The Interface of Mechanics and Nociception in Joint Pathophysiology: Insights From the Facet and Temporomandibular Joints

Sperry, Megan M.; Ita, Meagan E.; Kartha, Sonia; Zhang, Sijia; Yu, Ya‐Hsin; Winkelstein, Beth A.

doi:10.1115/1.4035647

Cited by 24 publications

(25 citation statements)

References 173 publications

(294 reference statements)

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“…This study used the RGS to assess spontaneous pain in a rat model of TMJ pain and compared RGS between groups with different TMJ sensitivity profiles to evaluate its ability to differentiate pain states (Figs 3 and 4 ). Although facial grimace scales have been used to characterize visceral, inflammatory, and neuropathic pain in rodent models of skin and joint inflammation, cervical radiculopathy, peripheral neuropathy, bladder infection, and abdominal constriction 16 , 18 , 19 , 41 , this is the first report of facial grimace for TMJ pain and in the context of repeated joint over-loading, which is a major cause of joint degeneration and pain 42 – 45 . Since RGS is elevated over baseline during the TMJ loading period and one day after its cessation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Grading facial expression is a sensitive means to detect grimace differences in orofacial pain in a rat model

Sperry

Welch

et al. 2018

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Although pre-clinical models of pain are useful for defining relationships between biological mechanisms and pain, common methods testing peripheral sensitivity do not translate to the human pain experience. Facial grimace scales evaluate affective pain levels in rodent models by capturing and scoring spontaneous facial expression. But, the Rat Grimace Scale (RGS) has not assessed the common disorder of temporomandibular joint (TMJ) pain. A rat model of TMJ pain induced by jaw loading (1 hr/day for 7 days) was used to investigate the time course of RGS scores and compare them between different loading magnitudes with distinct peripheral sensitivity profiles (0N–no sensitivity, 2N–acute sensitivity, 3.5N–persistent sensitivity). In the 3.5N group, RGS is elevated over baseline during the loading period and one day after loading and is correlated with peripheral sensitivity (ρ = −0.48, p = 0.002). However, RGS is not elevated later when that group exhibits peripheral sensitivity and moderate TMJ condylar cartilage degeneration. Acutely, RGS is elevated in the 3.5N loading group over the other loading groups (p < 0.001). These findings suggest that RGS is an effective tool for detecting spontaneous TMJ pain and that spontaneous pain is detectable in rats that develop persistent TMJ sensitivity, but not in rats with acute resolving sensitivity.

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Section: Discussionmentioning

confidence: 99%

Grading facial expression is a sensitive means to detect grimace differences in orofacial pain in a rat model

Sperry

Welch

et al. 2018

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“…1). Since these key features are shared across different synovial joints with OA (Tonge et al 2014;Sperry, Ita, et al 2017), the broader literature provides mechanistic insights into joint degeneration and disability. OA is initiated by multiple factors, including injury, aging, abnormal joint mechanics, and atypical joint shape (Loeser et al 2012).…”

Section: Osteoarthritis Painmentioning

confidence: 99%

Experimental Methods to Inform Diagnostic Approaches for Painful TMJ Osteoarthritis

et al. 2019

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Temporomandibular joint (TMJ) osteoarthritis (OA) is a degenerative disease of the joint that can produce persistent orofacial pain as well as functional and structural changes to its bone, cartilage, and ligaments. Despite advances in the clinical utility and reliability of the Diagnostic Criteria for Temporomandibular Disorders, clinical tools inadequately predict which patients will develop chronic TMJ pain and degeneration, limiting clinical management. The challenges of managing and treating TMJ OA are due, in part, to a limited understanding of the mechanisms contributing to the development and maintenance of TMJ pain. OA is initiated by multiple factors, including injury, aging, abnormal joint mechanics, and atypical joint shape, which can produce microtrauma, remodeling of joint tissues, and synovial inflammation. TMJ microtrauma and remodeling can increase expression of cytokines, chemokines, and catabolic factors that damage synovial tissues and can activate free nerve endings in the joint. Although studies have separately investigated inflammationdriven orofacial pain, acute activity of the trigeminal nerve, or TMJ tissue degeneration and/or damage, the temporal mechanistic factors leading to chronic TMJ pain are undefined. Limited understanding of the interaction between degeneration, intra-articular chemical factors, and pain has further restricted the development of targeted, disease-modifying drugs to help patients avoid long-term pain and invasive procedures, like TMJ replacement. A range of animal models captures features of intra-articular inflammation, joint overloading, and tissue damage. Although those models traditionally measure peripheral sensitivity as a surrogate for pain, recent studies recognize the brain's role in integrating, modulating, and interpreting nociceptive inputs in the TMJ, particularly in light of psychosocial influences on TMJ pain. The articular and neural contributors to TMJ pain, imaging modalities with clinical potential to identify TMJ OA early, and future directions for clinical management of TMJ OA are reviewed in the context of evidence in the field.

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“…3 A number of systemic risk factors for OA have been described, including age, gender, ethnicity, hormones, genetics, obesity, and nutrition, as well as biomechanical factors, including prior injury, muscle weakness, joint deformity, and ligament laxity. 1,[4][5][6] Despite the growing awareness of these risk factors, the pathophysiology of OA is still unresolved. Emerging clinical and experimental research suggests that the nervous system may play an essential role in mediating the pathophysiology and symmetrical manifestation of OA.…”

Section: Introductionmentioning

confidence: 99%

“…Emerging clinical and experimental research suggests that the nervous system may play an essential role in mediating the pathophysiology and symmetrical manifestation of OA. 4,5,7,8 OA has been traditionally considered an asymmetrical disease; however, studies have shown a predilection over time in humans toward symmetrical involvement, especially in knees 9 and hands. 10 Research shows that experimentally induced unilateral knee OA in animals results in symmetrical spread of neurogenically mediated inflammation and articular degeneration to contralateral homologous joints.…”

Section: Introductionmentioning

confidence: 99%

Increased Substance P Immunoreactivity in Ipsilateral Knee Cartilage of Rats Exposed to Lumbar Spine Injury

et al. 2018

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Augmented expression of substance P (SP) in the cartilaginous tissue has been shown to promote degenerative changes in the cartilaginous matrix of distal contralateral articular joints via neurogenic inflammation post monoarthritis-induction contributing to the symmetrical spread of osteoarthritis (OA). However, no studies have explored whether similar changes are also present within neurosegmentally linked ipsilateral heterologous cartilage. Objective The present study aimed to investigate whether experimentally induced lumbar facet-joint OA lead to degenerative changes and enhanced SP expression within the ipsilateral neurosegmentally linked tibiofemoral cartilage. Methods Adult male Sprague-Dawley rats were assigned to left side L5-L6 facet mechanical compression injury (surgery) ( n = 6), L5-L6 facet exposure with no compression (sham) ( n = 5), or naïve (no surgery) ( n = 4) groups. The morphology of the tibiofemoral articular cartilage was assessed using a modified Mankin scoring system. Immunohistochemistry was used to examine the density of chondrocytes stained positive for SP (cells/cm2) in the ipsilateral tibiofemoral cartilage at 28 days postintervention. Results Tibiofemoral cartilage in the surgery group showed consistent loss of superficial zone chondrocytes, mild roughening of the articular surface and occasional chondrocyte clusters as well as a greater density of SP mainly in the superficial cartilage zone compared with sham and naïve groups, although they also had a basic SP-expression. Conclusion Our results support the hypothesis that neurogenic mechanisms may mediate the spread of SP to neurosegmentally linked heterologous joints affecting the distal cartilage homeostasis. These findings contribute additional insight into the potential role of neurogenic inflammation with implications in the pathophysiology of chronic inflammatory joint disease and OA.

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The Interface of Mechanics and Nociception in Joint Pathophysiology: Insights From the Facet and Temporomandibular Joints

Cited by 24 publications

References 173 publications

Grading facial expression is a sensitive means to detect grimace differences in orofacial pain in a rat model

Grading facial expression is a sensitive means to detect grimace differences in orofacial pain in a rat model

Experimental Methods to Inform Diagnostic Approaches for Painful TMJ Osteoarthritis

Increased Substance P Immunoreactivity in Ipsilateral Knee Cartilage of Rats Exposed to Lumbar Spine Injury

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