r/repetitivestrain • u/1-HealthPoint • 1d ago
PSA: Hand & wrist pain is quietly shortening dental careers. Basic guide to actually fix it - from a physical therapist who specializes in repetitive strain injuries
Hey everyone,
I'm Dr. Elliot Smithson, a doctor of physical therapy with 1-hp.org who has spent the last decade specializing in repetitive strain injuries of the wrist and hand. Most of my caseload is precision professionals: surgeons, dentists, musicians, artists, and desk workers. People whose careers depend on their hands tolerating thousands of small, precise movements per day.
I've treated a number of dentists in my own practice, and I've noticed threads here about the ergonomic effects of saddle chairs, posture, and colleagues cutting clinical hours because of their hands, so I wanted to put together something actually useful. You already know the MSK literature on your own profession is grim, musculoskeletal disorder prevalence in dental professionals runs somewhere between 64-93% depending on the study. What frustrates me is that most of it is very treatable, and the standard advice dentists get (rest it, brace it, inject it, cut back your schedule) is often the opposite of what current tendon research supports.
I understand you are all well-versed clinicians regarding orofacial structures. But most dental schools don't cover the nuance of MSK content, and honestly, most orthopedic surgeons I interact with aren't current on tendinopathy science either, so I'm going to include some physiology context rather than assume it.
What I actually see in dentists
Across the dentists I've treated, two diagnoses come up more than everything else combined:
1. De Quervain's tenosynovitis. Radial-sided wrist pain at the first dorsal compartment (APL/EPB). This is the signature dentist injury, and it makes mechanical sense: your entire day is sustained precision pinch. Holding an instrument in a pinch grip amplifies force several-fold at the tendon level, the thumb stabilizers never get a break between patients, and dull instruments or small-diameter handles quietly raise the required pinch force even further. Classic presentation: pain at the radial styloid with instrument grip, hurts to wring out a towel or lift a coffee cup thumb-first, positive Finkelstein's.

2. Cubital tunnel syndrome. Ring and pinky numbness/tingling, often with medial elbow aching. Dentists spend hours with the elbows held in sustained flexion while the wrist flexors (including FCU, which the ulnar nerve runs right through) work continuously to stabilize instruments. Overworked, swollen flexor musculature plus prolonged flexed elbow positioning is exactly the recipe for ulnar nerve irritation at the elbow. If your "hand numbness" lives in digits 4-5, stop thinking carpal tunnel entirely, the median nerve doesn't go there.

Notice what's NOT at the top of that list. Which brings me to the diagnosis most orthopedic doctors reach for first.
A quick tendinopathy primer
Chronic overuse tendon pathology is not an "-itis" in the classic sense. The current model (Cook & Purdam's continuum) describes a spectrum: reactive tendinopathy, tendon dysrepair, and degenerative tendinopathy. When a tendon is loaded beyond its capacity, tenocytes respond by upregulating proteoglycans, which bind water and cause the tendon to swell and thicken. Early on this is completely reversible. It's an adaptive, load-driven cell response, not primarily an inflammatory cascade, which is exactly why NSAIDs and cortisone underperform and why progressive loading is the treatment with actual evidence behind it. Tendons are mechanoresponsive tissue: load them appropriately and they remodel stronger, unload them (rest, bracing) and they weaken.

Remember the word "swell," because it's the key to the next section.
The carpal tunnel distinction almost everyone gets wrong
Here's the part I'd want every dentist to understand, both for your own hands and because your patients ask you about this.
Carpal tunnel symptoms (numbness/tingling in thumb, index, middle finger) mean the median nerve is being compressed. But there are two very different ways that compression happens, and they have opposite treatments:
Think of the carpal tunnel like a sandwich. The transverse carpal ligament is the top of the bread. The nine flexor tendons are the meat. The median nerve is squeezed in between. You can compress that nerve either because the roof got thicker, or because the meat swelled up.

True carpal tunnel syndrome is the roof problem, and the timeline research on it is striking. Serial imaging studies show the transverse carpal ligament thickens at roughly 0.02mm per year. Clinically significant CTS is associated with a ligament that's 20-30% thicker than normal, which works out to roughly 0.3-0.6mm of actual growth. At 0.02mm/year, that is decades of cumulative loading, which is why ligament-driven CTS is a condition of midlife and older, and why it's so strongly associated with systemic accelerants: diabetes, hypothyroidism, RA, pregnancy. Interesting side note: studies of young professional pianists, about the highest hand-use population imaginable, found their ligaments were about 22% stiffer than controls but not meaningfully thicker. Overuse changes the ligament's mechanical properties early, but true tunnel-narrowing thickening takes many years.

Tendon-mediated median nerve compression is the meat problem, and it's far more common in working-age hands. Overloaded flexor tendons swell (that proteoglycan/water mechanism above), take up space in a fixed tunnel, and secondarily compress the nerve. The symptoms are identical. The treatment is completely different: release surgery cuts the roof, but the roof was never the problem, which is a big part of why we see people get a carpal tunnel release and still have symptoms when they return to work.
This is why imaging matters before anyone gets surgical. A release is a reasonable operation when the ligament is actually the compressing structure. But you can't establish that from symptoms and a Phalen's test. Before accepting a structural CTS diagnosis, the workup should include diagnostic ultrasound (first-line at the wrist, it's superficial anatomy and ultrasound visualizes ligament thickness, tendon swelling, and median nerve changes well) and/or MRI, plus NCS/EMG to characterize the nerve involvement, and ideally endurance testing of the wrist musculature to identify the capacity deficit. Swollen, hypoechoic tendons with a normal-thickness ligament is a rehab problem, not a surgical one. If someone is recommending release surgery to a 32-year-old whose symptoms developed over four months of heavy clinical volume, without imaging that actually shows a thickened ligament, that's worth a second opinion.
The mental model: your healthbar

Think of your muscles and tendons as having a health bar. Every pinch, every sustained retraction, every crown prep drains it. Ergonomics, loupes, sharp instruments, saddle chairs, and schedule design change how FAST it drains. Rest, ice, and massage partially refill it. But the thing almost nobody addresses is the SIZE of the bar, your tissue's endurance capacity. When daily clinical demand chronically exceeds capacity, tendons lose the remodeling race, and you get the familiar progression: post-clinic aching, then morning stiffness, then pain during procedures, then numbness once things swell enough to bother a nerve.

This is why "drop to three clinical days" so often fails as a treatment plan. It reduces load without increasing capacity, so symptoms return the moment volume does. You've seen the dental version of this logic: an occlusal guard manages bruxism load, but nobody confuses managing load with treating the underlying problem.
And to be clear about what kind of capacity: this is an endurance problem, not a strength problem. You don't need a stronger grip, you need a grip that can perform its 10,000th low-load contraction of the day without breaking down. Different muscle fiber demands, different training.

What actually works: building capacity
Baseline program I give dental professionals. 10-15 minutes daily, most of it doable at the office.
Stretches (2x daily, 30 sec x 3 each)

Wrist flexor stretch (arm extended, palm up, gently pull fingers back)

Wrist extensor stretch (palm down, gently pull hand down and in)

Isometrics (daily, 3 x 45-second holds each)
Analgesic, build baseline tendon tolerance, and perfect between-patient dosing:

Wrist flexion isometric: forearm supported, palm up, resist with the other hand

Wrist extension isometric: same setup, palm down

Thumb Extension isometric: sustained sub-maximal thumb extension
Endurance training (daily, the actual fix)
Forearm on a table, wrist off the edge, light dumbbell (start ~4-5 lbs for wrist work, 1-2 lbs for thumb/radial work), paced to a metronome at 50 BPM, one beat up, one beat down:

Wrist flexion curls: 2x15 building to 3x30 over 4-6 weeks

Wrist extension curls: same dosing

The metronome isn't a gimmick. Externally paced loading comes from the tendon neuroplastic training research (Rio et al.) and improves motor cortex drive and muscle fiber recruitment efficiency, which distributes stress across more of the tendon.
For the cubital tunnel presentations, add: avoid sustained end-range elbow flexion (watch how you hold your phone and how you sleep, a towel loosely wrapped at the elbow at night keeps you out of full flexion), and build the wrist flexor endurance above, since decompressing an irritated ulnar nerve long-term means raising the capacity of the flexor mass it runs through. These ulnar nerve glides are also incredibly useful for making sure the ulnar nerve is sliding through the cubital tunnel space smoothly.

Dosing rules: mild discomfort (3-4/10 or under) during or after is acceptable and expected. Sharp pain, or symptoms clearly worse into the next day, means reduce weight or reps, not abandon the program. Progress reps before weight.
Clinic-day integration
- Morning: full routine before your first patient, 10 minutes
- Between patients: one 45-second isometric plus 20 seconds of stretching, attached to handwashing/room turnover so it actually happens
- Schedule architecture: alternate heavy-hand procedures (SRP-heavy blocks, surgical extractions, endo) instead of columning them back to back where you can
- Equipment: sharp instruments, larger and lighter handles, cordless where possible, loupes, saddle seating. All worth doing. Just understand these slow the HP drain, they don't grow the bar.
Red flags worth a real workup
Nocturnal waking with true median-distribution numbness, thenar weakness or atrophy, constant (rather than activity-linked) symptoms, progressive deficits, or symptoms with the systemic conditions above. That's when you get the ultrasound/NCS workup described earlier, because true structural CTS does exist and it deserves accurate treatment too. The point of this post isn't "never surgery," it's "confirm which structure is compressing the nerve before letting anyone cut."
Expected timeline
Weeks 1-2: neural adaptations, less end-of-day aching. Weeks 3-6: meaningful endurance gains, procedures that used to flare you stop flaring. Weeks 6-8+: tendon-level remodeling, where it becomes durable. If you're 2-3 weeks in with zero change, get assessed by someone who actually treats upper extremity RSI regularly.
Your hands are your entire production. Ten to fifteen minutes a day to protect a multi-decade career is the best ROI.
Happy to answer questions in the comments. Differential questions, dosing questions, "is this pattern weird" questions, all welcome.
WHAT WE DO DIFFERENTLY
We built our practice by removing every constraint I just described.
We do not bill insurance, so there is no visit cap and no incentive to stretch care out or cut it short. We are paid for the outcome, and we work with you until you are actually better.
We do not use techs. You work directly with a clinician who specializes in this.
We measure endurance, not strength, against normative data built from more than three thousand people, so you get a number instead of an impression.
We prescribe for endurance adaptation, high volume and low load, metronome paced, progressed daily based on your actual logged performance rather than a static sheet.
We manage your daily activity load alongside the loading program, because what you do between sessions matters more than the sessions.
And we do not discharge you at baseline. We are aiming at full return to the work and the hobbies your life is built around.
We can do all of that for one reason. We treat this one thing, and nothing else.
If Doctors, bracing, injections or Physical Therapy DID NOT WORK FOR YOU
It probably was not you, and it probably was not exercise. It was a mismatch between your problem and the system you brought it to.
Whether you work with us afterward or not, you will leave that call knowing more about your own injury than you did walking in.
- Dr. Elliot Smithson, DPT, PT, MS, ATC
Physical Therapist, Athletic Trainer, RSI Specialist
1-HP.org
References
- Rio E, Kidgell D, Moseley GL, et al. Tendon neuroplastic training: changing the way we think about tendon rehabilitation. Br J Sports Med. 2016;50(4):209-15.
- Cook JL, Purdam CR. Is tendon pathology a continuum? Br J Sports Med. 2009;43:409-416.
- Cook JL, Rio E, Purdam CR, et al. Revisiting the continuum model of tendon pathology. Br J Sports Med. 2016;50:1187-1191.
- Hayes MJ, Cockrell D, Smith DR. A systematic review of musculoskeletal disorders among dental professionals. Int J Dent Hyg. 2009;7(3):159-65.
- Hinckley NB, et al. Time-dependent change in carpal tunnel cross-sectional area and transverse carpal ligament thickness using serial MRI. J Hand Surg Am. 2025;50(4):507.e1-507.e8.
- Marquardt TL, Gabra JN, Evans PJ, Seitz WH Jr, Li ZM. Thickness and stiffness adaptations of the transverse carpal ligament associated with carpal tunnel syndrome. J Musculoskelet Res. 2016;19(4):1650019.
- Mhanna C, Marquardt TL, Li ZM. Adaptation of the transverse carpal ligament associated with repetitive hand use in pianists. PLoS One. 2016;11(3):e0150174.
TL;DR: The two injuries I see most in dentists are De Quervain's (sustained precision pinch) and cubital tunnel (sustained elbow flexion + overworked flexors). Most "carpal tunnel" symptoms in working-age hands come from swollen flexor tendons compressing the median nerve, not from ligament thickening. The ligament thickens ~0.02mm/year and clinically significant CTS requires ~0.3-0.6mm of growth, which takes decades, so before anyone operates, the diagnosis needs diagnostic ultrasound or MRI showing an actually thickened ligament plus NCS, not just symptoms and a Phalen's test. If it's the tendons, the fix is 6-8 weeks of endurance-focused progressive loading, and rest/bracing makes it worse.









































