Carolina Joint and Arthritis

01/14/2026

The swimming coach who led the 2016 USA Women’s Olympic Team to more than 30 medals has joined the push for an Olympic-class swimming facility in the Wilmington area. David Marsh, who has coached more than 60 Olympians from over a dozen different countries and led Auburn University’s swim progra...

11/12/2025

President Trump announced on September 30, 2025, the creation of TrumpRx, a government-backed direct-to-consumer website designed to allow Americans to purchase prescription drugs at significantly discounted prices, aiming to address high U.S. drug costs. This initiative is part of a broader strategy to enforce "most-favored-nation" (MFN) pricing, ensuring U.S. prices match the lowest rates paid by other developed nations, and to bypass middlemen like pharmacy benefit managers (PBMs) that inflate costs.
Key Details of TrumpRx and Related Efforts

How It Works: TrumpRx functions as an online platform where patients can buy medications directly, with prices negotiated to undercut current market rates. It's tied to deals with pharmaceutical companies, starting with Pfizer, to reduce costs on a wide range of drugs. For example, it promotes transparency and eliminates "secret kickbacks" to PBMs, passing savings directly to consumers.
Recent Deals and Impact:
Pfizer Agreement (Sept 30, 2025): Lowers prices on many products; Pfizer gets a tariff grace period in exchange.
Eli Lilly & Novo Nordisk (Nov 2025): Slashes GLP-1 drugs (e.g., Ozempic, Wegovy, Mounjaro, Zepbound) for Medicare/Medicaid to $245/month, with copays as low as $50 for beneficiaries—down from $1,300+. This expands access for diabetes, obesity, and heart disease treatments.
Five Total Deals by Nov 6, 2025: Covering high-expenditure drugs, providing "substantial price relief" for millions.
Fertility Drugs: Recent MFN application offers massive discounts by cutting PBM involvement.

Broader Context: U.S. drug prices are ~3x higher than in peer nations due to foreign discounts subsidized by American buyers. Trump's May 2025 executive order mandates MFN pricing across Medicare, Medicaid, and private insurance, including weight-loss drugs. It includes tariffs on imports unless manufacturers comply.

Potential Limitations

Not a Full Elimination: While aiming for deep cuts (Trump has claimed up to 500% reductions in some rhetoric), it won't make all drugs free—focus is on alignment with international lows (e.g., 50-80% savings on select meds). Critics note it may not overhaul supply chain issues fully.
Reversals: Trump recently ended some Biden-era pilots for generic copays and gene therapy affordability, potentially shifting priorities away from certain cost controls.
Implementation: Rollout is ongoing; full effects depend on manufacturer compliance and congressional support. Past efforts (2018-2020) saw modest wins like price freezes but faced legal hurdles.

This builds on Trump's first-term actions (e.g., gag clause bans, rebate rule) but escalates with direct negotiation and TrumpRx as a consumer-facing tool. For updates, check whitehouse.gov or HHS announcements.

President Donald J. Trump and Vice President JD Vance are committed to lowering costs for all Americans, securing our borders, unleashing American energy dominance, restoring peace through strength, and making all Americans safe and secure once again.

11/08/2025

Fun Facts. Unfortunately most things that you can't understand without an explanation, you can't understand with one. What's missing from this?

Scientific Explanation: The Rate-Limiting Step in Osteoarthritis is Subchondral Bone Stiffening
The rate-limiting step in the progression of osteoarthritis (OA) — particularly in load-bearing joints — is the initial stiffening of subchondral bone, which precedes and drives cartilage degeneration. This concept challenges the traditional view that cartilage loss is the primary event. Instead, altered subchondral bone mechanics initiate a biomechanical vicious cycle that amplifies joint damage.
Molecular & Biomechanical Sequence Leading to Stiffening

Early Mechanical Overload
Repetitive or excessive joint loading (e.g., obesity, malalignment, trauma) induces microdamage in subchondral trabeculae. This triggers mechanosensitive signaling in osteocytes via integrins, connexin-43 hemichannels, and purinergic receptors (P2X7, P2Y), releasing ATP and prostaglandins.
TGF-β1 Hyperactivation
Microdamage upregulates transforming growth factor-β1 (TGF-β1) in subchondral bone marrow mesenchymal stem cells (MSCs) and osteocytes. TGF-β1 induces osteoblast hyperactivity and angiogenesis via VEGF, leading to uncoupled bone remodeling.
RANKL/OPG Imbalance → Transient Resorption
Early OA shows increased RANKL expression, promoting osteoclastogenesis and bone resorption. This increases porosity and temporarily reduces tissue stiffness.
Shift to Net Bone Formation (Sclerosis)
As disease progresses, osteoprotegerin (OPG) expression rises (up to 5-fold in OA osteocytes), inhibiting osteoclasts. This shifts remodeling toward net bone formation. New bone is hypomineralized (low hydroxyapatite density) but deposited in thicker, denser trabeculae → increased structural stiffness.
Young’s Modulus Paradox
Tissue-level Young’s modulus (intrinsic material stiffness) decreases due to hypomineralization.
Apparent (structural) stiffnessincreases due to trabecular thickening and reduced porosity.
→ The subchondral plate becomes rigid and non-compliant.

Rate-Limiting Biomechanical Effect
A stiffer subchondral plate reduces shock absorption and increases peak stresses on overlying cartilage by up to 3–5 fold during gait. This exceeds the cartilage’s adaptive capacity, triggering:
Chondrocyte apoptosis
MMP-13, ADAMTS-5 upregulation
Collagen II and aggrecan degradation
Cartilage thinning and fissuring

Thus, subchondral stiffening is rate-limiting: it is the earliest irreversible biomechanical alteration that locks the joint into a degenerative cascade. Once cartilage begins to fail, inflammatory crosstalk (IL-1β, TNF-α from synovium) amplifies bone remodeling, but the initial trigger and sustaining force is subchondral rigidity.

2. Simple Explanation (For Posters or Lay Audience)

Think of your joint like a car suspension:

Cartilage = shock absorber (soft, squishy)
Subchondral bone = metal spring underneath

In a healthy joint, the spring is flexible enough to absorb bumps.
In OA, the spring gets over-reinforced with thick, brittle metal — it becomes too stiff.
Now every bump in the road (walking, running) slams directly into the shock absorber, wearing it out fast.
The stiff spring doesn’t break first — but it CAUSES the shock to fail.
That’s why stiffening of the bone under the cartilage is the “rate-limiting step” — it starts the whole breakdown.

3. Joint-Specific Application: Knee, Hip, and Shoulder

JointLoading PatternSubchondral Stiffening MechanismClinical & Imaging CorrelationKneeHigh compressive load (3–6× body weight during gait); varus/valgus malalignmentMedial tibial plateau shows earliest sclerosis due to focal overload. TGF-β1 clusters nestin+ MSCs → trabecular thickening + plate densification. Reduced compliance → medial cartilage collapse.MRI: T2* ↓ (mineral ↑), μCT: BV/TV ↑, Tb.Th ↑
X-ray: Joint space narrowing (medial > lateral)HipBall-and-socket; shear + compression; acetabular rim overloadSuperior acetabulum and femoral head show focal stiffening. Cam/pincer impingement → microinstability → TGF-β1 surge → subchondral cyst → reactive sclerosis. Stiff focal zone → cartilage delamination.MRI: Bone marrow lesions (BMLs) → sclerosis on follow-up

CT: Subchondral plate thickening >1.5 mmShoulder (Glenohumeral)Low load but high range; instability (rotator cuff tear) → eccentric loadingGlenoid subchondral bone stiffens in response to posterosuperior overload (e.g., in cuff tear arthropathy). Wnt/β-catenin activation → osteophyte + sclerosis at glenoid rim. Stiffness alters humeral head translation → cartilage wear in concentric pattern.MRI: Glenoid version changes, BMLs → sclerosis
X-ray: “Cuff tear arthropathy” with acetabularization
Key Universal Principle:

Any joint that experiences repetitive focal overload → TGF-β1-driven subchondral remodeling → structural stiffening → loss of cartilage compliance → OA progression.

Even in non-weight-bearing joints (e.g., hand DIP/PIP), repetitive microtrauma (typing, gripping) induces the same pathway: microdamage → TGF-β1 → sclerosis → cartilage loss. It's the exact same mechanism in every joint and it CAN be reversed at least to some degree in most joint. Find out early.

10/29/2025

We get asked a LOT about why we use Medial Unloader Bracing with the Össur Rebound Cartilage for Unicompartmental Varus Gonarthrosis. 'varus gonarthrosis means you have arthritis because you're bow-legged from a musculoskeletal standpoint. We also get asked about orthotics. Let's GO!

Core problem: Varus alignment shifts the ground reaction force (GRF) vector medially, so >70% of total knee load compresses the medial compartment during gait (peak forces 3–4× body weight). This overloads the medial tibial plateau, initiating the rate-limiting step in OA: subchondral bone stiffening (Young’s modulus ↑ from 1–2 GPa to 5–10 GPa). Stiffer bone fails to dampen impact, driving microfractures → sclerosis → elevated intraosseous pressure (40–60 mmHg) → cartilage shear → ECM breakdown via MMP-13/ADAMTS-5 → sterile inflammation (DAMPs → TLR/NF-κB → IL-1β/TNF-α).

Mechanism of the Össur® Rebound Cartilage unloader The Rebound Cartilage is a three-point leverage brace that laterally distracts the knee: (this is the best and most expensive brace your insurance will pay for)

1. Condylar pad + hinge system applies a valgus moment (counterforce) at the distal femur and proximal tibia.
2. Dynamic unloading strap tightens in extension → mid-stance, reducing medial compartment pressure by 10–30% (confirmed via in-brace pressure mapping and gait lab studies).
3. Redistributes load: Shifts GRF vector laterally, dropping medial contact stress from >5 MPa to ~2–3 MPa (within cartilage tolerance).
Direct effects on pathophysiology
• ↓ Subchondral stress → halts microfracture → prevents sclerosis progression.
• ↓ Intraosseous pressure → relieves bone marrow edema (seen on MRI wetmap resolution). combined with bone marrow concentrate this causes the subchondral bone to remodel and regain it's 'elasticity' and reverses the degenerative changes seen otherwise.
• ↓ Cartilage shear → reduces MMP/ADAMTS activity → slows GAG loss. (Biochemical factors) DM us for more information.
• ↓ Synovial inflammation → less DAMP release → reduced IL-1β/TNF-α → less pain.
Clinical evidence
• Randomized trials (Briggs et al., 2019): 30% reduction in KOOS pain at 6 months vs. neutral brace. 90% when combined with BMC Nanoplasty
• Gait analysis: Medial compartment unloading = 0.5–1.0 kN during stance (equivalent to losing 50–100 kg of load).
• Long-term: Delays need for high tibial osteotomy (HTO) or TKA by 3–7 years in 60% of patients.

Why Lateral Heel Wedge Orthotics Work for Medial Compartment OA

Principle: A 5–7° lateral heel wedge (placed under the lateral border of the foot) tilts the calcaneus into valgus, altering the tibial alignment and GRF vector.
Biomechanical chain
1. Calcaneal valgus → talar dorsiflexion → tibial external rotation + valgus tilt.
2. GRF vector shifts laterally by 2–4 mm at the knee (measured via pressure plate studies).
3. Reduces external knee adduction moment (EKAM) by 5–15% (peak EKAM ↓ from 4.5% to 3.8% BW·Ht).
o EKAM is the primary driver of medial compartment load.
Effects on subchondral bone & cartilage
• ↓ Medial compressive impulse → less subchondral microdamage → preserves bone elasticity.
• ↓ EKAM = ↓ medial contact stress (finite element models: ~20% load transfer to lateral compartment).
• ↓ Pain via reduced bone edema pressure and mechanoreceptor firing.
Evidence
• Meta-analysis (Reeves & Bowling, 2011): Lateral wedges reduce EKAM by 6–10% and improve WOMAC pain by 15–20% at 12 weeks.
• Best responders: Early OA (KL 1–2) + varus

10/23/2025

What's on your mind? Just ask your favorite AI App. Here's what you might be wondering and will definitely find interesting! Always ask, "Why?"

Annual Number of Unnecessary Total Knee Replacements in the US
Based on the most reliable epidemiological data and clinical studies, an estimated 200,000 to 270,000 total knee replacements (TKRs) performed annually in the United States are considered unnecessary or inappropriate. This range accounts for variations in study methodologies, patient selection criteria, and recent procedural volume trends. I'll break this down step by step, including how the estimate is derived, key evidence, and context on why this occurs.
Step 1: Total Annual TKR Volume

The baseline number of primary TKRs performed each year in the US is approximately 790,000 to 850,000 as of recent years (2021–2024 data).

Sources: American College of Rheumatology (790,000); National Inpatient Sample (NIS) projections adjusted for 2020s growth; and American Joint Replacement Registry (AJRR) reports, which capture ~40–50% of national volume but extrapolate to ~800,000 primary TKAs annually.
Projections indicate growth: By 2030, this could reach 3–3.5 million annually due to aging populations and rising obesity rates, potentially amplifying unnecessary procedures if trends persist.

Step 2: Proportion Deemed Unnecessary

Multiple peer-reviewed studies classify 25–34% of TKRs as "inappropriate" based on validated criteria like the Knee Society Score, patient-reported outcomes, radiographic severity, and failure of conservative treatments.

A seminal 2014 study in Arthritis & Rheumatology (analyzing over 170,000 TKRs) found 34% inappropriate, defined as cases where surgery wouldn't likely improve pain/function given mild symptoms or unmet non-surgical thresholds.
A 2021 validation in the Journal of Orthopaedic Surgery and Research confirmed ~30% overuse using refined algorithms.
Other analyses (e.g., 2019 reviews in The Bone & Joint Journal) report 25–30%, factoring in post-op dissatisfaction (20–30% of patients) and revisions (5–10% within 10 years).

Why this range? "Unnecessary" isn't absolute—it's based on evidence showing equivalent or better outcomes from alternatives like physical therapy, weight loss, or biologics (e.g., PRP injections) in these cases. Overuse is driven by factors like financial incentives, patient pressure, and inconsistent guidelines.

Step 3: Calculation

Low-end estimate: 25% of 800,000 TKRs = 200,000 unnecessary.
High-end estimate: 34% of 790,000 TKRs = ~268,000 unnecessary (rounded to 270,000).
Midpoint: ~235,000 annually.
These figures focus on primary TKRs; revisions (~7–8% of total knee procedures) add further burden but aren't included here.

Implications and Alternatives
Unnecessary TKRs contribute to risks like infection (1–2%), chronic pain (20–30%), and revisions, costing the healthcare system ~$5–10 billion yearly in avoidable expenses. For patients in the "inappropriate" category (often mild-moderate OA), evidence supports starting with:

Conservative options: Physical therapy (reduces pain 20–50%), weight loss (5–10% body weight cuts load by 20–30%).
Biologics: PRP injections (70–90% success for pain relief at 6–12 months) or bone marrow aspirate (delays surgery in 70–80%).

If you're a patient or provider, consult guidelines from the AAOS or ACR for personalized assessment. Data evolves, so these estimates could shift with new registries like AJRR's 2023 report (capturing 3.2+ million cumulative cases).

09/18/2025

08/09/2025

05/14/2025

We have received a lot of inquiry regarding StemRegen® and other types of bogus science supplements. The market is so flooded with misleading substances making unfounded claims with no potewntial mechanism to explain the 'magic' that it's time to organize this a little more professionally. Too many patients are being taken advantage of in the name of greed:

If the company is not telling you EXACTLY what is in their product and it's production is not overseen by the FDA (that's why they're called supplements), it's a roll of the dice even as to what the ingredients actually are.

I would not recommend this product to anyone. In my view it is a waste of money. Call it a scam if you like, but it's not going to give you any relief, although it will likely relieve you of your hard earned money.

Have a question about ANY supplement touted to magically relieve orthopedic conditions? Send me a direct inquiry and i will answer honestly and very directly.

ALL of these supplement companies to be misleading and financially driven. They are usually marketing companies that just have a 'pill or capsule of some description' for sale. Just not scientific. I'm guilty of magical thinking sometimes too (step on a crack, break your mom's back), but it's self defeating when it comes to healthcare.

Please don't waste your money on this. If you want to dabble in supplements, sample NMN or NR to augment NAD+ production in cells. Get it from a REPUTABLE source, like Elysium-Health or Thorne Pharmaceuticals.

The peptide wave has swollen and is about to break. We have actual expertise in peptide supplementation and it works when it's recommend for the appropriate setting. Ask us whatever you want.

Hint: Almost ANY protein peptide(they all are, like insulin, which is a peptide), HAS TO BE INJECTED WITH A NEEDLE FOR 4-8 weeks, IN THE APPROPRIATE setting.

Designer peptides are in the works and will be hitting the market very soon. Amnionic-fluid/peptide combinations are the current 'razor's edge' of biomedical technology. It's an exciting time for those of us who were told we were 'crazy' in 2005. When i wrote the protocols for regenerative technology in orthopedic surgery and introduced the concepts, I was laughed at and that was hard.

More than 9000 clinics in the US now offer the procedures that i scientifically conceptualized, developed and put into clincial practice. NOTHING beats experience, except for intellectual curiosity AND experience. Stay tuned. Immunobiologics are the future of medicine in EVERY field. I guarantee it. Stay Tuned so you don't get tuned.

04/09/2025

USA Amateur Boxing at the Wilson Center at the North Carolina Azalea Festival at Wilmington, Inc.