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Author Response

Enrique Lluch Girbés, Rafael Torres-Cueco, Jo Nijs
DOI: 10.2522/ptj.2013.93.9.1278 Published 1 September 2013
Enrique Lluch Girbés
E. Lluch Girbés, PT, Department of Physical Therapy, University of Valencia, Valencia, Spain, and Pain in Motion Research Group, Departments of Human Physiology and Physiotherapy, Faculty of Physical Education & Rehabilitation, Vrije Universiteit Brussel, Brussels, Belgium.
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Rafael Torres-Cueco
R. Torres-Cueco, PT, Department of Physical Therapy, University of Valencia.
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Jo Nijs
J. Nijs, PT, PhD, Pain in Motion Research Group, Departments of Human Physiology and Physiotherapy, Faculty of Physical Education & Rehabilitation, Vrije Universiteit Brussel, and Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels, Belgium.
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We thank Gentzel for his careful reading of our article.1 His letter to the editor2 is enriching, as it facilitates the international debate regarding pain treatment and pain mechanisms in osteoarthritis (OA). Below we respond to each of the issues raised.

As correctly indicated by Gentzel, the aim of our article was to emphasize the role of the hyperexcitability of the central nervous system (or central sensitization [CS]) on pain in patients with OA rather than updating the readers with our current understanding of OA etiology and joint pathophysiology. Considering both peripheral and central aspects for a comprehensive approach to OA pain does not imply “ignorance” of the chronic inflammatory condition, as suggested by Genztel. As the scientific community is well informed about the pathological changes in joint structures in patients with OA, the central pain mechanisms require more attention. Our article reviewed and evaluated the existing scientific evidence addressing CS in OA pain in order to establish whether there were enough arguments to support the role of CS in chronic pain related to OA. To cite our own article, “[i]n addition to the pathological changes in articular structures, changes in central pain processing or central sensitization appear to be involved in osteoarthritis pain.”1(p842)

We do not doubt the role that tissue modification and destruction, typically observed in patients with OA, can have in explaining pain during the early stages of the disease. However, it is now well recognized that the central nervous system becomes hyperexcitable as pain is prolonged in time. This hyperexcitability often implies that patients' symptoms become less associated with what is happening in the peripheral tissues, including the joints, which may explain the common observation of discrepancies between radiological changes identified in patients with OA and the degree of pain and disability3,4 and the fact that some patients with OA show symptoms even after prosthetic substitution.5 Nevertheless, even in a person with chronic pain, peripheral nociceptive input from the damaged joint can modulate CS, as has been shown by modulation of central hyperexcitability in patients with OA in the form of amelioration of widespread analgesia6–8 and restoration of altered spinal reflexes9 after implementation of different treatment modalities, mainly addressing the affected joints (eg, by joint replacements). Thus, tissues can be important even in cases of chronic, localized OA pain.

Central sensitization is not present in all patients with chronic OA pain. Moreover, we acknowledge that CS is unlikely to be the etiological mechanism in a subgroup of the OA population (chronic inflammation is not etiologic to OA either), but there is increasing evidence suggesting that the presence of CS in this OA subgroup is of clinical importance.10–12 Probably the main goal of our article was to alert clinicians about this subgroup where CS can be the most dominant pain mechanism (ie, pain experience disproportionate to the nature and extent of injury, widespread pain distribution, generalized allodynia, and hyperalgesia). In those cases, we suggest a broader management approach, focusing treatment more on diminishing the hypersensitivity of the central nervous system than on addressing the joint dysfunctions.

We recognize that clinically categorizing patients with OA as having CS can be challenging, as no gold standard method of assessment exists. In fact, pain hypersensitivity in OA has been identified mostly within laboratory settings using equipment that is costly and not readily available to clinicians (ie, psychophysical testing with various stimuli,13 brain imaging studies14). That is why we propose to use a mechanism-based model mostly based on recognition of signs and symptoms for diagnosing CS,15 following recommendations of renowned authors in the field of pain.16 We do not think these models are “open to too much conjecture” or can lead to “entrenching of informational cascades,” as Gentzel suggests, although more evidence-based and validated clinical strategies are needed to more readily and systematically identify CS in patients with OA pain. Classification of pain in terms of mechanism should constitute a priority, considering that interventions at the peripheral tissue level (eg, surgery) are less successful when CS is suspected.4

The biomedical model falls short in explaining chronic musculoskeletal pain.17 Despite the fact that “[s]cience is busy identifying the causes of many chronic disease conditions such as OA,” unfortunately physical therapists continue dealing every day with people with chronic pain due to OA. So, in the same way Gentzel reflected on the relevant question of at what point of tissue degradation does OA become incurable, we suggest an alternative question: At what point in time does the transition from acute to chronic OA pain occur? In other words: when CS develops in patients with OA pain, will it still be possible to reverse the situation, or will this be less likely? There is evidence showing sensitization occurring in people with subacute musculoskeletal pain18 and evidence pointing to the ability of CS to modulate the transition from acute to chronic pain.18,19 In addition, CS has been shown to mediate the effects of interventions applied to peripheral tissues.4

As has been pointed out by Dieppe and Lohmander,19 OA joint damage may be associated with clinical problems, but the severity of joint disease is only weakly related to that of the clinical problem. They stated that clinicians dealing with OA are faced with a complex interaction between local events in the joint, pain sensitization, the cortical experience of pain, context (ie, psychosocial, economic, and other factors), and what people are doing in their everyday lives.19 Therefore, we should move on our thinking and broaden our view from only addressing joint dysfunctions to a more comprehensive approach addressing the brain, the central pain mechanisms, and the biopsychosocial model applied to chronic OA pain.17

We think Gentzel's criticism of our use of the term “might” or “may” throughout the text is not justified because our article was intended to be a proposal for chronic pain management in patients with OA, and not a statement of fact. He also alerts us that animal models of musculoskeletal pain do not closely mirror the human condition.20 Indeed, we know pain is a complex, multidimensional, personal, and subjective experience that only humans can express.21 However, curiously, little attention to psychosocial aspects of human OA pain was detected in Gentzel's reasoning, as addressing “basic malfunctions of normal physiology” was stated to be one his main end purposes.

In conclusion, it is key for physical therapists to acknowledge that an important subgroup of patients with OA develop hyperexcitability of the central nervous system and that CS plays a crucial role in the pain reported by these patients. Recent studies published in well-respected journals support our arguments.22–25

Footnotes

  • This letter was posted as a Rapid Response on July 10, 2013 at ptjournal.apta.org.

  • © 2013 American Physical Therapy Association

References

  1. ↵
    1. Lluch Girbés E,
    2. Nijs J,
    3. Torres-Cueco R,
    4. López Cubas C
    . Pain treatment for patients with osteoarthritis and central sensitization. Phys Ther. 2013;93:842–851.
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Gentzel JB
    . On “Pain treatment for patients with osteoarthritis and central sensitization.” Phys Ther. 2013;93:1276–1277.
    OpenUrlFREE Full Text
  3. ↵
    1. Arendt-Nielsen L,
    2. Nie H,
    3. Laursen MB,
    4. et al
    . Sensitization in patients with painful knee osteoarthritis. Pain. 2010;149:573–581.
    OpenUrlCrossRefPubMedWeb of Science
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    1. Bedson J,
    2. Croft PR
    . The discordance between clinical and radiographic knee osteoarthritis: a systematic search and summary of the literature. BMC Musculoskelet Disord. 2008;9:116
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    1. Lundblad H,
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    . Prediction of persistent pain after total knee replacement for osteoarthritis. J Bone Joint Surg Br. 2008;90:166–171.
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    1. Graven-Nielsen T,
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    3. Langford RM,
    4. et al
    . Normalization of widespread hyperesthesia and facilitated spatial summation of deep-tissue pain in knee osteoarthritis patients after knee replacement. Arthritis Rheum. 2012;64:2907–2916.
    OpenUrlCrossRefPubMedWeb of Science
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    1. Moss P,
    2. Sluka K,
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    . The initial effects of knee joint mobilization on osteoarthritic hyperalgesia. Man Ther. 2007;12:109–118.
    OpenUrlCrossRefPubMedWeb of Science
  8. ↵
    1. Vance CG,
    2. Rakel BA,
    3. Blodgett NP,
    4. et al
    . Effects of transcutaneous electrical nerve stimulation on pain, pain sensitivity, and function in people with knee osteoarthritis: a randomized controlled trial. Phys Ther. 2012;92:898–910.
    OpenUrlAbstract/FREE Full Text
  9. ↵
    1. Courtney CA,
    2. Witte PO,
    3. Chmell SJ,
    4. Hornby TG
    . Heightened flexor withdrawal response in individuals with knee osteoarthritis is modulated by joint compression and joint mobilization. J Pain. 2010;11:179–185.
    OpenUrlCrossRefPubMedWeb of Science
  10. ↵
    1. Murphy SL,
    2. Lyden AK,
    3. Phillips K,
    4. et al
    . Subgroups of older adults with osteoarthritis based upon differing comorbid symptom presentations and potential underlying pain mechanisms. Arthritis Res Ther. 2011;13:R135.
    OpenUrlCrossRefPubMed
  11. ↵
    1. Hochman JR,
    2. French MR,
    3. Bermingham SL,
    4. Hawker GA
    . The nerve of osteoarthritis pain. Arthritis Care Res (Hoboken). 2010;62:1019–1023.
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  12. ↵
    1. Hochman JR,
    2. Gagliese L,
    3. Davis AM,
    4. Hawker GA
    . Neuropathic symptoms in a community knee osteoarthritis cohort. Osteoarthritis Cartilage. 2011;19:647–654.
    OpenUrlCrossRefPubMedWeb of Science
  13. ↵
    1. Suokas AK,
    2. Walsh DA,
    3. McWilliams DF,
    4. et al
    . Quantitative sensory testing in painful osteoarthritis: a systematic review and meta-analysis. Osteoarthritis Cartilage. 2012;20:1075–1085.
    OpenUrlCrossRefPubMedWeb of Science
  14. ↵
    1. Jones AK,
    2. Huneke NT,
    3. Lloyd DM,
    4. et al
    . Role of functional brain imaging in understanding rheumatic pain. Curr Rheumatol Rep. 2012;14:557–567.
    OpenUrlCrossRefPubMed
  15. ↵
    1. Nijs J,
    2. Van Houdenhove B,
    3. Oostendorp RAB
    . Recognition of central sensitization in patients with musculoskeletal pain: application of pain neurophysiology in manual therapy practice. Man Ther. 2010;15:135–141.
    OpenUrlCrossRefPubMed
  16. ↵
    1. Woolf CJ
    . Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 suppl):S2–S15.
    OpenUrlCrossRefPubMedWeb of Science
  17. ↵
    1. Nijs J,
    2. Roussel N,
    3. Paul van Wilgen C,
    4. et al
    . Thinking beyond muscles and joints: therapists' and patients' attitudes and beliefs regarding chronic musculoskeletal pain are key to applying effective treatment. Man Ther. 2013;18:96–102.
    OpenUrlCrossRefPubMed
  18. ↵
    1. Sterling M,
    2. Jull G,
    3. Vicenzino B,
    4. Kenardy J
    . Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain. 2003;104:509–517.
    OpenUrlCrossRefPubMedWeb of Science
  19. ↵
    1. Dieppe PA,
    2. Lohmander LS
    . Pathogenesis and management of pain in osteoarthritis. Lancet. 2005;365:965–973.
    OpenUrlCrossRefPubMedWeb of Science
  20. ↵
    1. Arendt-Nielsen L,
    2. Curatolo M,
    3. Drewes A
    . Human experimental pain models in drug development: translational pain research. Curr Opin Investig Drugs. 2007;8:41–53.
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    1. Arendt-Nielsen L,
    2. Yarnitsky D
    . Experimental and clinical applications of quantitative sensory testing applied to skin, muscles and viscera. J Pain. 2009;10:556–572.
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  22. ↵
    1. Chiarotto A,
    2. Fernandez-de-Las-Peñas C,
    3. Castaldo M,
    4. Villafañe JH
    . Bilateral pressure pain hypersensitivity over the hand as potential sign of sensitization mechanisms in individuals with thumb carpometacarpal osteoarthritis. Pain Med. 2013 Jun 26 [Epub ahead of print]. doi: 10.1111/pme.12179.
  23. ↵
    1. Aranda-Villalobos P,
    2. Fernández-de-Las-Peñas C,
    3. Navarro-Espigares JL,
    4. et al
    . Normalization of widespread pressure pain hypersensitivity after total hip replacement in patients with hip osteoarthritis is associated with clinical and functional improvements. Arthritis Rheum. 2013;65:1262–1270.
    OpenUrlCrossRefPubMedWeb of Science
  24. ↵
    1. Skou ST,
    2. Graven-Nielsen T,
    3. Rasmussen S,
    4. et al
    . Widespread sensitization in patients with chronic pain after revision total knee arthroplasty. Pain. 2013 Apr 20 [Epub ahead of print]. doi: 10.1016/j.pain.2013.04.033.
  25. ↵
    1. Finan PH,
    2. Buenaver LF,
    3. Bounds SC,
    4. et al
    . Discordance between pain and radiographic severity in knee osteoarthritis: findings from quantitative sensory testing of central sensitization. Arthritis Rheum. 2013;65:363–372.
    OpenUrlCrossRefPubMedWeb of Science
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Vol 93 Issue 9 Table of Contents
Physical Therapy: 93 (9)

Issue highlights

  • Work Reintegration for Veterans With Mental Disorders
  • Dynamic Plantar Pressure During Loaded Gait
  • Sleep Deprivation and Dynamic Visual Acuity
  • Utilization of Rehabilitation Services by Patients With Amputation in the VA System
  • Effect of Two Different Exercise Regimens on Trunk Muscle Morphometry and Endurance
  • Undetected Pectoralis Major Tendon Rupture
  • Physical Therapist Point-of-Care Decisions in the Military Health Care System
  • Meaning of Occupation, Occupational Need, and Occupational Therapy in a Military Context
  • Returning Service Members to Duty Following Mild Traumatic Brain Injury
  • Role of US Military Physical Therapists in Recent Combat Campaigns
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Author Response
Enrique Lluch Girbés, Rafael Torres-Cueco, Jo Nijs
Physical Therapy Sep 2013, 93 (9) 1278-1280; DOI: 10.2522/ptj.2013.93.9.1278

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Author Response
Enrique Lluch Girbés, Rafael Torres-Cueco, Jo Nijs
Physical Therapy Sep 2013, 93 (9) 1278-1280; DOI: 10.2522/ptj.2013.93.9.1278
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