An Evaluation of the     Relationship Between    Acute and Chronic Pain        Can Acute Pain Become a Chronic            ...
Acute Dental PainHeaivilin et al., JDR 2011
Acute PainChronic Pain
Acute PainChronic Pain
Acute Pain     ?Chronic Pain
Pain: An unpleasant  sensory and emotionalexperience associated with actual or potential tissue damage, or described in  t...
All Chronic Pain Was At One Time Acute
Chronic Pain: Pain thatpersists beyond the healing    phase of an injury
Clinical definition ofchronic pain comes     down to.....
Pain History
Pain History   “The tooth hurt for about    3 months before the root     canal”
Pain History                     “The tooth                   hurt for about                      3 months                ...
Pain History                     “The tooth         “The root                   hurt for about    canal was one of        ...
Pain History                     “The tooth         “The root                   hurt for about    canal was one of        ...
Pain History                      “The tooth         “The root                    hurt for about    canal was one of      ...
Pain History                      “The tooth         “The root                    hurt for about    canal was one of      ...
Pain History                      “The tooth           “The root                    hurt for about      canal was one of  ...
Pain History                      “The tooth           “The root                    hurt for about      canal was one of  ...
TIMELINE3 mo              9 mo            ?  RCT Completed          PG Endo NYU
TIMELINE       ONE YEAR!3 mo              9 mo            ?  RCT Completed          PG Endo NYU
Where we’ll go today
Epidemiology/Risk Factors of Chronic Pain
Epidemiology/     Mechanisms ofRisk Factors of     Acute and Chronic Pain      Chronic Pain
Epidemiology/                Mechanisms ofRisk Factors of                Acute and Chronic Pain                 Chronic Pa...
Epidemiology/ Risk Factors  of Chronic     Pain          Chronic Pain is            Common
Epidemiology/ Risk Factors  of Chronic     Pain
Epidemiology/ Risk Factors  of Chronic     Pain46%          54%
Epidemiology/ Risk Factors  of Chronic    No Pain     Pain       Chronic Pain46%          54%
Epidemiology/      Risk Factors       of Chronic             No Pain          Pain                Chronic Pain     46%    ...
Epidemiology/      Risk Factors       of Chronic                         No Pain          Pain                            ...
Epidemiology/      Risk Factors       of Chronic                                       No Pain          Pain              ...
Epidemiology/      Risk Factors       of Chronic                                       No Pain          Pain              ...
Epidemiology/      Risk Factors       of Chronic                                       No Pain          Pain              ...
Epidemiology/ Risk Factors  of Chronic     Pain    Chronic Pain Can  Often Be Neuropathic
Epidemiology/ Risk Factors  of Chronic     Pain                Neuropathic Pain: Pain                   arising as a direc...
Epidemiology/ Risk Factors  of Chronic     Pain                Post-Traumatic NeuropathyTrauma                          CR...
Epidemiology/ Risk Factors  of Chronic     Pain                Post-Traumatic NeuropathyTrauma                          CR...
Epidemiology/ Risk Factors  of Chronic     Pain                Post-Traumatic NeuropathyTrauma                          CR...
Epidemiology/ Risk Factors  of Chronic     Pain                Post-Traumatic NeuropathyTrauma                          CR...
Epidemiology/ Risk Factors  of Chronic     Pain     Neuropathic Pain is       not as common
Epidemiology/ Risk Factors  of Chronic     Pain
Epidemiology/ Risk Factors  of Chronic    No Pain     Pain       Neuropathic Pain
Epidemiology/ Risk Factors  of Chronic    No Pain     Pain       Neuropathic Pain        8%          92%
Epidemiology/ Risk Factors  of Chronic                 No Pain     Pain                    Neuropathic Pain          8%   ...
Epidemiology/ Risk Factors  of Chronic                      No Pain     Pain                         Neuropathic Pain     ...
Epidemiology/ Risk Factors  of Chronic                           No Pain     Pain                              Neuropathic...
Epidemiology/ Risk Factors  of Chronic     Pain  Chronic Post-Surgical          Pain
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Epidemiology/ Risk Factors  of Chronic                         4- Point Definition     Pain                              of...
Phantom Tooth PainAtypical Odontalgia  Persistent Post-  Treatment Pain
Epidemiology/ Risk Factors  of Chronic     PainMajority of CPSP  cases have neuropathiccharacteristics
Epidemiology/     Risk Factors      of Chronic         Pain         Chronic Pain 1 Year After SurgeryBandolier, Accessed 4...
Epidemiology/ Risk Factors  of Chronic     PainKehlet, Jensen, Woolf, Lancet 2006
Epidemiology/ Risk Factors  of Chronic     PainKehlet, Jensen, Woolf, Lancet 2006
Epidemiology/    Risk Factors     of Chronic        PainBallantyne, et al., IASP Clinical Update, January 2011
Epidemiology/    Risk Factors     of Chronic        PainBallantyne, et al., IASP Clinical Update, January 2011
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      B...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      B...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      1...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      1...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      1...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                      1...
Epidemiology/ Risk Factors  of Chronic     Pain       Individual     Predisposition        for CPSP                       ...
Epidemiology/ Risk Factors  of Chronic     Pain   What are some of the   risk factors for CPSP?                Patient   S...
Epidemiology/ Risk Factors       Patient  of Chronic     Pain           Specific   The most consistent  predictor of CPSP i...
Epidemiology/ Risk Factors                 Patient  of Chronic     Pain                     Specific   The most consistent ...
Epidemiology/ Risk Factors                                            Patient  of Chronic     Pain                        ...
Epidemiology/ Risk Factors       Patient  of Chronic     Pain           Specific     Females are More at        Risk for CPSP
Epidemiology/ Risk Factors      Patient  of Chronic     Pain          Specific     Persons of Younger    Age are More at Ri...
Epidemiology/ Risk Factors                     Patient  of Chronic     Pain                         Specific     Psychosoci...
Epidemiology/ Risk Factors                           Patient  of Chronic     Pain                               Specific   ...
Epidemiology/ Risk Factors                        Patient  of Chronic     Pain                            Specific         ...
Epidemiology/ Risk Factors                        Patient  of Chronic     Pain                            Specific         ...
Epidemiology/ Risk Factors                        Patient  of Chronic     Pain                            Specific         ...
Epidemiology/ Risk Factors                                 Patient  of Chronic     Pain                                   ...
Epidemiology/ Risk Factors  of Chronic     Pain   What are some of the   risk factors for CPSP?                Patient   S...
Epidemiology/ Risk Factors  of Chronic                     Surgery     Pain            Specific     Longer complicated    s...
Epidemiology/ Risk Factors  of Chronic                                          Surgery     Pain                          ...
Epidemiology/ Risk Factors  of Chronic                                              Surgery     Pain                      ...
Epidemiology/ Risk Factors  of Chronic                           Surgery     Pain                  Specific         Minimiz...
Epidemiology/ Risk Factors  of Chronic     Pain       But Could Teeth Be           Different?
Epidemiology/ Risk Factors  of Chronic     Pain   1. The Trigeminal System   2. Use of LA in dental procedures   3. Biolog...
Epidemiology/ Risk Factors  of Chronic     Pain   1. The Trigeminal System   2. Use of LA in dental procedures            ...
Epidemiology/ Risk Factors  of Chronic     Pain   1. The Trigeminal System   2. Use of LA in dental procedures   3. Biolog...
Epidemiology/ Risk Factors  of Chronic     Pain        Does CPSP Occur In          Endodontics?                   Polycarp...
Epidemiology/ Risk Factors  of Chronic     Pain        Does CPSP Occur In          Endodontics?                   Polycarp...
Epidemiology/ Risk Factors  of Chronic     Pain        Risk Factor       OR     95% CI          Pre-op Pain     7.8   (1.7...
Epidemiology/ Risk Factors  of Chronic     Pain        Does CPSP Occur In          Endodontics?                   Nixdorf,...
Epidemiology/ Risk Factors  of Chronic     Pain    Can We Prevent CPSP      with Analgesics?
Epidemiology/ Risk Factors  of Chronic     Pain                Katz and Seltzer, Exp Rev                Neurotherapeutics,...
Epidemiology/ Risk Factors  of Chronic     Pain       Conclusions     Chronic Post Surgical Pain (CPSP) can occur     afte...
Epidemiology/ Risk Factors  of Chronic     Pain       In The Future     Inform Our Patients About the Risk Factors for    ...
Epidemiology/         Mechanisms ofRisk Factors of         Acute and Chronic Pain          Chronic Pain              Imagi...
Mechanismsof Acute andChronic Pain               Trigeminal (Vth) nerve               (Peripheral)  The Trigeminal System
Mechanismsof Acute andChronic Pain               Trigeminal (Vth) nerve               (Peripheral) Central Sensitization
Mechanismsof Acute andChronic Pain               Trigeminal (Vth) nerve               (Peripheral) Central Sensitization
Mechanismsof Acute andChronic Pain                      4 Days   3 Weeks         Neuroplasticity               Taylor PE e...
Mechanismsof Acute andChronic Pain   NormalInflammation         Neuroplasticity               Rodd HD et al., Arch Oral Bio...
Mechanismsof Acute andChronic Pain           Neuroplasticity               Zhang et al., Exp Brain Res, 1995
Mechanismsof Acute andChronic Pain        Ectopic Activity               Contributes to spontaneous pain  Occurs in damage...
Mechanismsof Acute andChronic Pain       Reduced Descending Inhibition    A-Beta Fiber Mediated Mechanical                ...
Mechanismsof Acute andChronic PainDeafferentation    Somatotopic   Reorganization More Spontaneously   Active Neurons Incr...
Mechanisms    of Acute and                          Control    Chronic Pain   Induction of      Glial     Activity        ...
Mechanismsof Acute andChronic Pain   Conclusions  Multiple Mechanisms Contribute to  Development of Chronic Pain  In Anima...
Epidemiology/         Mechanisms ofRisk Factors of         Acute and Chronic Pain          Chronic Pain              Imagi...
NO BRAIN…………………NO PAINImaging the  Brain inChronic Pain
Imaging the  Brain inChronic Pain     fMRI
Woollett and Maguire: Current Biology, 2011
Woollett and Maguire: Current Biology, 2011
Woollett and Maguire: Current Biology, 2011
Brain Imaging in the       Media
Brain Imaging in the       Media
Brain Imaging in the       Media
Can Brain ImagingLet Us “See” Pain?
The PainMatrix
Measuring Chronic Pain isMore Challenging
Watching Chronic                       Pain in the BrainBaliki, MN et al., J Neurosci 2006
Changes in Brain                                Anatomy with                                 Chronic PainApkarian AV, et a...
Changes in Brain                                Anatomy with                                 Chronic PainApkarian AV, et a...
Changes in Brain                                Anatomy with                                 Chronic PainApkarian AV, et a...
What is theConsequence of Grey Matter  Atrophy?
Functional                           Consequence of                        Cortical DegenerationApkarian VA et al., Pain 2...
Functional                           Consequence of                        Cortical DegenerationApkarian VA et al., Pain 2...
Functional                           Consequence of                        Cortical DegenerationApkarian VA et al., Pain 2...
DLPFC        Amygdala                 S2 cortex insular cortex                Brainstem        ACCRodriguez-Raecke, et al....
Every Type of                      Chronic Pain is                        DifferentApkarian AV, et al., Pain 2011
Every Type of                      Chronic Pain is                        DifferentApkarian AV, et al., Pain 2011
Limitations of Brain  Imaging Studies
MultipleComparisons  Problem
Multiple              Small SampleComparisons                 Sizes  Problem
Multiple                    Small SampleComparisons                       Sizes  Problem              Over         Simplifi...
MultipleComparisons  Problem Bennett C.M et. al., Human Brain Mapping Conference                         2009
SmallSample Sizes
OverSimplification   of Brain  Function
OverSimplification   of Brain  Function
Brain Imaging:     Conclusions1. Subjective Experience of  Pain Can Be Objectively   Measured Using Brain          Imaging
Brain Imaging:     Conclusions2. Acute Pain and Chronic  Pain Activate Distinct   Regions of the Brain
Brain Imaging:      Conclusions3. Chronic Pain Causes Long   Term Changes in Brain Structure That May Relate    to Cogniti...
Epidemiology/         Mechanisms ofRisk Factors of         Acute and Chronic Pain          Chronic Pain              Imagi...
Chronic Pain is a    DiseaseNot just a symptom anymore
Real knowledge is toknow the extent of one’signorance.Confucius
★ Avoid damaging nerves
★ Avoid damaging nerves★ Get patients out of pain asap
★ Avoid damaging nerves★ Get patients out of pain asap★ Minimize intraoperative pain  experience
★ Avoid damaging nerves★ Get patients out of pain asap★ Minimize intraoperative pain  experience★ Minimize post-operative ...
THANKYOU !
Acute to chronic pain endodontics
Acute to chronic pain endodontics
Acute to chronic pain endodontics
Acute to chronic pain endodontics
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Acute to chronic pain endodontics

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Exploring the relationship between acute and chronic pain and relevance to endodontics

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  • \n
  • Our arena as endodontists and generalists is usually acute pain. Toothache or odontalgia is one of the most common types of moderate-severe pain experienced by both adults and children. We know that acute tooth pain is causes a fairly dramatic disruption in activities of daily living, affecting work attendance, mood, ability to eat, and generally is causes stress and anxiety for the person experiencing it. -Explain word cloud-Acute pain management certainly has challenges- pulpal anesthesia can be incredibly difficult, and patient management can be challenging for the person experiencing an acute pulpitis. Although we would still benefit from evidence based research in management of acute odontogenic pain, for the most part, we can get someone out of pain. \n
  • Where we get lost as clinicians is what does it mean when the pain doesn’t go away. We want to get our patients out of pain. But is it possible that sometimes no matter what we do, some patients aren’t going to get better. \n
  • Where we get lost as clinicians is what does it mean when the pain doesn’t go away. We want to get our patients out of pain. But is it possible that sometimes no matter what we do, some patients aren’t going to get better. \n
  • Pain is subjective. It’s influenced by your current emotional state and your past experiences with injury. It means something different to every person. \nImportant to note in the definition that there’s a sensory component and an emotional component. You don’t actually have to experience tissue injury to experience pain. Examples: empathetic pain, phantom limb pain. \n
  • But we need a starting point- so let’s begin with this statement. The burden on chronic pain is so profound that there is a big push to identify preventive factors that could prevent patients from developing chronic pain.\n
  • Because it’s hard to determine when the healing phase has ended a more common clinical definition involved a fixed time of persistent pain after it’s onset. \n
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  • Usually between 3 months or 6 months. Chronic back pain it’s 6 months. For herpes zoster/PHN it’s 3 months. For chronic post-surgical pain in medicine it’s usually 2 months after surgery. Since, to my knowledge we don’t have a strong evidence base for this in endodontics, it seems\n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
  • By some definitions this was already a chronic pain patient before she even got the initial root canal treatment. Now, she certainly is a chronic pain patient. \n\nThis case raises so many questions- it sounds like it was odontogenic pain to start with... Was it her cumulative experience of pain that led her to have this persistent pain problem now. If so would aggressively treating her acute pain have prevented her current chronic pain?\n\nDoes she have TMD and would intervention to control TMD pain aid her “tooth” pain?\n\nIs she genetically susceptible to chronic pain? I think the take home message today is that “It’s complicated”. And the more we learn about pain the more complicated it gets. I’m going to raise a lot of questions that I don’t necessarily have answers to, but I will present our current evidence and theories of chronic pain that I hope will shed some light on these important questions. \n\nI think this is a case of chronic post-treatment pain. \n
  • Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
  • Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
  • Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
  • Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
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  • Some other characteristics of neuropathic pain include the observation that nerve damage is necessary but not sufficient to generate this type of pain. That is not everyone who has nerve damage will develop neuropathic pain and in fact the number that will is actually quite small. So we can take the case of painful diabetic neuropathy. Of all diabetic patients approximately 50% will develop neuropathy meaning altered sensory thresholds, usually manifesting as decreased sensitivity to mechanical or thermal sensitivity, relative to age matched healthy controls. Now neuropathy does not necessarily mean pain. Of those that exhibit neuropathy only 20-30% report pain meaning the patient now reports pain that can be spontaneous, dysesthesias, and thermal or mechanical allodynia or hyperalgesia. Most chronic post surgical pain is neuropathic \n\n
  • Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
  • Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
  • Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
  • Again with the definitions....When it comes to actually defining things, things get complicated. \n
  • Some of these items are more difficult to define than others. \n
  • Some of these items are more difficult to define than others. \n
  • Some of these items are more difficult to define than others. \n
  • Some of these items are more difficult to define than others. \n
  • Let’s think about our case and whether using the criteria, if it could be classified as CPSP\n
  • Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
  • Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
  • Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
  • Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
  • A quick word on nomenclature. There are other terms to describe the phenomena I’m describing today. Phantom Tooth Pain was first described in the late 70s. The main distinction I’m making today is to use a terminology that’s rapidly gaining traction in the medical field, and to see if this might help us to better see through the murk. Atypical odontalgia is still difficult to define clinically. \n
  • It is thought that nerve damage is necessary, but not sufficient to cause CPSP. Most surgical procedures involve some damage to major or minor nerve branches. There is the potential however, that chronic inflammatory process could contribute. \n
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  • When you look at the amount of severe, disabling chronic pain, it’s much less, but still significant. \n
  • They are starting to be universal recognition that dental \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
  • The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
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  • What we’re talking about is pre-operative pain and post-operative pain. The presence of preoperative pain, or its intensity or duration, is a risk factor for the development of severe early acute postoperative pain, as well as long term post-surgical pain, and ultimately the development of chronic pain. It’s likely that the mechanisms we’ll talk about in a bit, that occur in acute pain, if left unchecked cause changes to the nervous system that put the patient at risk for chronic pain. \n
  • I think we’re very familiar with this concept in endodontics. We have a lot of studies showing how pre-operative pain predicts post-operative pain. Here’s one example that stands out for the large number of cases involved. \n1191 cases, looking at post-operative pain at 7days after completion of RCT.\nWhat’s missing in our literature is what happens to these patients after 7 days. \n
  • Like many chronic pain conditions females are generally at a greater risk of developing CPSP\n
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  • Numerous studies have shown the relationship between pre-op anxiety levels and post-operative or chronic post-surgical pain.\n\nCatastrophizing: a tendency to exaggerated pessimism about outcome. \n\nFear of pain. \n
  • Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
  • Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
  • Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
  • The studies I just described are just one example of a gene shown to be involved in pain experience. There are many others including the gene that encodes the serotonin transporter, IL-1B and others. Important to point out that these studies don’t show whether the gene is affecting pain itself or associated with a pathological state that has pain as a comorbidity. Also there is not yet any specific association with any of these genes and CPSP.\n
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  • Minimally invasive procedures that spare nerve injury as much as possible are recommended. \n
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  • Small sample size, but suggestive of the fact that less invasive procedures are less likely to cause chronic pain. Perhaps a more realistic example is RCT on #30 and #31 is less likely to cause chronic pain than EXT and placement of 2 implants. Highly speculative of course. \n\n
  • Surgeries that avoid major nerve damage are less likely to have CPSP. I think we have a good understanding of this in endodontics. We’re more worried about surgeries that impinge on mental nerve or IAN nerve. However any trauma, surgical or otherwise to soft tissue, bone, etc. can damage nerve endings and lead to chronic pain. This line of research has led to recommendations for preventive strategies that we’ll discuss at the end.\n\n
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  • Maybe somehow the nerves in the trigeminal system are different and less susceptible to the mechanisms which occur after nerve injury – we actually know there are potentially important differences between the TG and the spinal system- example sprouting of sympathetic fibers into the DRG after nerve injury but not into the TG. On the other hand we know there’s plenty of neuropathic pain in the head and neck so this really isn’t that great of an argument.\n\n
  • The eruption and exfoliation of primary teeth represents one of the few examples of a biologically programmed denervation that occurs. Maybe there’s some evolutionary protective mechanisms to against the neuroplastic changes contributing to chronic pain in pulpal neurons. \n\n
  • We’re really good at local anesthesia. Unlike most of our medical colleagues, we perform almost all of our procedures under local anesthesia. Preventing the barrage of peripheral signal into the central nervous system may reduce the incidence of chronic pain. Evidence of this from the work of Sharon Gordon in 3rd molar ext studies. That same argument could be used to speculate on how chronic pain could develop in a typical toothache case. Lots of pre-op pain, barriers to receiving care, difficult local anesthsia when they do come in for treatment, sever post-op pain due to inadequate post-op analgesics. \n\n
  • Attempted to recall 400 sequential patients who had undergone surgical or non-surgical rct. Only recalled about half of them so there could be some bias in the study based on the patients they were able to recall; i.e. those with more pain were more likely to come in. Patients were brought in for a clinical and radiographic exam and evaluated for any persistent disease. Pre-op pain was recorded prospectively which makes this a stronger study. Another limitation of this study and pretty much any study that looks at endodontic outcomes is that we’re limited in our ability to detect disease. Just because there is no detectable disease does that mean there really isn’t any? Maybe with better diagnostics this number could go down. However that fact remains that although the number might go down it likely will not go down to 0. So even if it were 2%, 3%, 1% we would still have a serious problem on our hands given the MILLIONS of procedures performed annually. \n\n
  • It’s good to think back to our “chicken or egg” problem when thinking about this data. Did some of these patients have something else going on that looked like odontogenic pain, which then did not resolve with endodontics. \n\n
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  • Can we prevent the progression to CPSP?\nExample of successful intervention to prevent post-op pain. Important point that this was multimodal analgesia. \nRemember where gabapentin is working, centrally. There’s a lot of examples of unsuccessful trials, many with NSAIDS and Local anesthetics. Is the gabapentin key? Unsure. \n
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  • Sprouting of CGRP fibers evident after drilling into cervical dentin. Hardware changes.\n
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  • Neuroplasticity occurs on a larger scale with nerve injury. We’re going to talk more about neuroplasticity in the last part of the talk where we talk about brain imaging studies. \n
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  • Let’s go back to the current definition of pain: “ An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Peripheral Nociception- the act of a painful stimulus activating peripheral neurons (example of giving an injection) pain. However, the actual experience of pain is influenced by a number of factors. The same stimulus can be interpreted differently based on a number of factors- a relaxed person versus an anxious person, a distracted person versus someone anticipating the painful response. Also, there are instances when you don’t need the peripheral input at all to experience pain. Consider phantom limb syndrome. In that case the peripheral input is completely absent but the experience of pain is quite real. Therefor discussion of the brain is essential to our understanding of chronic pain. \n\n\n\n
  • Non invasive imaging of the human brain has allowed for numerous opportunities to explore brain function both in health and disease. There are several ways to image the brain including MEG, PET, EEG but the most common is functional MRI, an example of which is being shown in the image above. fMRI measures brain activity by measuring small changes in blood flow. In addition to functional activity you can also measure structural changes in the brain\n
  • Examples of brain imaging studies have made it into mainstream media. For example this study of London Taxi Drivers. \nIn order to qualify as a licensed London taxi driver, a trainee must learn the complex and irregular layout of London's ∼25,000 streets (Figure 1) within a 6-mile radius of Charing Cross train station, along with the locations of thousands of places of interest. This spatial learning is known as acquiring “the Knowledge” and typically takes between 3 and 4 years, leading to a stringent set of examinations, called “appearances,” which must be passed in order to obtain an operating license from the Public Carriage Office (PCO, the official London taxi-licensing body). This comprehensive training and qualification procedure is unique among taxi drivers anywhere in the world.\n\nIn this study Woollett and Maguire imaged brains of persons entering the training program and were able to compare those who successfully completed the training, those who didn’t , and a control group. What they see is a specific increase the grey matter volume in the posterior hippocampal grey area. \n\nFor the first time we’re able to quantitatively measure changes in the brain that correlate with changes in how the brain is functioning. You could imaging that imaging dental students brains before and after learning the waxing during the first years you might see some changes in brain structure involved in fine motor skills. \n\n
  • Examples of brain imaging studies have made it into mainstream media. For example this study of London Taxi Drivers. \nIn order to qualify as a licensed London taxi driver, a trainee must learn the complex and irregular layout of London's ∼25,000 streets (Figure 1) within a 6-mile radius of Charing Cross train station, along with the locations of thousands of places of interest. This spatial learning is known as acquiring “the Knowledge” and typically takes between 3 and 4 years, leading to a stringent set of examinations, called “appearances,” which must be passed in order to obtain an operating license from the Public Carriage Office (PCO, the official London taxi-licensing body). This comprehensive training and qualification procedure is unique among taxi drivers anywhere in the world.\n\nIn this study Woollett and Maguire imaged brains of persons entering the training program and were able to compare those who successfully completed the training, those who didn’t , and a control group. What they see is a specific increase the grey matter volume in the posterior hippocampal grey area. \n\nFor the first time we’re able to quantitatively measure changes in the brain that correlate with changes in how the brain is functioning. You could imaging that imaging dental students brains before and after learning the waxing during the first years you might see some changes in brain structure involved in fine motor skills. \n\n
  • There are numerous examples that have made it to mainstream media describing how the \n
  • There are numerous examples that have made it to mainstream media describing how the \n
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  • What came out of this line of research is called “The Pain Matrix”.The pain matrix is a network of connected structures distributed throughout the brain. Includes structures involved in sensory discrimination as well as structures involved in affect, cognition and evaluation. These areas of the brain consistently light up when a painful stimulus is applied in an experimental setting. However, there is a lot of individual variability in this matrix. Also important to note that there isn’t one pain center in the brain. So ablating or taking out one of these structures or even all of them wouldn’t necessarily eliminate pain. In other words these structures might not be necessary for the experience of pain.\n
  • The areas that are pain matrix are the most frequent to show activity in pain studies, but this is only relevant to acute simulated pain in healthy volunteers. What happens in chronic pain is more complex. Different etiology, different anatomical structures involved, different time courses. \n
  • Vania Apkarian’s group took a different experimental approach. They reasoned that the most burdensome and clinically relevant aspect of pain for the chronic pain patient is the experience of spontaneous pain. So they put patients in the scanner and they would record their spontaneous pain while their brain was imaged, without any external stimulation. This allowed them measure what parts of their brain were active when they were in pain as well as correlate brain activity with spontaneous pain intensity. What they found was that the brain areas activated by acute pain stimuli were only marginally associated with the experience of spontaneous pain in chronic pain patients, and seemed to be activated upon initiation of a bout of spontaneous pain. A distinct area of the brain was active during sustained periods of intense spontaneous pain called located within the medial prefrontal cortex. This brain areas is involved in emotion, cognition, and motivation. Based on other work that associated brain activities with this region, the researchers hypothesize that this activity reflects a negative emotional state in reference to the self. Perhaps suffering. \n
  • In another series of studies by Vania Apkarian, again using patients with Chronic Back Pain, they evaluated gross changes in brain morphology in pain patients versus age matched healthy controls. What they found was surprising. First, they found that total volume of grey matter was reduced in the pain patients compared to the healthy controls. They had to take into account age because as we age our grey matter volume decreases by about 0.5% per year. They found that having chronic back pain caused an brain matter atrophy equivalent to 10-20 years of aging.They also looked at specific regions of grey matter loss and found the greatest loss in the DLPFC as well as the thalamus. Both of these regions are activated with acute pain.They also found the loses in the DLPFC were more significant in patients with neuropathic back pain rather than non-neuropathic back pain. It was interesting that the DLPFC seemed to be more significantly related to chronic pain since this area is involved in working memory and executive function. So complex decision making- this area is involved in deciding which responses should be executed. Pain in some way seemed to be overloading the decision making system and possibly atrophying the system.\n
  • In another series of studies by Vania Apkarian, again using patients with Chronic Back Pain, they evaluated gross changes in brain morphology in pain patients versus age matched healthy controls. What they found was surprising. First, they found that total volume of grey matter was reduced in the pain patients compared to the healthy controls. They had to take into account age because as we age our grey matter volume decreases by about 0.5% per year. They found that having chronic back pain caused an brain matter atrophy equivalent to 10-20 years of aging.They also looked at specific regions of grey matter loss and found the greatest loss in the DLPFC as well as the thalamus. Both of these regions are activated with acute pain.They also found the loses in the DLPFC were more significant in patients with neuropathic back pain rather than non-neuropathic back pain. It was interesting that the DLPFC seemed to be more significantly related to chronic pain since this area is involved in working memory and executive function. So complex decision making- this area is involved in deciding which responses should be executed. Pain in some way seemed to be overloading the decision making system and possibly atrophying the system.\n
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  • Again, the same group studied how chronic pain patients performed on a specific task that involved emotional decision making. Patients performed a test called the “Iowa Gambling Task” where they drew cards from four decks of cards. Two of the decks were “good” decks (c and d) and two of the decks were “bad” decks (a and b) in the long run. Then they measure how long it takes the subject to figure out which decks pay off for them in the long run. It’s also interesting to note that healthy persons given acute pain stimuli are not affected in performing this task. This effect seems to be specific to chronic pain\n
  • Again, the same group studied how chronic pain patients performed on a specific task that involved emotional decision making. Patients performed a test called the “Iowa Gambling Task” where they drew cards from four decks of cards. Two of the decks were “good” decks (c and d) and two of the decks were “bad” decks (a and b) in the long run. Then they measure how long it takes the subject to figure out which decks pay off for them in the long run. It’s also interesting to note that healthy persons given acute pain stimuli are not affected in performing this task. This effect seems to be specific to chronic pain\n
  • This study looked at patients with chronic osteoarthritis pain in one hip. Like many other studies they found a loss in grey matter volume in particular areas of the brain. Hip replacement actually improves pain to a profound extent in most of these patients so they were able to scan these patients before and after hip replacement and determine whether pain relief reverses the loss of grey matter. The first bar is before hip replacement, the second is 6-8 weeks after, and the last is 16-18 weeks after surgery. The third scan showed a significant increase in grey matter volume relative to the first and second scans. Suggests that the changes observed in chronic pain patients are reversible.\n
  • The activation in the pre-frontal cortex that was related to pain in CBP patients was much less so in other pain states. \n
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  • One mature atlantic salmon participated in the study. The salmon was not alive at the time of the study. The salmon was shown a series of photographs depicting human individuals in social situations with a specified emotional valence\nIn fMRI, the problem is particularly severe. An MRI scan divides the brain up into cubic units called voxels. There are over 40,000 in a typical scan. Most fMRI analysis treats every voxel independently, and tests to see if each voxel is "activated" by a certain stimulus or task. So that's at least 40,000 separate comparisons going on - potentially many more, depending upon the details of the experiment. The conclusion of this “study” is that correction for multiple comparisons is essential for brain imaging studies. \n\n
  • Cost is about $500-$600 for a research scan. As a consequence large studies are often cost prohibitive. \n
  • The Human Connectome Project (HCP) is a project to construct a map of the complete structural and functional neural connections in vivo within and across individuals. The HCP represents the first large-scale attempt to collect and share data of a scope and detail sufficient to begin the process of addressing deeply fundamental questions about human connectional anatomy and variation. Uses Diffusion Tensor Imaging Technique that is still a type of neuroimaging, but not a lot of functional data techniques. Scientist at MIT are attemption to map every connection in the human brain. There are about 100 billion neurons in the brain and each neuons makes about 7000 synpatic connections with other neurons so this is an incredible challenge. As important and a bigger project than the human genome project. \n
  • Much of the brain imaging data we have so far is not so different from phrenology. Phrenology was a “scientific” area of study popular in the first half of the 19th century where it was thought measuring the skull would reveal certain truths about the functioning of the brain. By not accounting for the complex interactions and communication between individual neurons and brain regions and how they communicate, we’re running the risk of \n
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  • So different mechanisms. \n
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  • So where does this leave us? We spoke about some of the risk factors for chronic pain, we dug into what we know about CPSP and how it may or may not be relevant to us in dentistry. And finally we spoke about what we’ve learned about how the brain changes when it’s in pain. \n
  • Like many diseases, preventive strategies are often more useful than trying to reverse the disease. \n
  • I think is some respects you might find this talk unsatisfying, because there is so much that we don’t know. There’s not much practical advice to give at this point, but it’s more a glimpse into what I hope we’ll be able to understand in the future. \n
  • Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
  • Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
  • Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
  • Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
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  • Acute to chronic pain endodontics

    1. 1. An Evaluation of the Relationship Between Acute and Chronic Pain Can Acute Pain Become a Chronic Problem? Jennifer L. Gibbs MAS, DDS, PhDNew York University Department of Endodontics
    2. 2. Acute Dental PainHeaivilin et al., JDR 2011
    3. 3. Acute PainChronic Pain
    4. 4. Acute PainChronic Pain
    5. 5. Acute Pain ?Chronic Pain
    6. 6. Pain: An unpleasant sensory and emotionalexperience associated with actual or potential tissue damage, or described in terms of such damage.
    7. 7. All Chronic Pain Was At One Time Acute
    8. 8. Chronic Pain: Pain thatpersists beyond the healing phase of an injury
    9. 9. Clinical definition ofchronic pain comes down to.....
    10. 10. Pain History
    11. 11. Pain History “The tooth hurt for about 3 months before the root canal”
    12. 12. Pain History “The tooth hurt for about 3 months before the root canal” “The pain was so bad after thetreatment I had to go back and get vicodin ”
    13. 13. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after thetreatment I had to go back and get vicodin ”
    14. 14. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after thetreatment I had to go back and “The pain get vicodin ” never really went away”
    15. 15. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after the Pre-Op Paintreatment I had to go back and “The pain get vicodin ” never really went away”
    16. 16. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after the Pre-Op Paintreatment I had to go back and “The pain get vicodin ” never really went away”Post-Op Pain
    17. 17. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after the Pre-Op Pain Intra-Op Paintreatment I had to go back and “The pain get vicodin ” never really went away”Post-Op Pain
    18. 18. Pain History “The tooth “The root hurt for about canal was one of 3 months the most painful before the root experiences of canal” my life” “The pain was so bad after the Pre-Op Pain Intra-Op Paintreatment I had to go back and “The pain get vicodin ” never really went away”Post-Op Pain Chronic Pain?
    19. 19. TIMELINE3 mo 9 mo ? RCT Completed PG Endo NYU
    20. 20. TIMELINE ONE YEAR!3 mo 9 mo ? RCT Completed PG Endo NYU
    21. 21. Where we’ll go today
    22. 22. Epidemiology/Risk Factors of Chronic Pain
    23. 23. Epidemiology/ Mechanisms ofRisk Factors of Acute and Chronic Pain Chronic Pain
    24. 24. Epidemiology/ Mechanisms ofRisk Factors of Acute and Chronic Pain Chronic Pain Imaging the Brain in Chronic Pain
    25. 25. Epidemiology/ Risk Factors of Chronic Pain Chronic Pain is Common
    26. 26. Epidemiology/ Risk Factors of Chronic Pain
    27. 27. Epidemiology/ Risk Factors of Chronic Pain46% 54%
    28. 28. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain46% 54%
    29. 29. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain 46% 54%Elliott et al., Lancet 1999
    30. 30. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain 46% 48% 54% 52%Elliott et al., Lancet 1999
    31. 31. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain 46% 48% 54% 52% Torrance et al., J PainElliott et al., Lancet 1999 2006
    32. 32. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain 31% 46% 48% 54% 52% 69% Torrance et al., J PainElliott et al., Lancet 1999 2006
    33. 33. Epidemiology/ Risk Factors of Chronic No Pain Pain Chronic Pain 31% 46% 48% 54% 52% 69% Torrance et al., J Pain Bouhassira et al., PainElliott et al., Lancet 1999 2006 2008
    34. 34. Epidemiology/ Risk Factors of Chronic Pain Chronic Pain Can Often Be Neuropathic
    35. 35. Epidemiology/ Risk Factors of Chronic Pain Neuropathic Pain: Pain arising as a direct consequence of a lesion or disease affecting the somatosensory system. Image from:georgiapainphysicians.com
    36. 36. Epidemiology/ Risk Factors of Chronic Pain Post-Traumatic NeuropathyTrauma CRPS Neuropathic Pain= Nerve Injury
    37. 37. Epidemiology/ Risk Factors of Chronic Pain Post-Traumatic NeuropathyTrauma CRPSSurgery Neuropathic Pain= Nerve Injury
    38. 38. Epidemiology/ Risk Factors of Chronic Pain Post-Traumatic NeuropathyTrauma CRPSSurgery Neuropathic Pain= Nerve Injury
    39. 39. Epidemiology/ Risk Factors of Chronic Pain Post-Traumatic NeuropathyTrauma CRPSSurgery Chronic Post-Surgical Pain Neuropathic Pain= Nerve Injury
    40. 40. Epidemiology/ Risk Factors of Chronic Pain Neuropathic Pain is not as common
    41. 41. Epidemiology/ Risk Factors of Chronic Pain
    42. 42. Epidemiology/ Risk Factors of Chronic No Pain Pain Neuropathic Pain
    43. 43. Epidemiology/ Risk Factors of Chronic No Pain Pain Neuropathic Pain 8% 92%
    44. 44. Epidemiology/ Risk Factors of Chronic No Pain Pain Neuropathic Pain 8% 92% Torrance et al., J Pain 2006
    45. 45. Epidemiology/ Risk Factors of Chronic No Pain Pain Neuropathic Pain 8% 7% 92% 93% Torrance et al., J Pain 2006
    46. 46. Epidemiology/ Risk Factors of Chronic No Pain Pain Neuropathic Pain 8% 7% 92% 93% Torrance et al., J Pain Bouhassira et al., Pain 2006 2008
    47. 47. Epidemiology/ Risk Factors of Chronic Pain Chronic Post-Surgical Pain
    48. 48. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Macrae and Davies, IASP Press 1999
    49. 49. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed After a Surgical Procedure Macrae and Davies, IASP Press 1999
    50. 50. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed Pain of at Least After a Surgical 2 Month Procedure Duration Macrae and Davies, IASP Press 1999
    51. 51. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed Pain of at Least After a Surgical 2 Month Procedure Duration Exclude the Possibility that Pain is Continuing From a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    52. 52. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed Pain of at Least After a Surgical 2 Month Procedure Duration Exclude the Other Causes Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    53. 53. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed Pain of at Least After a Surgical 2 Month Procedure Duration Exclude the Other Causes Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    54. 54. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed Pain of at Least After a Surgical 2 Month Procedure Duration Exclude the Other Causes Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    55. 55. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed After a Surgical Procedure p Pain of at Least 2 Month Duration Exclude the Other Causes Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    56. 56. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed After a Surgical Procedure p Pain of at Least 2 Month Duration p Exclude the Other Causes Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    57. 57. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed After a Surgical Procedure p Pain of at Least 2 Month Duration p Exclude the Other Causes ?p Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    58. 58. Epidemiology/ Risk Factors of Chronic 4- Point Definition Pain of CPSP Pain Developed After a Surgical Procedure p Pain of at Least 2 Month Duration p Exclude the Other Causes ?p ?p Possibility that for the Pain Pain is Have Been Continuing From Excluded a Pre-Existing Problem Macrae and Davies, IASP Press 1999
    59. 59. Phantom Tooth PainAtypical Odontalgia Persistent Post- Treatment Pain
    60. 60. Epidemiology/ Risk Factors of Chronic PainMajority of CPSP cases have neuropathiccharacteristics
    61. 61. Epidemiology/ Risk Factors of Chronic Pain Chronic Pain 1 Year After SurgeryBandolier, Accessed 4/2012. www. medicine.ox.ac.uk
    62. 62. Epidemiology/ Risk Factors of Chronic PainKehlet, Jensen, Woolf, Lancet 2006
    63. 63. Epidemiology/ Risk Factors of Chronic PainKehlet, Jensen, Woolf, Lancet 2006
    64. 64. Epidemiology/ Risk Factors of Chronic PainBallantyne, et al., IASP Clinical Update, January 2011
    65. 65. Epidemiology/ Risk Factors of Chronic PainBallantyne, et al., IASP Clinical Update, January 2011
    66. 66. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP Bruce, J. et al., Pain 2003
    67. 67. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP Bruce, J. et al., Pain 2003
    68. 68. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP 12% Bruce, J. et al., Pain 2003
    69. 69. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP 12% Bruce, J. et al., Pain 2003
    70. 70. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP 12% 9% Bruce, J. et al., Pain 2003
    71. 71. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP 12%p=0.12 x 0.09 =0.01 or 1% 9% Bruce, J. et al., Pain 2003
    72. 72. Epidemiology/ Risk Factors of Chronic Pain Individual Predisposition for CPSP 12%p=0.12 x 0.09 =0.01 or 1% Incidence of Chronic Pain at Both Sites= 9% 18% Bruce, J. et al., Pain 2003
    73. 73. Epidemiology/ Risk Factors of Chronic Pain What are some of the risk factors for CPSP? Patient Surgery Specific Specific
    74. 74. Epidemiology/ Risk Factors Patient of Chronic Pain Specific The most consistent predictor of CPSP is....
    75. 75. Epidemiology/ Risk Factors Patient of Chronic Pain Specific The most consistent predictor of CPSP is.... pain itself
    76. 76. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Severe Pain Mod Pain No Pain 100 75 % 50 25 0 No Pre-Op Pain Pre-Op Pain Genet J.M et al., IEJ 1986
    77. 77. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Females are More at Risk for CPSP
    78. 78. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Persons of Younger Age are More at Risk for CPSP
    79. 79. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Psychosocial Factors ANXIETY CATASTROPHIZING FEAR
    80. 80. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Genetics COMT Diatchenko L et al., Human Mol Genetics 2005
    81. 81. Epidemiology/ Risk Factors Patient of Chronic Pain Specific COMT Diatchenko L et al., Human Mol Genetics 2005
    82. 82. Epidemiology/ Risk Factors Patient of Chronic Pain Specific COMT Diatchenko L et al., Human Mol Genetics 2005
    83. 83. Epidemiology/ Risk Factors Patient of Chronic Pain Specific COMT Diatchenko L et al., Human Mol Genetics 2005
    84. 84. Epidemiology/ Risk Factors Patient of Chronic Pain Specific Genetics Dr. Paul Rosenberg- Saturday 1:45
    85. 85. Epidemiology/ Risk Factors of Chronic Pain What are some of the risk factors for CPSP? Patient Surgery Specific Specific
    86. 86. Epidemiology/ Risk Factors of Chronic Surgery Pain Specific Longer complicated surgeries associated with higher incidence of chronic pain
    87. 87. Epidemiology/ Risk Factors of Chronic Surgery Pain Specific MASTECTOMY + RECONSTRUCTION 49%* MASTECTOMY 31% BREAST REDUCTION 22% Wallace MS et al., Pain 1996
    88. 88. Epidemiology/ Risk Factors of Chronic Surgery Pain Specific SURGICAL ENDO 23.8%* NON-SURGICAL ENDO 10.7% Polycarpou N. et al., IEJ 2005
    89. 89. Epidemiology/ Risk Factors of Chronic Surgery Pain Specific Minimize Chances of Nerve Injury By Surgical Strategy
    90. 90. Epidemiology/ Risk Factors of Chronic Pain But Could Teeth Be Different?
    91. 91. Epidemiology/ Risk Factors of Chronic Pain 1. The Trigeminal System 2. Use of LA in dental procedures 3. Biologically programmed denervation But Could Teeth Be Different? Bennet G., J Oraf Pain 2004
    92. 92. Epidemiology/ Risk Factors of Chronic Pain 1. The Trigeminal System 2. Use of LA in dental procedures Text 3. Biologically programmed denervation But Could Teeth Be Different? Bennet G., J Oraf Pain 2004
    93. 93. Epidemiology/ Risk Factors of Chronic Pain 1. The Trigeminal System 2. Use of LA in dental procedures 3. Biologically programmed denervation But Could Teeth Be Different? Bennet G., J Oraf Pain 2004
    94. 94. Epidemiology/ Risk Factors of Chronic Pain Does CPSP Occur In Endodontics? Polycarpou N. et al., IEJ 2005
    95. 95. Epidemiology/ Risk Factors of Chronic Pain Does CPSP Occur In Endodontics? Polycarpou N. et al., IEJ 2005
    96. 96. Epidemiology/ Risk Factors of Chronic Pain Risk Factor OR 95% CI Pre-op Pain 7.8 (1.7, 35.6) Chronic Pain 4.5 (1.5, 13.5) Inter Appt Pain 3.9 (1.4, 10.7) Gender 4.5 (1.2, 16.4) Surgery 4.0 (1.0, 14.6)
    97. 97. Epidemiology/ Risk Factors of Chronic Pain Does CPSP Occur In Endodontics? Nixdorf, DE et al., JOE 2010
    98. 98. Epidemiology/ Risk Factors of Chronic Pain Can We Prevent CPSP with Analgesics?
    99. 99. Epidemiology/ Risk Factors of Chronic Pain Katz and Seltzer, Exp Rev Neurotherapeutics, 2009
    100. 100. Epidemiology/ Risk Factors of Chronic Pain Conclusions Chronic Post Surgical Pain (CPSP) can occur after dental surgeries including RCT. Management of Pain, Pre-Op, Intra-Op, and Post-Op to Minimize Risk Minimize Invasive Procedures to Minimize Risk
    101. 101. Epidemiology/ Risk Factors of Chronic Pain In The Future Inform Our Patients About the Risk Factors for Chronic Pain After All Dental Procedures (RCT, EXT, IMPLANT) Estimate an Individuals Risk for Developing CPSP Using Atypical Analgesics (e.g. Gabapentin) in High Risk Cases Emphasis on preserving vital pulp when possible???
    102. 102. Epidemiology/ Mechanisms ofRisk Factors of Acute and Chronic Pain Chronic Pain Imaging the Brain in Chronic Pain
    103. 103. Mechanismsof Acute andChronic Pain Trigeminal (Vth) nerve (Peripheral) The Trigeminal System
    104. 104. Mechanismsof Acute andChronic Pain Trigeminal (Vth) nerve (Peripheral) Central Sensitization
    105. 105. Mechanismsof Acute andChronic Pain Trigeminal (Vth) nerve (Peripheral) Central Sensitization
    106. 106. Mechanismsof Acute andChronic Pain 4 Days 3 Weeks Neuroplasticity Taylor PE et al., Brain Research, 1988
    107. 107. Mechanismsof Acute andChronic Pain NormalInflammation Neuroplasticity Rodd HD et al., Arch Oral Biol, 2002
    108. 108. Mechanismsof Acute andChronic Pain Neuroplasticity Zhang et al., Exp Brain Res, 1995
    109. 109. Mechanismsof Acute andChronic Pain Ectopic Activity Contributes to spontaneous pain Occurs in damaged and adjacent undamaged neurons Nerve! Injury!
    110. 110. Mechanismsof Acute andChronic Pain Reduced Descending Inhibition A-Beta Fiber Mediated Mechanical Allodynia Glia**
    111. 111. Mechanismsof Acute andChronic PainDeafferentation Somatotopic Reorganization More Spontaneously Active Neurons Increased Receptive Field Size Hu et al., J Phys, 1986
    112. 112. Mechanisms of Acute and Control Chronic Pain Induction of Glial Activity 7D Post Pulp Exp Increased GFAP Expression After Pulp Exposure.Stephenson & Byers Exp Neurol 1995
    113. 113. Mechanismsof Acute andChronic Pain Conclusions Multiple Mechanisms Contribute to Development of Chronic Pain In Animal Models Similar Mechanisms of Pulpal Deafferentation and Other Types of Nerve Injury Biologically Pulpal Degeneration or Removal Has the Potential to Cause Chronic Pain
    114. 114. Epidemiology/ Mechanisms ofRisk Factors of Acute and Chronic Pain Chronic Pain Imaging the Brain in Chronic Pain
    115. 115. NO BRAIN…………………NO PAINImaging the Brain inChronic Pain
    116. 116. Imaging the Brain inChronic Pain fMRI
    117. 117. Woollett and Maguire: Current Biology, 2011
    118. 118. Woollett and Maguire: Current Biology, 2011
    119. 119. Woollett and Maguire: Current Biology, 2011
    120. 120. Brain Imaging in the Media
    121. 121. Brain Imaging in the Media
    122. 122. Brain Imaging in the Media
    123. 123. Can Brain ImagingLet Us “See” Pain?
    124. 124. The PainMatrix
    125. 125. Measuring Chronic Pain isMore Challenging
    126. 126. Watching Chronic Pain in the BrainBaliki, MN et al., J Neurosci 2006
    127. 127. Changes in Brain Anatomy with Chronic PainApkarian AV, et al. J Neurosci 2004
    128. 128. Changes in Brain Anatomy with Chronic PainApkarian AV, et al. J Neurosci 2004
    129. 129. Changes in Brain Anatomy with Chronic PainApkarian AV, et al. J Neurosci 2004
    130. 130. What is theConsequence of Grey Matter Atrophy?
    131. 131. Functional Consequence of Cortical DegenerationApkarian VA et al., Pain 2004
    132. 132. Functional Consequence of Cortical DegenerationApkarian VA et al., Pain 2004
    133. 133. Functional Consequence of Cortical DegenerationApkarian VA et al., Pain 2004
    134. 134. DLPFC Amygdala S2 cortex insular cortex Brainstem ACCRodriguez-Raecke, et al., J. Neurosci, 2009
    135. 135. Every Type of Chronic Pain is DifferentApkarian AV, et al., Pain 2011
    136. 136. Every Type of Chronic Pain is DifferentApkarian AV, et al., Pain 2011
    137. 137. Limitations of Brain Imaging Studies
    138. 138. MultipleComparisons Problem
    139. 139. Multiple Small SampleComparisons Sizes Problem
    140. 140. Multiple Small SampleComparisons Sizes Problem Over Simplification of Brain Function
    141. 141. MultipleComparisons Problem Bennett C.M et. al., Human Brain Mapping Conference 2009
    142. 142. SmallSample Sizes
    143. 143. OverSimplification of Brain Function
    144. 144. OverSimplification of Brain Function
    145. 145. Brain Imaging: Conclusions1. Subjective Experience of Pain Can Be Objectively Measured Using Brain Imaging
    146. 146. Brain Imaging: Conclusions2. Acute Pain and Chronic Pain Activate Distinct Regions of the Brain
    147. 147. Brain Imaging: Conclusions3. Chronic Pain Causes Long Term Changes in Brain Structure That May Relate to Cognitive Changes
    148. 148. Epidemiology/ Mechanisms ofRisk Factors of Acute and Chronic Pain Chronic Pain Imaging the Brain in Chronic Pain
    149. 149. Chronic Pain is a DiseaseNot just a symptom anymore
    150. 150. Real knowledge is toknow the extent of one’signorance.Confucius
    151. 151. ★ Avoid damaging nerves
    152. 152. ★ Avoid damaging nerves★ Get patients out of pain asap
    153. 153. ★ Avoid damaging nerves★ Get patients out of pain asap★ Minimize intraoperative pain experience
    154. 154. ★ Avoid damaging nerves★ Get patients out of pain asap★ Minimize intraoperative pain experience★ Minimize post-operative pain ★ follow up ★ multi-modal analgesia
    155. 155. THANKYOU !
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