM 8, TRPV 1
El Karim IA, Linden GJ, Curtis TM, et al. Human odontoblasts express functional thermo-sensitive TRP channels:
implications for dentin sensitivity. Pain. 2011;152:2211–2223.

20. Mechanical allodynia
• Mechanical Allodynia is a
common finding in patients
presenting with signs and
symptoms consistent with
irreversible pulpitis.
• Several hypotheses have
been proposed to explain the
concurrent presentation of
mechanical allodynia with
irreversible pulpitis
Owatz CB, Khan AA, Schindler WG, et al. The incidence of mechanical allodynia in patients with
irreversible pulpitis. J Endod. 2007;33:552–556.

21. HYPOTHESIS 1
• mechanical allodynia is mediated by
mechanoreceptive neurons innervating the pulp.
This is supported by the findings that odontoblasts
express the mechanoreceptors and that pulpal
afferent A-fibers respond to mechanical stimulation.
• Given that not all patients with symptomatic
irreversible pulpitis present with mechanical
allodynia, it is unlikely that the mechanical allodynia
in odontogenic pain patients is activated via
sensitization of pulpal mechanoreceptors.

22. HYPOTHESIS 1 HYPOTHESIS 2
HYPOTHESIS 3

23. HYPOTHESIS 2
• inflammatory mediators and microbial byproducts
from inflamed pulps diffuse into the periradicular
space and activate or sensitize mechanoreceptors in
the periodontal ligament.
• mechanical allodynia in teeth with irreversible
pulpitis is due to activation of mechanoreceptors in
the periodontal ligament.
• Proof 1 : histologic findings that periapical changes
occur in teeth with vital pulps (prior to complete
pulpal necrosis)

24. • Proof 2 :
[Pope O, Sathorn C, Parashos P. A comparative investigation of cone-beam computed tomography and
periapical radiography in the diagnosis of a healthy periapex. J Endod. 2014;40: 360–365]
• Proof 3:
[Abella F, Patel S, Durán-Sindreu F, Mercadé M, Bueno R, Roig M. An evaluation of the periapical status of
teeth with necrotic pulps using periapical radiography and cone-beam computed tomography. Int Endod J.
2014;47:387–396]
CBCT IOPA
detected periapical radiolucencies ≥1 mm
in diameter of almost 20% of teeth with
vital pulps
no detectable radiolucencies in the
periapical radiographs.
CBCT IOPA
13.7% of teeth diagnosed with irreversible
pulpitis had periapical lesions
only 3.3% on periapical radiographs.

25. HYPOTHESIS 3:
• mechanical allodynia results from central sensitization
following activation of pulpal nociceptors.
• This is supported by preclinical studies showing that
acute sensitization of TRPA1, expressing pulpal
nociceptors, induces mechanical allodynia at distant
sites.
• A clinical study found that patients diagnosed with
irreversible pulpitis and mechanical allodynia reported
higher spontaneous pain as compared to those with
irreversible pulpitis and normal periapical tissues.
• Interestingly, the mechanical pain thresholds of the
normal contralateral teeth in patients with irreversible
pulpitis were lower than those in asymptomatic
patients.

26. • MANAGEMENT
1. determined based on the type of pulpitis and
presence of infection involving the periapical area.
TYPE T/t
Reversible pulpitis Excavation followed by restorations
Irreversible pulpitis Root canal treatment
Acute spreading infection additional drainage intra or extraorally via
drainage of involved tissue tissue spaces.

27. APICAL PAIN
• Caused by infection
spreading through the apical
foramen of the tooth causing
apical periodontitis and
ultimately a dental abscess (if
left untreated ).
• T/t :root canal treatment or
extraction of the tooth with
or without concomitant
course of antibiotics .
• Iatrogenic apical pain may
result after dental treatment
including premature contact
if a restoration is left high in
occlusion.

28. • Characterized by an initial sharp pain which becomes
duller after a period. The pain is due to a recent tooth
restoration that is ‘high’ compared with the normal
occlusion when biting together and to other areas of the
mouth.
• Symptoms : cause the patient to have difficulty sleeping
and may be exacerbated by lying down. Heat may make
the pain worse whereas cold may alleviate it.
• Duration of pain : intermittent with no regular pattern and
may have occurred over months or years.
• If there is periapical infection present, patients may no
longer complain of pain in response to a thermal
stimulus, but rather of sensitivity on biting

29. CRACKED TOOTH OR CRACKED CUSP
SYNDROME
• Occurs when a crack has occurred in the enamel or
dentine and reaches the pulp chamber. The crack is usually
not visible to the naked eye.
• Cause : Application of excessive force on a normal tooth or
physiologic forces applied to a weakened tooth.

30. • Diagnosis : often tricky.
• Radiography is not helpful in detection of fractures,
as cracks occur in a mesiodistal direction, parallel to
that of the plane of the film.
• Simple test is to have patient bite on a cotton roll
that evokes a sharp pain.
• Type of Pain: sharp and shooting in nature, and is
usually associated with biting and chewing.
• Hot and cold stimuli also evoke the pain.
• T/t :Restorable teeth should be treated
endodontically, followed by a full-coverage
restoration of tooth. However, tooth with large
cracks may require extraction

32. PERIAPICAL PERIODONTITIS (periapical
abscess, granuloma, and cyst)
• It includes acute/chronic nonsuppurative inflammation and
suppurative inflammation.
• Causes:
1. chronic inflammation without pus = Periapical granuloma
2. inflammation involving pus = periapical abscess .
3. Chemical irritation.

33. i. Acute periapical abscess
• Characterized by :
1. severe pain in the area of the nonvital tooth particularly
on percussion
2. inflammation
3. or complaint of pus drainage (with its associated foul
taste).
• Type of Pain : severe , pain also typically interferes with sleep.
• Treatment : includes drainage through an opening in the tooth
itself or through the soft tissue surrounding the jaw, if cellulitis has
developed.
• If patients with abscess have systemic signs of infection (e.g.,
fever), an oral antimicrobial is prescribed (amoxicillin 500 mg
every 8 hours; for patients allergic to penicillin, clindamycin 150 or
300 mg every 6 hours).
• On resolution of the abscess, the patient should undergo root
canal therapy or extraction

34. ii. Periapical granulomas or cysts
• Cause : inadequate drainage of acute pulpal infection.
• Type of Pain : dull pain or may be asymptomatic.
• Radiographically, abscesses, granulomas, or cysts have
the same features and microscopic examination should
be done for distinction.
• T/t : Teeth with periapical granulomas are nonvital and
needs root canal treatment or removal. Root canal
treatment done competently leads to healing even if
cystic phase has started.
• Persistence of periapical radiolucency after 6–
12 months may be due to technical faults associated
with root canal treatment. In such a case, apical
curettage with apicoectomy may be indicated

35. TRAUMATIC PERIODONTITIS
• painful condition that arises because of injury to the
periodontium due to trauma from excessive
occlusal forces.
Primary occlusal trauma Secondary occlusal trauma Combined occlusal trauma
Tooth or teeth with normal
periodontal support enduring
increased occlusal loads
Tooth or teeth with
inadequate periodontal
support if subjected to
normal occlusal forces
Excessive occlusal force on a
diseased periodontium may
lead to combined occlusal
trauma.
Causes :
• bruxism,
• overextended margins of
restorations,
• excessive loading during
orthodontic movements,
• recent fitting of a new
partial denture.
Cause : parafunctional
movements such as bruxism

36. Clinical features :
• pain on chewing/biting or percussion,
• progressive tooth mobility,
• nonphysiological movement of tooth during function
(fremitus).
• Additionally, there can be gingival inflammation with
pocket formation in combined occlusal trauma.
Radiographic features : evidence of circumferential
and furcal bone loss, in combination with widening
of the periodontal ligament space.

37. • Management :
Primary occlusal trauma Secondary occlusal trauma Combined occlusal trauma
Analysis and correction of
occlusion.
Progressive tooth mobility
may be reduced by occlusal
adjustment.
Managing the periodontal
inflammation is of primary
importance
One or more of the following
steps can do occlusal
adjustments:
• tooth movements,
• tooth removal,
• dental restorations,
• coronoplasty etc.
• Pain occurring due to
hypermobility can be
managed by splinting of
teeth.
• The aim of splinting is to
increase the resistance of
dentition to the occlusal
forces through
stabilization.
• It involves joining of two
or more teeth
• Premature occlusal
contacts usually contribute
to the progression of
periodontitis.
• tackled by simple
correction of the occlusion
eradicating the premature
occlusal contacts
Shaikh S. Management of Odontogenic and Nonodontogenic Oral Pain (From Conventional to
Innovative Approaches for Pain Treatment). 10.5772/intechopen.83837

38. PERIODONTAL ABSCESS
• Arises due to acute infection of a periodontal
pocket.
• Associated with vital tooth.
• Causes :
1. Primarily incomplete calculus removal
2. Occasionally, it may occur following root planing,
as the trauma to pocket lining implants bacteria
into the periodontal tissues.
3. food packing down between teeth with poor
contact points or foreign body (e.g., fish bone)
driven through the floor of a pocket.
4. Poorly controlled diabetes mellitus.

39. • Clinical features :
1. Periodontal abscess has a rapid onset.
2. gingival swelling and inflammatory edema prevent
drainage through the pocket orifice.
3. initial gingival tenderness progresses to throbbing pain
(well localized).
4. +ve on tender to percussion or biting.
5. tooth mobility with its elevation in socket.
6. Pus exudation may occur from the pocket; however, a
deep abscess has a sinus tract that points on the
alveolar mucosa.
7. Fever and regional lymphadenopathy (occasionally)
(The vitality of tooth, deep pocketing, and less severe
tenderness helps to differentiate between a periodontal
and pulpal abscess)

40. • T/t :
1. Before initiating T/t, evaluation
of patient’s medical history,
dental history, and systemic
conditions is crucial to
determine the need for
antibiotics.
2. Ideally, it should be drained
through pocket or occasionally
by an incision through the
gingiva.
3. If abscess is too large and
drainage cannot be done,
subgingival scaling and root
planing or deferring the surgical
access until the major clinical
signs have subsided.

41. 1. indications for antimicrobial therapy
are fever, lymphadenopathy,
evidence of spreading of infection
(cellulitis), deep periodontal
pocketing, and immunosuppression.
2. Administration of antibiotics alone
without the local drainage of the
abscess is contraindicated.
3. The drainage is mandatory in order to
eliminate the etiologic factors.
4. Extraction can be considered as a last
resort, if there is poor response to
therapy, horizontal tooth mobility
exceeding 1 mm, pocketing exceeding
8 mm, and more than 40% alveolar
bone resorption

42. Perio-endo, endo-perio, and combined
lesions
• In perio-endo lesions, microorganisms from the
periodontal pockets can reach the pulp through
accessory canals, thereby leading to pulpal
inflammation and necrosis.
• In endo-perio lesions, pulpal necrosis leads to
involvement and destruction of the periodontal
ligament and adjacent alveolar bone. Clinically
endo-perio lesions present as deep periodontal
probing depth extending to the apex of the tooth.

44. • Management :
1. Making an accurate diagnosis as to the source of
infection is a critical determinant of the treatment
outcome.
2. Sequence of the disease process can be an
important factor in determining the exact nature
of lesions: perio-endo and endo-perio lesions.
3. Conventional root canal therapy (RCT) alone leads
to a complete resolution of the periodontal defects
arising from primary pulpal infection.
4. However, pulpal infections resulting from primary
periodontal infections require both endodontic
and periodontal treatments for achieving complete
healing

45. ACUTE ALVEOLAR OSTEITIS (DRY SOCKET)
• Most common complication after
extraction whereby clot formation
within socket fails at 3–5 days.
• Healing fails, resulting in an empty
socket which traps food and debris.
• The resultant pain is caused by
necrotic foodstuff aggravating bony
nerve endings.
• This condition is devoid of the usual
acute inflammatory markers
(absence of lymphadenopathy ,
local inflammation and swelling).

46. • Type of pain : A dull throbbing pain develops two to
four days after a tooth extraction.
• Predisposing factor :commonly, Smoking as it
reduces the blood supply
• Features: The tissue around the socket is very
tender and white necrotic bone is exposed in the
socket.
Halitosis is very common.
• Incidence : between 1-9%. (Patients undergoing
mandibular surgical tooth removal should be
routinely warned of a possible incidence of 5%)

47. Management :
1. Irrigation of the socket using saline or
chlorhexidine and then an obtundant dressing
usually soaked in bacteriorstatic solution (alvogyl
paste, BIPP (bismuth iodoform paraffin paste),
cotton wool or gauze soaked in iodoform).
2. Immediate pain relief is usually attained and
patients rarely re-present for additional treatment.
3. Patients should be shown how to irrigate the area
and told to do this regularly.

48. 1. Analgesics are indicated as pain may persist for
several days.
2. Although opinion is divided as to whether or not
dry socket is an infective condition, use of
antibiotics is not recommended.
3. It is crucial that the reason for infection is
determined such as retained root or bony
fragments. A radiograph can be helpful. Surgical
extraction is indicated for removal of root tip or
bone sequestrum

49. ACUTE PERICORONITIS
• It is the inflammation of the flap of tissues (operculum)
around an erupting tooth, and most commonly
associated with impacted mandibular third molars.
• The chief complaints in this condition are severe pain
that can radiate to surrounding areas and swelling of
the pericoronal tissues.
• The hyperplastic-inflamed flap of tissue can become a
hotbed for bacteria, as it readily holds food particles
and debris.
• This scenario leads to bacterial infection with clinical
manifestations of discharge of pus, trismus, fever,
regional lymphadenopathy, and in some cases spread
of the infection to adjacent tissue spaces.

50. • Management :
Local measures :
1. If the pain and inflammation are limited to the
tooth, local measures, such as debridement of
food debris and plaque, irrigation with normal
saline or hydrogen peroxide, and avoidance of
occlusal trauma are recommended.
2. Antimicrobial therapy is indicated for patients
presenting with fever, trismus, and pus exudation.
3. Metronidazole 400 mg three times a day for
5 days is to be prescribed in combination with
phenoxymethylpenicillin 500 mg four times a day
for 5 days.

51. Operculectomy:
1. If it is envisaged that the tooth can be useful for
chewing and patient also has the desire to retain
the tooth, hyperplastic pericoronal tissue should
be excised out through a minor oral surgery
procedure known as operculectomy
2. Allows better access to properly clean the area and
prevent the accumulation of bacteria and food
debris.
3. In some unfortunate instances, the gum tissue may
grow back and create the same problem

52. Extraction:
1. Since impacted teeth frequently are unfavorably
aligned and do not erupt completely, extraction of
such tooth is commonly performed. This method
eliminates any chance of recurrence of
pericoronitis.
2. The risks and benefits of removal of impacted
molars are mired in controversy, as extraction can
lead to inferior alveolar nerve damage; retention
can precipitate serious, even life-threatening
infection.

53. CONCLUSION
The prudent clinician appreciates the importance of
listening to the patients’ pain history, using
appropriate diagnostic tests and replicating the chief
complaint in order to arrive at the right diagnosis.

54. BIBLIOGRAPHY
• Rotstein I, Ingle JI. Ingle’s Endodontics, 7/e.
Raleigh (North Carolina) : PMPH USA Ltd ; 2019
• Grossman’s Endodontic Practice, 13th edition.
New Delhi: Wolters Kluwer (India)Pvt. Ltd ; 2014
• Newman, Takei & Carranza. Clinical
Periodontology , 9/e. Pennsylvania : Saunders ;
2003
• Malik N. Textbook of Oral and Maxillofacial
Surgery, first edition. Noida (India) : Jaypee
Brothers Medical Publishers (P) Ltd ; 2002