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Jennifer A Haythornthwaite - One of the best experts on this subject based on the ideXlab platform.
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exploring the role of negative cognitions in the relationship between ethnicity sleep and pain in women with Temporomandibular Joint Disorder
The Journal of Pain, 2018Co-Authors: Sheera F Lerman, Michael T Smith, C Campbell, L Buenaver, Mary Medak, Jane Phillips, Michelle Polley, Jennifer A HaythornthwaiteAbstract:Negative cognitions are central to the perpetuation of chronic pain and sleep disturbances. Patients with Temporomandibular Joint Disorder (TMJD), a chronic pain condition characterized by pain and limitation in the jaw area, have a high comorbidity of sleep disturbances that possibly exacerbate their condition. Ethnic group differences are documented in pain, sleep, and coping, yet the mechanisms driving these differences are still unclear, especially in clinical pain populations. We recruited 156 women (79% white, 21% African American) diagnosed with TMJD as part of a randomized, controlled trial evaluating the effectiveness of interventions targeting sleep and pain catastrophizing on pain in TMJD. Analysis of baseline data demonstrated that, relative to white participants, African Americans exhibited higher levels of clinical pain, insomnia severity, and pain catastrophizing, yet there was no ethnic group difference in negative sleep-related cognitions. Mediation models revealed pain catastrophizing, but not sleep-related cognitions or insomnia severity, to be a significant single mediator of the relationship between ethnicity and clinical pain. Only the helplessness component of catastrophizing together with insomnia severity sequentially mediated the ethnicity-pain relationship. These findings identify pain catastrophizing as a potentially important link between ethnicity and clinical pain and suggest that interventions targeting pain-related helplessness could improve both sleep and pain, especially for African American patients. Perspective:Pain-related helplessness and insomnia severity contribute to ethnic differences found in clinical pain among woman with TMJD. Findings can potentially inform interventions that target insomnia and catastrophizing to assist in reducing ethnic disparities in clinical pain.
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sleep continuity and architecture associations with pain inhibitory processes in patients with Temporomandibular Joint Disorder
European Journal of Pain, 2009Co-Authors: Robert R Edwards, Estherann Grace, Stephen Peterson, Brendan Klick, Jennifer A Haythornthwaite, Michael T SmithAbstract:Recent research suggests bi-directional interactions between the experience of pain and the process of sleep; pain interferes with the ability to obtain sleep, and disrupted sleep contributes to enhanced pain perception. Our group recently reported, in a controlled experimental study, that sleep fragmentation among healthy adults resulted in subsequent decrements in endogenous pain inhibition. The present report follows up that observation by extending this line of research to a sample of patients experiencing persistent pain. Patients with chronic Temporomandibular Joint Disorder (TMD) pain were studied using polysomnography and psychophysical evaluation of pain responses. We assessed whether individual differences in sleep continuity and/or architecture were related to diffuse noxious inhibitory controls (DNIC), a measure of central nervous system pain inhibition. Among 53 TMD patients, higher sleep efficiency and longer total sleep time were positively associated with better functioning of DNIC (r = 0.42–0.44, p < 0.01; ps < 0.05 for the multivariate analyses). These results suggest the possibility that disrupted sleep may serve as a risk factor for inadequate pain-inhibitory processing and hint that aggressive efforts to treat sleep disturbance early in the course of a pain condition might be beneficial in reducing the severity or impact of clinical pain.
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sleep Disorders and their association with laboratory pain sensitivity in Temporomandibular Joint Disorder
Sleep, 2009Co-Authors: Michael T Smith, Robert R Edwards, Stephen Peterson, Brendan Klick, L Buenaver, Emerson M Wickwire, Edward G Grace, Jennifer A HaythornthwaiteAbstract:Temporomandibular Joint Disorder (TMD) HAS BEEN DESCRIBED AS A PROTOTYPIC IDIOPATHIC PAIN SYNDROME CHARACTERIZED BY POORLY understood, episodic, masticatory muscle and/or Joint pain. TMD affects an estimated 12% of the population.1 As in other idiopathic pain Disorders such as fibromyalgia and irritable bowel syndrome, patients often present with overlapping signs and symptoms including psychological distress, neuroendocrine abnormalities, and chronic insomnia.2,3 Recent theoretical perspectives have proposed that these “central sensitivity syndromes” share a common central nervous system substrate characterized by heightened processing of noxious input, which contributes to overlapping daytime sequelae among these Disorders.4 Several cross-sectional studies have demonstrated that compared to controls, TMD patients exhibit enhanced responsivity to a variety of painful stimuli measured both at facial and extracranial anatomic sites.5–7 Pain sensitivity at “unaffected” (i.e., non-jaw) sites suggests the involvement of central pain processing mechanisms, beyond peripheral contributions. Recent longitudinal work has reported that enhanced laboratory pain sensitivity in pain free individuals is linked to genetic polymorphisms that predict the development of new onset TMD.8 This suggests that central processes associated with pain amplification may be critical to understanding the etiopathophysiology of TMD. Clinical factors that contribute to pain amplification in TMD, however, are poorly understood. Our group has focused on the possibility that sleep disturbance is one such factor that may directly contribute to central sensitization and pain amplification.9 We recently reported, for example, that sleep onset insomnia symptoms predict the development of chronic pain following serious burn injury.10 While it is often assumed that insomnia or sleep loss occurring in the context of chronic pain occurs secondarily to the sleep interrupting effects of pain, we and others have demonstrated that insomnias associated with chronic pain are often phenotypically similar to primary insomnia.11 Shared features include high levels of pre-sleep cognitive rumination and evidence of maladaptive coping strategies that may exist prior to the development of pain and/or independently contribute to insomnia symptoms. It is unknown, however, whether primary insomnia is associated with alterations in laboratory pain sensitivity when it occurs either as a sole condition or as part of a chronic pain Disorder such as TMD. Only a handful of investigations have systematically sought to evaluate the sleep quality of TMD patients. These studies have consistently found that the majority ( > 50%) of TMD patients report poor sleep quality, and that subjective ratings of poor sleep are associated with increased clinical pain severity and psychological distress.12–14 Fundamental descriptive data using polysomnography and standard research diagnostic interviews to quantify the range of sleep Disorders in TMD and determine their possible associations with laboratory measures of pain sensitivity are lacking. The extant literature has largely focused on possible relationships between sleep bruxism and TMD.15,16 Sleep bruxism, however, has not been found to be associated with either poor sleep quality or polysomnographic measures of sleep continuity or architecture disturbances.17–19 The objective of this study was to address two critical gaps in the literature: (1) characterize the spectrum of sleep Disorders in a well-described sample of myofascial TMD patients, using polysomnography and state-of-the art structured diagnostic interviews; and (2) evaluate possible associations between observed sleep Disorder indices and laboratory measures of pain threshold. We hypothesized that rates of primary insomnia would be substantive in TMD and that primary insomnia would be associated with reductions in pain threshold at both masseter and extracranial sites.
Michael T Smith - One of the best experts on this subject based on the ideXlab platform.
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exploring the role of negative cognitions in the relationship between ethnicity sleep and pain in women with Temporomandibular Joint Disorder
The Journal of Pain, 2018Co-Authors: Sheera F Lerman, Michael T Smith, C Campbell, L Buenaver, Mary Medak, Jane Phillips, Michelle Polley, Jennifer A HaythornthwaiteAbstract:Negative cognitions are central to the perpetuation of chronic pain and sleep disturbances. Patients with Temporomandibular Joint Disorder (TMJD), a chronic pain condition characterized by pain and limitation in the jaw area, have a high comorbidity of sleep disturbances that possibly exacerbate their condition. Ethnic group differences are documented in pain, sleep, and coping, yet the mechanisms driving these differences are still unclear, especially in clinical pain populations. We recruited 156 women (79% white, 21% African American) diagnosed with TMJD as part of a randomized, controlled trial evaluating the effectiveness of interventions targeting sleep and pain catastrophizing on pain in TMJD. Analysis of baseline data demonstrated that, relative to white participants, African Americans exhibited higher levels of clinical pain, insomnia severity, and pain catastrophizing, yet there was no ethnic group difference in negative sleep-related cognitions. Mediation models revealed pain catastrophizing, but not sleep-related cognitions or insomnia severity, to be a significant single mediator of the relationship between ethnicity and clinical pain. Only the helplessness component of catastrophizing together with insomnia severity sequentially mediated the ethnicity-pain relationship. These findings identify pain catastrophizing as a potentially important link between ethnicity and clinical pain and suggest that interventions targeting pain-related helplessness could improve both sleep and pain, especially for African American patients. Perspective:Pain-related helplessness and insomnia severity contribute to ethnic differences found in clinical pain among woman with TMJD. Findings can potentially inform interventions that target insomnia and catastrophizing to assist in reducing ethnic disparities in clinical pain.
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sleep continuity and architecture associations with pain inhibitory processes in patients with Temporomandibular Joint Disorder
European Journal of Pain, 2009Co-Authors: Robert R Edwards, Estherann Grace, Stephen Peterson, Brendan Klick, Jennifer A Haythornthwaite, Michael T SmithAbstract:Recent research suggests bi-directional interactions between the experience of pain and the process of sleep; pain interferes with the ability to obtain sleep, and disrupted sleep contributes to enhanced pain perception. Our group recently reported, in a controlled experimental study, that sleep fragmentation among healthy adults resulted in subsequent decrements in endogenous pain inhibition. The present report follows up that observation by extending this line of research to a sample of patients experiencing persistent pain. Patients with chronic Temporomandibular Joint Disorder (TMD) pain were studied using polysomnography and psychophysical evaluation of pain responses. We assessed whether individual differences in sleep continuity and/or architecture were related to diffuse noxious inhibitory controls (DNIC), a measure of central nervous system pain inhibition. Among 53 TMD patients, higher sleep efficiency and longer total sleep time were positively associated with better functioning of DNIC (r = 0.42–0.44, p < 0.01; ps < 0.05 for the multivariate analyses). These results suggest the possibility that disrupted sleep may serve as a risk factor for inadequate pain-inhibitory processing and hint that aggressive efforts to treat sleep disturbance early in the course of a pain condition might be beneficial in reducing the severity or impact of clinical pain.
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sleep Disorders and their association with laboratory pain sensitivity in Temporomandibular Joint Disorder
Sleep, 2009Co-Authors: Michael T Smith, Robert R Edwards, Stephen Peterson, Brendan Klick, L Buenaver, Emerson M Wickwire, Edward G Grace, Jennifer A HaythornthwaiteAbstract:Temporomandibular Joint Disorder (TMD) HAS BEEN DESCRIBED AS A PROTOTYPIC IDIOPATHIC PAIN SYNDROME CHARACTERIZED BY POORLY understood, episodic, masticatory muscle and/or Joint pain. TMD affects an estimated 12% of the population.1 As in other idiopathic pain Disorders such as fibromyalgia and irritable bowel syndrome, patients often present with overlapping signs and symptoms including psychological distress, neuroendocrine abnormalities, and chronic insomnia.2,3 Recent theoretical perspectives have proposed that these “central sensitivity syndromes” share a common central nervous system substrate characterized by heightened processing of noxious input, which contributes to overlapping daytime sequelae among these Disorders.4 Several cross-sectional studies have demonstrated that compared to controls, TMD patients exhibit enhanced responsivity to a variety of painful stimuli measured both at facial and extracranial anatomic sites.5–7 Pain sensitivity at “unaffected” (i.e., non-jaw) sites suggests the involvement of central pain processing mechanisms, beyond peripheral contributions. Recent longitudinal work has reported that enhanced laboratory pain sensitivity in pain free individuals is linked to genetic polymorphisms that predict the development of new onset TMD.8 This suggests that central processes associated with pain amplification may be critical to understanding the etiopathophysiology of TMD. Clinical factors that contribute to pain amplification in TMD, however, are poorly understood. Our group has focused on the possibility that sleep disturbance is one such factor that may directly contribute to central sensitization and pain amplification.9 We recently reported, for example, that sleep onset insomnia symptoms predict the development of chronic pain following serious burn injury.10 While it is often assumed that insomnia or sleep loss occurring in the context of chronic pain occurs secondarily to the sleep interrupting effects of pain, we and others have demonstrated that insomnias associated with chronic pain are often phenotypically similar to primary insomnia.11 Shared features include high levels of pre-sleep cognitive rumination and evidence of maladaptive coping strategies that may exist prior to the development of pain and/or independently contribute to insomnia symptoms. It is unknown, however, whether primary insomnia is associated with alterations in laboratory pain sensitivity when it occurs either as a sole condition or as part of a chronic pain Disorder such as TMD. Only a handful of investigations have systematically sought to evaluate the sleep quality of TMD patients. These studies have consistently found that the majority ( > 50%) of TMD patients report poor sleep quality, and that subjective ratings of poor sleep are associated with increased clinical pain severity and psychological distress.12–14 Fundamental descriptive data using polysomnography and standard research diagnostic interviews to quantify the range of sleep Disorders in TMD and determine their possible associations with laboratory measures of pain sensitivity are lacking. The extant literature has largely focused on possible relationships between sleep bruxism and TMD.15,16 Sleep bruxism, however, has not been found to be associated with either poor sleep quality or polysomnographic measures of sleep continuity or architecture disturbances.17–19 The objective of this study was to address two critical gaps in the literature: (1) characterize the spectrum of sleep Disorders in a well-described sample of myofascial TMD patients, using polysomnography and state-of-the art structured diagnostic interviews; and (2) evaluate possible associations between observed sleep Disorder indices and laboratory measures of pain threshold. We hypothesized that rates of primary insomnia would be substantive in TMD and that primary insomnia would be associated with reductions in pain threshold at both masseter and extracranial sites.
Yasunori Okada - One of the best experts on this subject based on the ideXlab platform.
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Aggrecanase analysis of synovial fluid of Temporomandibular Joint Disorders
Oral Diseases, 2005Co-Authors: Kan Yoshida, Shigeyuki Takatsuka, Eriko Hatada, Akira Tanaka, Hiroyuki Nakamura, Kiyomasa Nakagawa, Yasunori OkadaAbstract:Objectives: To determine whether or not aggrecanase in synovial fluid can be used as a biochemical marker in the diagnosis of Temporomandibular Joint Disorder (TMJD). Materials and methods: Forty-four samples of synovial fluid were obtained from 35 patients with internal derangement or osteoarthritis and 15 control samples from 10 asymptomatic volunteers. Aggrecanase in the synovial fluid was examined by immunoblotting. Result: The incidence of aggrecanase expression in TMJD group were significantly higher than that in the normal control group (P
Masato Kaku - One of the best experts on this subject based on the ideXlab platform.
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Correction of skeletal class II severe open bite with Temporomandibular Joint Disorder treated by miniscrew anchorage and molar extraction: a case report
Journal of Medical Case Reports, 2019Co-Authors: Masato Kaku, Taeko Yamamoto, Yuka Yashima, Jin Izumino, Haruka Kagawa, Kazutaka Ikeda, Kotaro TanimotoAbstract:Background Little information is available on the treatment of open bite with Temporomandibular Joint Disorder by intrusion of molars using miniscrews. Case presentation This case report describes a 42-year-old Japanese woman with a skeletal class II severe anterior open bite and Temporomandibular Joint Disorder. The pretreatment magnetic resonance imaging of both Temporomandibular Joints revealed osteoarthritis and anterior disc displacement without reduction in both Temporomandibular Joints. A stabilization splint was used before orthodontic treatment and bilateral upper and lower premolars were extracted. Miniscrews were inserted into the palatal region to intrude the maxillary molars and avoid loss of anchorage. The maxillary left first molar was also extracted to improve the molar relationship and the dental midline. Normal overjet and overbite with Angle class I molar relationship were achieved, and the upper and lower midlines coincided. Our patient’s teeth continued to be stable and her Temporomandibular Joint was asymptomatic after a retention period of 2 years. Conclusions Intrusion of molars by miniscrews is available for skeletal class II severe open bite.
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correction of skeletal class ii severe open bite with Temporomandibular Joint Disorder treated by miniscrew anchorage and molar extraction a case report
Journal of Medical Case Reports, 2019Co-Authors: Masato Kaku, Taeko Yamamoto, Yuka Yashima, Jin Izumino, Haruka Kagawa, Kazutaka Ikeda, Kotaro TanimotoAbstract:Little information is available on the treatment of open bite with Temporomandibular Joint Disorder by intrusion of molars using miniscrews. This case report describes a 42-year-old Japanese woman with a skeletal class II severe anterior open bite and Temporomandibular Joint Disorder. The pretreatment magnetic resonance imaging of both Temporomandibular Joints revealed osteoarthritis and anterior disc displacement without reduction in both Temporomandibular Joints. A stabilization splint was used before orthodontic treatment and bilateral upper and lower premolars were extracted. Miniscrews were inserted into the palatal region to intrude the maxillary molars and avoid loss of anchorage. The maxillary left first molar was also extracted to improve the molar relationship and the dental midline. Normal overjet and overbite with Angle class I molar relationship were achieved, and the upper and lower midlines coincided. Our patient’s teeth continued to be stable and her Temporomandibular Joint was asymptomatic after a retention period of 2 years. Intrusion of molars by miniscrews is available for skeletal class II severe open bite.
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treatment of a case of skeletal class ii malocclusion with Temporomandibular Joint Disorder using miniscrew anchorage
Cranio-the Journal of Craniomandibular Practice, 2011Co-Authors: Masato Kaku, Hiroyuki Koseki, Aki Kawazoe, Sara Abedini, Shunichi Kojima, Masahide Motokawa, Junji Ohtani, Tadashi Fujita, Toshitsugu Kawata, Kazuo TanneAbstract:AbstractAt the present time, there are no reports in the literature on the treatment of Temporomandibular Joint Disorder (TMD) by intrusion of molars using mini-screws. This case report describes the treatment for a female patient, aged 19 years seven months, with a TMD and an excessive lower anterior facial height. Overjet and overbite were +5.0 mm and +0.5 mm, respectively. The patient had a history of orthodontic treatment in which her first premolars were all extracted. During the first orthodontic treatment, a clockwise mandibular rotation was observed as a result of the increase of posterior dentoalveolar height. She had Temporomandibular Joint (TMJ) pain during mouth opening and complained of difficulty in eating due to masticatory dysfunction. The pretreatment Schuller views of both TMJ showed a posterior condyle position. In order to correct the overjet, molar relationship and the mandibular condyle position, a miniscrew was inserted into the palatal region of the upper first molar to intrude the...
Kotaro Tanimoto - One of the best experts on this subject based on the ideXlab platform.
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Correction of skeletal class II severe open bite with Temporomandibular Joint Disorder treated by miniscrew anchorage and molar extraction: a case report
Journal of Medical Case Reports, 2019Co-Authors: Masato Kaku, Taeko Yamamoto, Yuka Yashima, Jin Izumino, Haruka Kagawa, Kazutaka Ikeda, Kotaro TanimotoAbstract:Background Little information is available on the treatment of open bite with Temporomandibular Joint Disorder by intrusion of molars using miniscrews. Case presentation This case report describes a 42-year-old Japanese woman with a skeletal class II severe anterior open bite and Temporomandibular Joint Disorder. The pretreatment magnetic resonance imaging of both Temporomandibular Joints revealed osteoarthritis and anterior disc displacement without reduction in both Temporomandibular Joints. A stabilization splint was used before orthodontic treatment and bilateral upper and lower premolars were extracted. Miniscrews were inserted into the palatal region to intrude the maxillary molars and avoid loss of anchorage. The maxillary left first molar was also extracted to improve the molar relationship and the dental midline. Normal overjet and overbite with Angle class I molar relationship were achieved, and the upper and lower midlines coincided. Our patient’s teeth continued to be stable and her Temporomandibular Joint was asymptomatic after a retention period of 2 years. Conclusions Intrusion of molars by miniscrews is available for skeletal class II severe open bite.
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correction of skeletal class ii severe open bite with Temporomandibular Joint Disorder treated by miniscrew anchorage and molar extraction a case report
Journal of Medical Case Reports, 2019Co-Authors: Masato Kaku, Taeko Yamamoto, Yuka Yashima, Jin Izumino, Haruka Kagawa, Kazutaka Ikeda, Kotaro TanimotoAbstract:Little information is available on the treatment of open bite with Temporomandibular Joint Disorder by intrusion of molars using miniscrews. This case report describes a 42-year-old Japanese woman with a skeletal class II severe anterior open bite and Temporomandibular Joint Disorder. The pretreatment magnetic resonance imaging of both Temporomandibular Joints revealed osteoarthritis and anterior disc displacement without reduction in both Temporomandibular Joints. A stabilization splint was used before orthodontic treatment and bilateral upper and lower premolars were extracted. Miniscrews were inserted into the palatal region to intrude the maxillary molars and avoid loss of anchorage. The maxillary left first molar was also extracted to improve the molar relationship and the dental midline. Normal overjet and overbite with Angle class I molar relationship were achieved, and the upper and lower midlines coincided. Our patient’s teeth continued to be stable and her Temporomandibular Joint was asymptomatic after a retention period of 2 years. Intrusion of molars by miniscrews is available for skeletal class II severe open bite.
