Targeting the neurological amplifier that makes joint pain so severe — not just the joint itself
Ketamine for arthritis and joint pain in Baltimore costs $1,499.99 per session ($1,125 for Vitality Circle members — a $374.99 saving) and is anesthesiologist-led care, under the medical direction of Dr. Brijen Joshi MD, a board-certified Johns Hopkins anesthesiologist. This off-label intravenous infusion is evaluated for osteoarthritis (OA) and inflammatory arthritis (rheumatoid, psoriatic, ankylosing spondylitis). It works through two mechanisms: for OA, NMDA receptor blockade resets central sensitization — the neurological amplifier that makes joint pain far more severe than the structural damage alone predicts; for inflammatory arthritis, ketamine additionally reduces pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). Each session is a private, monitored infusion — not a nurse-only or spa drip. Ketamine is not disease-modifying — DMARDs, biologics, and rheumatology care continue alongside evaluation.
Mon–Fri: 1PM–8PM · Sat: 10AM–2PM
513 Bayview Blvd, Canton Baltimore MD 21224
(443) 563-1059
Answer a few quick questions — our clinical team reaches out within 1 business day to discuss whether ketamine therapy may be right for you.
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Arthritis is not a single disease — it is a broad category covering degenerative and inflammatory joint conditions with distinct pathologies. The clinical rationale for ketamine differs between these two categories, though both ultimately involve NMDA receptor dysregulation in the chronic pain phase.
OA involves gradual degeneration of articular cartilage — producing bone-on-bone contact, joint space narrowing, osteophyte formation, and chronic pain. The knees, hips, hands, and spine are most commonly affected. OA pain is initially driven by peripheral joint changes, but in the chronic phase, NMDA-mediated central sensitization amplifies pain signals far beyond what the structural damage predicts. Many OA patients' pain intensity does not correlate with the severity of radiographic findings — a hallmark of central sensitization.
Inflammatory arthritis conditions involve autoimmune-driven joint inflammation through pro-inflammatory cytokines — TNF-α, IL-6, IL-1β — that attack synovial tissue, cause joint erosion, and produce systemic inflammation. DMARDs and biologics suppress the autoimmune process but do not always fully control pain — particularly in patients who develop central sensitization in the chronic phase.
One of the most clinically important and least explained phenomena in arthritis pain is the mismatch between structural findings and pain severity. This is not exaggeration — it is the neurological signature of central sensitization.
is the range, across population studies, of people with radiographic knee OA who actually report knee pain — in many studies only about half — while many with severe pain have mild X-ray findings. The pain–imaging disconnect is a documented clinical phenomenon in OA. (Bedson & Croft, 2008; BMC Musculoskeletal Disorders)
The explanation is central sensitization — NMDA receptor hyperactivity in the spinal cord and brain that amplifies joint pain signals far beyond the peripheral structural damage. Once central sensitization is established, the nervous system generates and amplifies pain largely independently of what is happening in the joint itself.
Gwilym et al. (2009, Arthritis & Rheumatism) combined quantitative sensory testing with functional MRI in hip OA patients with referred pain — finding increased activity in the brainstem periaqueductal gray, a central pain-modulating hub, consistent with central sensitization that had become self-sustaining beyond the joint itself. Soni et al. (2019, Arthritis & Rheumatology) later showed the same brainstem signature in a subset of knee OA patients, and those patients did worse after joint replacement. This is the mechanism ketamine targets: not the joint, but the neurological amplification system that is making the joint pain so severe.
Ketamine's relevance to arthritis pain operates through two distinct pathways. For OA, the NMDA mechanism dominates. For inflammatory arthritis, both pathways contribute.
References: Loix S, De Kock M, Henin P (2011). The anti-inflammatory effects of ketamine: state of the art. Acta Anaesthesiol Belg 62(1):47-58. PubMed · Sakai T et al. (2000). Ketamine suppresses endotoxin-induced NF-κB expression. Can J Anaesth 47(10):1019-24. PubMed · Sun J et al. (2004). Ketamine suppresses endotoxin-induced NF-κB activation and cytokines production in the intestine. Acta Anaesthesiol Scand 48(3):317-21. PubMed
The following limitations must be understood before evaluation is pursued.
Ketamine is not a disease-modifying treatment. It does not slow or reverse the structural progression of osteoarthritis or the autoimmune process in rheumatoid, psoriatic, or ankylosing spondylitis. It is evaluated at Vita Nova for patients whose arthritis pain has not been adequately controlled by conventional approaches — addressing the neurological pain amplification dimension while disease-directed treatment continues.
The evidence base for ketamine in arthritis pain draws primarily from the central sensitization and chronic pain literature, supported by neuroimaging studies documenting central mechanisms in OA and anti-inflammatory mechanism research for inflammatory arthritis.
Quantitative sensory testing plus functional MRI in OA patients with referred pain and skin hypersensitivity — documenting increased activity in the brainstem periaqueductal gray, a central pain-modulating hub, that was not explained by the joint itself. This was among the first direct evidence that central sensitization is a measurable feature of chronic OA pain, and the authors named the central nervous system as a treatment target for what is largely a peripheral disease. The findings support NMDA-targeted therapy for OA patients whose pain exceeds their radiographic findings.
Systematic review of ketamine's anti-inflammatory effects documenting subanesthetic ketamine's reduction of TNF-α, IL-6, and IL-1β production — the core pro-inflammatory cytokines in rheumatoid and inflammatory arthritis. Provides the mechanistic basis for the second relevant pathway in inflammatory arthritis beyond NMDA central sensitization.
Longitudinal study of 865 RA patients documenting that clinically significant pain continued in a substantial subgroup of patients who met DAS28 remission criteria at both baseline and one year — pain that persisted even though measured disease activity was controlled. Together with the same group's work on central pain mechanisms in RA, it supports the clinical rationale for NMDA-targeted treatment in RA patients whose pain persists despite adequate disease-modifying therapy.
The foundational paper establishing NMDA receptors as the central mechanism of central sensitization — the same mechanism driving disproportionate pain in OA and the chronic pain component of inflammatory arthritis. The mechanistic foundation for all central sensitization-targeted therapies, including ketamine, in arthritis pain management.
| Service | Non-Member | Vitality Circle Member | Saving |
|---|---|---|---|
| Ketamine — Chronic Pain / session Off-Label | $1,499.99 | $1,125 | $374.99/session |
| Vitality Circle Membership / month | — | $99.99/month | Includes pain & MH discounts |
Co-occurring low mood alongside arthritis pain? Depression and chronic pain share the same NMDA-glutamate circuitry — and impaired mood weakens descending pain inhibition, the brain's natural pain brake. Addressing both through ketamine's mechanism may improve pain and mood together, and your provider evaluates both dimensions in one plan. See our co-occurring depression & chronic pain page.
Self-pay, with a superbill. Vita Nova is self-pay for ketamine. Each $1,499.99 session is a private, continuously monitored infusion under the medical direction of Dr. Brijen L. Joshi MD, a board-certified Johns Hopkins anesthesiologist — physician-led care, not a nurse-only or spa drip. Vitality Circle membership ($99.99/month) lowers each session to $1,125; the $374.99 saved covers the membership on a single visit, and members also receive 25% off premium IVs (NAD+, high-dose Vitamin C, Iron) plus a free monthly wellness perk. We provide an itemized superbill you can file with your insurance. HSA/FSA accepted; Community Heroes discounts available. Number of sessions determined individually at evaluation. Pricing August 2026 — subject to change. Full pricing guide →
Several wellness services at Vita Nova address physiological factors that amplify arthritis pain. Always coordinate with your rheumatologist before beginning supplemental therapy.
Magnesium naturally modulates NMDA receptor sensitivity — directly relevant to ketamine's central sensitization mechanism. Magnesium deficiency increases NMDA excitability, worsening pain amplification in both OA and inflammatory arthritis. Chronic inflammation depletes magnesium through urinary losses.
High-dose IV Vitamin C reduces oxidative stress and pro-inflammatory cytokine load — particularly relevant for inflammatory arthritis where elevated TNF-α and IL-6 drive both joint damage and pain sensitization. Also a cofactor in collagen synthesis relevant to cartilage and connective tissue health in OA.
NAD+ supports mitochondrial energy in both joint tissue and pain-processing neural circuits. Mitochondrial dysfunction is increasingly recognized as a contributing factor in OA cartilage metabolism and in the fatigue common in inflammatory arthritis.
Vitamin D3 deficiency is extremely common in arthritis patients — particularly those with limited mobility. Low D3 is associated with increased inflammatory activity in RA, worsened OA pain severity, and increased central sensitization. IM D3 achieves therapeutic blood levels rapidly and reliably.
Anemia of chronic disease is common in rheumatoid and inflammatory arthritis — driven by the same inflammatory cytokines (IL-6) that fuel joint pain. The resulting fatigue lowers pain tolerance and amplifies pain perception. IV iron corrects deficiency directly when oral iron is poorly tolerated or blocked by inflammation.
Clinical note: These wellness services are not treatments for arthritis and do not replace DMARDs, biologics, or rheumatology care. Always discuss supplemental therapy with your rheumatologist and prescribing physician — particularly if you are on immunosuppressive medications.
Veterans, first responders, and healthcare workers carry elevated rates of early-onset OA and inflammatory arthritis from the physical demands and occupational injuries of service.
Common questions from patients with osteoarthritis and inflammatory arthritis evaluating ketamine therapy in Baltimore.
Rheumatology care continues unchanged. No commitment required.
Book Consultation → View Self-Pay PricingWhen conventional arthritis treatments haven't controlled your pain, ketamine's NMDA mechanism targets the neurological amplifier that makes joint pain so severe. Rheumatology care continues unchanged. Off-label, self-pay with an itemized superbill you can file with your insurance. Community Heroes discounts available.
📍 513 Bayview Blvd · Canton, Baltimore MD 21224 · 🅿️ Free Parking
Mon–Fri: 1PM–8PM · Sat: 10AM–2PM · (443) 563-1059
A few blocks from Johns Hopkins Bayview Medical Center · Serving Canton, Highlandtown, Greektown, Brewers Hill, Fells Point & Dundalk
Canonical URL: https://vitanovawellnessclinic.com/ketamine-arthritis-baltimore/ · Last reviewed August 26, 2026
Medically reviewed by Dr. Brijen L. Joshi MD — Assistant Professor of Anesthesiology & Critical Care Medicine, Johns Hopkins University School of Medicine · Chief of Thoracic Anesthesia, Johns Hopkins Hospital · Medical Director, Vita Nova Ketamine & Wellness Clinic. · View full credentials →
Baltimore's physician-led clinic for Ketamine, IV vitamin infusions, Iron IV, and NAD+ therapy — serving our community with integrity and care.

Providing compliant, physician-led ketamine & IV therapy care — one of the few clinics certified in Maryland.
See Our Certification →Founded & directed by Dr. Brijen L. Joshi MD, Johns Hopkins School of Medicine faculty.
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