Spotlight on National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

Research Highlights

Four-Year Outcomes of Surgical Versus Non-surgical Treatment for Lower Back Pain

Initial results of the Spine Patients Outcomes Research Trial (SPORT), a large, multicenter clinical trial designed to compare the outcomes of surgery and nonoperative treatment for patients who suffer from back pain, revealed that patients in both treatment groups improved substantially over the first two years. 

After following the health of the patients for an average of four years after treatment, researchers have collected enough evidence to conclude that the patients who underwent surgery fared better than those who did not.  The surgical patients reported significantly greater improvement in pain, function, satisfaction with their symptoms and care, and self-rated progress than their counterparts who did not undergo surgery.  However, consistent with the earlier findings, the patients who received nonoperative treatments also improved with time. 

Reference:  Weinstein JN, et al.  Surgical Versus Nonoperative Treatment for Lumbar Disc Herniation: Four-Year Results for the Spine Patient Outcomes Research Trial (SPORT).  Spine, 2008 Dec 1, 33(25):2789-800. 

Pain May Contribute to Development, Expansion, and Worsening of Arthritis

Arthritis may develop from joint trauma, infection, or autoimmune diseases.  It is usually characterized by significant pain that often affects physical function and quality of life.  The pain pathway involves neurons that send sensory input to the brain, where it is processed, and may result in a motor neuron-muscle response to the pain stimulus (for example, pulling your finger from the fire).  This pain processing pathway is complex and includes sensitization of the primary sensory nerves that innervate the joint and transmit signals to the spine.  This stimulation from the sensory nerves can lead to neuroinflammation in the spine and central nervous system (CNS), including the activation of glia cells (supporting cells of the nervous system that participate in transmission of nerve signals) and the production of molecular mediators of inflammation, such as interleukin-1β (IL-1β).  Researchers conducted a study recently to determine whether the role of spinal IL-1β in the CNS processing of pain is also involved in the development of arthritis.  A feline virus was injected directly into the cisterna magna (an opening at the base of the brain which leads to the fluid layer surrounding the brain) of mice that develop an arthritis-like disease, to induce the production of IL-1β in the spinal area.  The mice were examined for behavioral and sensory changes, damage in the joint, and inflammation in the nervous system.  A series of experiments, using molecular or genetic approaches to block the effects of IL-1β, showed that arthritis, and subsequent pain, can be induced by the release of IL-1β centrally in the spinal cord.  These unique experiments suggest that there is bidirectional communication between the joints and the CNS that may contribute to the worsening of arthritis in the periphery by processes that originate in the nervous system.  This research extends and confirms the idea that the sensory nerves and CNS in the mouse can be involved in arthritis development, progression, and exacerbation.  Although the mechanisms and molecules remain unclear, these observations of peripheral and central nervous system crosstalk in peripheral tissue pathology is a paradigm-shifting concept, and provides a new area for therapeutic development of novel analgesics.

Reference:  Fiorentino PM, et al.  Spinal Interleukin-1β in a Mouse Model of Arthritis and Joint Pain.  Arthritis & Rheumatism, 2008 Oct., 58(10): 3100-3109. 

Highlights from NIAMS 2008 Scientific Retreat

Chronic Pain Session
Session Goals

In April 2008, the NIAMS leadership and scientific staff discussed how the NIAMS can more effectively study and contribute toward personalized treatment options for patients who suffer from chronic musculoskeletal pain.  The session was expected to position the NIAMS to capitalize on and contribute to what is known about how to prevent, identify, and manage chronic pain.  Leading experts from the extramural research community introduced the current status of pain research and contributed to the topical discussion.

Chronic pain can be an important aspect of many of the diseases that are part of the NIAMS' portfolio.  The contribution of chronic musculoskeletal pain to patient suffering and burden, particularly with acute exacerbations, is likely to increase substantially as the U.S. population ages.  The existence of chronic pain at a public health level suggests that clinically important aspects of pain are not adequately understood.  While there have been many developments in the understanding of pain and how it is treated, these have not been easily translated into interventions for chronic pain.

The chronic pain session explored certain emerging aspects of this patient-focused topic, described in the Venn diagram below.  Current thinking on the mechanisms of peripheral pain perception, transmission and central (brain) sensitization and how these processes might impact molecular and behavioral interventions was discussed.  Information that supports the commonly accepted notion of central nervous system plasticity, which suggests that chronic pain, at least in some patients, is no longer a symptom, but a disease itself offering potentially different targets for further study and treatment intervention was reviewed.  The role of genetic and environmental influences on chronic pain, along with efforts to obtain objective evidence of chronic pain (such as brain mapping and imaging techniques) was also presented.
In aggregate, this knowledge will help NIAMS identify gaps and opportunities toward achieving its mission of understanding the causes, treatment and prevention needs of chronic pain in both adults and children.  This session also discussed ongoing efforts by the NIH Pain Consortium to develop NIH Roadmap initiatives on biomarkers and risk factors for chronic pain.  The recognition that pain and itch are linked by common mechanisms was discussed throughout the session, as appropriate.  This link offers even more reason for the NIAMS to focus on new thinking and approaches on how to treat, cure, and even prevent these all too common problems that substantially impact patient function and quality of life.

• What aspects of pain research are appropriate for NIAMS to support? Which are of particular interest to the Institute? What elements are beyond the scope of its mission?
• Which diseases or conditions within the NIAMS mission can serve as models for studies of chronic pain prevention, diagnosis, and management of chronic pain?
• How can the NIAMS incorporate into existing efforts the latest knowledge about
• Pain plasticity?
• The genetic and environmental factors influencing chronic pain?
• The behavioral and psychosocial aspects of chronic pain?
• What other programs could facilitate the translation of biological information about chronic pain into diagnostic and therapeutic applications?
• Is there a place for chronic pain research in tomorrow's discussion about ancillary studies to large clinical projects?
• How can NIAMS-supported investigators participate in trans-NIH efforts, such as the Clinical and Translational Science Awards or the Pain Consortium's potential Roadmap initiatives?
• What specific steps can the NIAMS take to advance the investigation of chronic pain in skin, rheumatic, and musculoskeletal diseases?