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Arthritis and pain. Future targets to control osteoarthritis pain
1AstraZeneca R&D Montreal, Frederick Banting St, Montreal H4S 1Z9, Canada. Andy.Dray@astrazeneca.com
Abstract:
Clinical presentation of osteoarthritis (OA) is dominated by pain during joint use and at rest. OA pain is caused by aberrant functioning of a pathologically altered nervous system with key mechanistic drivers from peripheral nerves and central pain pathways. This review focuses on symptomatic pain therapy exemplified by molecular targets that alter sensitization and hyperexcitability of the nervous system, for example, opioids and cannabinoids. We highlight opportunities for targeting inflammatory mediators and their key receptors (for example, prostanoids, kinins, cytokines and chemokines), ion channels (for example, NaV1.8, NaV1.7 and CaV2.2) and neurotrophins (for example, nerve growth factor), noting evidence that relates to their participation in OA etiology and treatment. Future neurological treatments of pain appear optimistic but will require the systematic evaluation of emerging opportunities.
Insights
Osteoarthritis (OA) pain stems from nervous system dysfunction. This review explores novel molecular targets for symptomatic pain therapy, offering hope for future treatments.
Area of Science:
- Neuroscience
- Pharmacology
- Rheumatology
Background:
- Osteoarthritis (OA) clinical presentation is characterized by joint pain during activity and at rest.
- OA pain originates from aberrant functioning of the peripheral and central nervous systems.
- Understanding the nervous system's role is crucial for developing effective OA pain therapies.
Purpose of the Study:
- To review symptomatic pain therapy for osteoarthritis.
- To highlight molecular targets that modulate nervous system sensitization and hyperexcitability.
- To discuss emerging opportunities for neurological treatments of OA pain.
Main Methods:
- Focused review of scientific literature on OA pain mechanisms and therapeutic targets.
- Examination of molecular targets including opioids, cannabinoids, inflammatory mediators, ion channels, and neurotrophins.
- Analysis of evidence linking these targets to OA etiology and treatment outcomes.
Main Results:
- Symptomatic OA pain therapy can be achieved by targeting molecular mechanisms altering nervous system sensitization.
- Key targets include opioids, cannabinoids, inflammatory mediators (prostanoids, kinins, cytokines, chemokines), ion channels (NaV1.8, NaV1.7, CaV2.2), and neurotrophins (nerve growth factor).
- Evidence supports the involvement of these targets in OA pathogenesis and their potential for therapeutic intervention.
Conclusions:
- Neurological approaches to OA pain management hold significant promise.
- Targeting molecular pathways involved in nerve sensitization and hyperexcitability offers a viable strategy for symptomatic pain relief.
- Systematic evaluation of emerging neurological treatment opportunities is essential for advancing OA pain therapy.
