Sunday, May 10, 2026

"RSA has a lower revision rate than aTSA". Why that may not mean what you think it does.

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Disclaimers: I have no relationships with any implant company. I do love anatomic total shoulder arthroplasty. The below is my attempt to analyze the available data, but there is a dearth of high-level evidence. I am not a statistician, but here I share my attempt at a deep dive into an important and hotly discussed issue. It is not a quick read, but the topic deserves the depth.

The relative merits of anatomic and reverse total shoulder arthroplasty for osteoarthritis are—and probably will forever be—hotly debated. Many factors contribute to surgeons' views on this topic, including indications, relative difficulty of the procedure, cost, need for preoperative 3D/CT-based planning, need for transfer technologies (robotics, patient-specific instruments, virtual/augmented reality), and the patient's anticipated postoperative comfort, range of motion, and function. In this post, we take a look at the contention that patients whose osteoarthritis is treated with reverse total shoulder arthroplasty have lower rates of revision than those treated with anatomic total shoulder arthroplasty.

The word on the street is that patients having reverse total shoulder arthroplasty (RSA) are less likely to undergo revision than patients having anatomic total shoulder arthroplasty (aTSA). For example, the Australian Orthopaedic Association National Joint Replacement Registry's 2025 Annual Report puts the 10-year cumulative revision rate at 7.4% for aTSA and 5.4% for RSA [1]. The 14-year figures are 9.5% and 6.4%. These numbers are often cited in support of expanding RSA into indications it was not originally designed for—including osteoarthritis with an intact rotator cuff.

Set against those numbers, a finding from O’Malley and colleagues' 2025 National Joint Registry analysis of 21,918 patients should give us pause. RSA had nearly twice the prevalence of unsatisfactory function—Oxford Shoulder Score below 29—as aTSA: 27.0% versus 15.4%. Yet RSA patients with unsatisfactory function were less than half as likely to undergo revision (4.9% vs. 10.6%, p < 0.001) [6]. The implant with the lower revision rate (RSA) is the implant under which a larger proportion of patients are living with poor function.

That paradox is the subject of this post. Two sampling biases and one structural property of the metric itself combine to make revision rate a misleading proxy for clinical success when comparing aTSA to RSA. The first is a confounding mismatch between the patient populations the two operations are performed on. The second is an attrition mechanism that systematically removes the worst outcomes from any cohort with a minimum time to follow-up. The third—and the most important one is that revision rate measures what the surgeon decides to operate on again, not what the patient is living with. Strip these out and the registry-based case for RSA in osteoarthritis with intact cuff is weak.

Two biases and a metric problem

Bias 1: The patient populations are not the same

Restricting to osteoarthritis controls for the obvious confounders of other indications such as cuff tear arthropathy and fracture; even within that restriction, the AOANJRR shows aTSA at 7.7% revision at 10 years and RSA at 5.0% [1]. But the RSA-for-OA cohort is overwhelmingly older: 87.7% of cases are in patients aged 65 or older [1]. When attention is restricted to the demographic where the operations actually compete—younger patients with osteoarthritis—the favorable RSA signal disappears. Figure 1 shows the actual curves from the registry.

Figure 1.  Cumulative percent revision from the AOANJRR 2025 Annual Report. RSA for OA in patients aged <65 (n=3,439, Table ST85) versus aTSA with a polyethylene glenoid for OA, all ages (n=5,120, Table ST44). Markers at the registry's reported time points (1, 3, 5, 7, 10, 14 years); shaded bands show 95% confidence intervals. The RSA <65 curve runs above the aTSA curve at every reported time point. At 14 years RSA <65 reaches 13.2% (95% CI 9.6–17.9) versus 9.4% (95% CI 7.8–11.1) for aTSA—the ratio of point estimates is 1.40. The wide 14-year RSA confidence interval reflects the small number of patients still under follow-up at that time point (n=53), an example of the cohort attrition discussed under Bias 2.  aTSA n-at-risk approximated from Figure ST2 of the AOANJRR 2025 report (all-diagnosis polyethylene glenoid, n=5,413) scaled to the OA-only cohort. RSA n-at-risk taken directly from Table ST85.

Cautions about this comparison are in order. The under-65 RSA-OA cohort is itself selected: these patients typically have severe pathology not amenable to aTSA, so part of their failure rate may reflect disease severity rather than implant inferiority. And the aTSA comparison group is not age-matched. Thus the registry cannot fully answer the like-for-like question—younger patient with intact cuff, RSA versus aTSA—because surgeons mostly do not choose RSA for that patient, and so the comparison cases barely exist. What the registry can show is that the apparent RSA-OA advantage in the registry headline is overwhelmingly driven by older patients for whom aTSA was never going to be offered.

Bias 2: The cohorts are themselves selectively curated

Every minimum-follow-up cohort is, by construction, a survivor cohort. To be analyzed at minimum 2, minimum 5, or minimum 10 years, a patient must have remained alive, in clinic, and with the original implants in place. Patients are excluded if their shoulder was revised before the minimum follow-up, if they died, if they were lost to follow-up, or if they left the surgeon's practice. This is not random. The mechanism is the immortal time bias formalized by Suissa: when cohort entry depends on a span of time during which the outcome of interest (e.g., survivorship to the minimum follow-up time) could not occur, the estimated event rate is systematically biased toward the experience of survivors [2]. Including only patients with minimum two-year follow-up systematically excludes those revised or deceased before two years; the percentage excluded by this immortal time effect grows for minimum five-year follow-up and grows again for minimum ten-year follow-up. This exclusion leaves a “purified” sample of patients more likely to continue life without revision and does not reflect the overall revision risk of the initial cohort.

Three independent processes drive this attrition. Khan and colleagues used Medicare claims on 108,667 elective shoulder arthroplasty patients aged 65 or older and reported 5-year mortality of 14.9% in elective non-fracture cases [3]. Torrens and colleagues prospectively tracked 251 shoulder arthroplasty patients and reported cumulative loss to follow-up of 18.3% at 2 years, 31.5% at 5 years, and 34.3% at 7 years, with older, sicker, and more obese patients selectively lost (HR 1.05 per year of age, HR 2.44 for severe obesity, HR 1.93 per ASA point) [4]. After adding exclusion for pre-threshold revision, at minimum 10-year follow-up only a minority of the original cohort—roughly a quarter to a third—remains analyzable. The minimum-10-year revision rate commonly quoted from a published series is therefore drawn from the least at-risk fraction of the original patient population.

Figure 2.  Approximate share of an original elective shoulder arthroplasty cohort still available for analysis at minimum 2-, 5-, and 10-year follow-up. Mortality components anchored to Khan 2024 [3] (14.9% at 5 years extrapolated to ~30% at 10 years); loss-to-follow-up components anchored to Torrens 2022 [4] (18.3% at 2 years, 31.5% at 5 years, extrapolated to ~36% at 10 years); pre-threshold revision approximated from registry data.

This compounds asymmetrically with the demographic confounding above. RSA cohorts are older and have higher all-cause mortality, so these cohorts lose more patients to death between landmark thresholds. RSA's particular failure modes—acromial fracture, dissatisfaction with limited internal rotation, persistent pain—are also more likely to lead to patients quietly dropping out of follow-up because there is often no good surgical option for them to consider. A published “minimum 5-year RSA-OA revision rate” of 3.5% is best read as 3.5% of the best segment of the original cohort, not the entire cohort. The same dynamic appears directly in Figure 1: at the 14-year time point the RSA <65 cohort retains only 53 of the original 3,439 patients (1.5%), producing the wide confidence interval that runs from 9.6% to 17.9%.

The metric problem: failure is not the same as revision

This is the largest of the three issues, and the one with the most specific mechanism. Revision rate is commonly used as a surrogate for clinical failure. It is a particularly poor surrogate for RSA. Parada and colleagues reported a 10.7% complication rate and 5.6% revision rate for aTSA, versus 8.9% and 2.5% for RSA, in 1,128 cases at mean follow-up of 23 months [5]. The gap between complication and revision was 3.6-fold for RSA versus 1.9-fold for aTSA. The most common RSA complication—acromial or scapular fracture (2.5%)—had a 0% revision rate [5].

O’Malley and colleagues' finding closes the loop: twice the prevalence of unsatisfactory function after RSA, and less than half the rate at which that unsatisfactory function leads to revision [6]. The lower RSA revision rate does not reflect superior implant performance. It reflects a higher threshold for revision in an older, frailer cohort, combined with failure modes that are difficult to address surgically and that surgeon and patient usually choose to accept rather than trying to fix surgically.

Figure 3.  Cumulative revision rate (light bars) and cumulative clinical failure rate (dark bars) for aTSA and RSA at minimum 2-, 5-, and 10-year follow-up. Revision rates anchored to AOANJRR registry data [1]; clinical failure rates anchored to Parada complication rates [5] and O’Malley OSS<29 prevalence [6]. The clinical-failure-to-revision ratio is approximately 3-fold for aTSA across all time points and 5- to 6-fold for RSA.

The asymmetry has a specific cause: the failure modes that drive each operation's clinical burden carry very different probabilities of leading to revision. Most of the failure modes unique to RSA produce clinical problems that rarely lead to revision.

A mode-by-mode look

Figure 4.  Estimated cumulative incidence of patients clinically affected by each failure mode (light bars) versus the proportion undergoing revision attributable to that mode (dark bars). Constructed from AOANJRR revision-cause distributions [1], Parada complication rates [5], O’Malley OSS<29 prevalence [6], systematic-review data on acromial fracture [7–9], Young secondary cuff dysfunction rates [14], Papadonikolakis glenoid radiolucency rates [10], Olson RSA instability rates [15], and Rojas baseplate loosening rates [16].

Acromial and scapular fracture. This mode is unique to RSA and represents the largest disconnect in the literature. Three independent systematic reviews place the incidence at 2.8% (Mahendraraj 2019) [8], 4.0% (Kim 2019) [9], and 5.0% (Patterson 2020) [7]. Of 208 fractures in Patterson's review, only 9 (4.3%) underwent revision arthroplasty [7]. Function deteriorates after fracture regardless of treatment. The clinical-failure-to-revision ratio is approximately 25:1.

Persistent pain. Pain is a major driver of unsatisfactory function but rarely the documented reason for revision. The OSS<29 prevalence in O’Malley—15.4% for aTSA and 27.0% for RSA—captures pain alongside stiffness, ADL limitation, and overall functional compromise [6]. The cleanest reading is the one O’Malley reports directly: RSA patients with poor function are less than half as likely as aTSA patients with poor function to be revised. Some unknown proportion of persistent pain after shoulder arthroplasty represents occult Cutibacterium infection that goes undiagnosed; Pottinger and colleagues showed that 22% of revisions performed for stiffness, pain, or loosening had positive cultures for Cutibacterium despite being categorized clinically as aseptic [11]. Patients with low-grade unrecognized infection who do not undergo revision are invisible in registry data altogether.

Cuff and subscapularis failure. This mode is aTSA-specific. Cuff insufficiency accounts for roughly a quarter of aTSA-OA revisions in the AOANJRR data [1]. The actual prevalence of post-aTSA cuff failure is substantially higher. Young and colleagues, in a multicenter European study of 518 aTSAs followed for a mean of 8.6 years, reported a 16.8% rate of secondary rotator cuff dysfunction, with Kaplan–Meier survivorship free of secondary cuff dysfunction of 100% at 5 years, 84% at 10 years, and 45% at 15 years [14]. Most of this dysfunction was managed with rehabilitation or accepted as part of the clinical course; only a fraction underwent revision. RSA bypasses the rotator cuff biomechanically, so this mode does not apply to RSA. Importantly, aTSA failure due to cuff or glenoid component issues can be revised to RSA with patient-reported outcome improvements [12,13]—a salvage option that is less successful for some of the major RSA-specific failure modes.

Asymptomatic glenoid radiolucency and loosening. aTSA-specific. Papadonikolakis, Neradilek, and Matsen's 2013 systematic review of 27 articles representing 3,853 aTSAs reported asymptomatic glenoid radiolucent lines accumulating at 7.3% per year, symptomatic loosening at 1.2% per year, and surgical revision for loosening at 0.8% per year [10]. Radiographically apparent loosening occurs approximately nine times more frequently than revision. Most asymptomatic radiolucent lines do not progress to clinical failure within the patient's lifetime, but those that do represent a substantial population not captured in revision rates.

Dislocation and instability. Both operations can fail by this mode, but RSA more often. Olson and colleagues' systematic review of 17 studies including 7,885 RSAs reported a pooled instability rate of 2.5%, ranging from 1–5% in primary RSA cohorts and 1–49% in revision RSA [15]. Across studies, treatment was successful with closed reduction and casting in 28–100% of cases and with revision RSA in 55–100%; recurrent instability often required hemiarthroplasty or resection. The clinical-failure-to-revision ratio for instability is approximately 1.5:1 to 2:1—smaller than for the modes above, but RSA-specific risk factors (subscapularis insufficiency, proximal humerus fracture, fracture sequelae) load this mode disproportionately onto the older RSA-for-fracture population.

Baseplate failure (RSA) and overt infection (both RSA and aTSA). These are the modes with the smallest disconnect. Aseptic glenoid baseplate loosening is rare: Rojas and colleagues' meta-analysis of 103 studies including 6,583 RSAs reported a pooled prevalence of 1.16% (95% CI 0.80–1.69%), with 0.90% in primary RSA and 1.69% in revision RSA [16]. When symptomatic, baseplate loosening almost always progresses to revision. Overt infection is similarly almost always revised. Both modes have clinical-failure-to-revision ratios close to 1:1—but the Pottinger finding indicates that the population of patients with low-grade unrecognized infection may be substantially larger than overt-infection counts suggest, and many of those patients neither receive a revision nor appear in registry infection data [11].

Bottom line

The AOANJRR shows a population-level revision-rate advantage for RSA over aTSA. It does not show a like-for-like advantage. Two sampling biases compound: an age and indication mismatch that places most RSA-for-OA cases in older patients to whom aTSA was never going to be offered, and an immortal time bias that removes most of an original cohort from the analyzed group at the 10-year mark, with the older RSA population hit hardest. The third issue is structural rather than statistical. Revision rate measures the surgeon's and patient's thresholds for re-operation, and does not reflect the patient's clinical outcome. The clinical-failure-to-revision ratio is two to three times larger for RSA than for aTSA.

This is not an artifact. It has a specific mechanism. RSA's distinctive failure modes—acromial fracture, persistent pain, scapular notching, dissatisfaction with internal rotation—are largely uncountable in revision data because there is often no good surgical option to consider. By contrast, aTSA failures from cuff or subscapularis tear and from glenoid component loosening can be revised to RSA with clinically significant outcome improvements [12,13]. Revision rate as a quality metric privileges the operation (RSA) whose failures are less likely to be surgically correctable.

Evidence for restricting RSA to its established indications—cuff arthropathy, irreparable cuff tear, selected fractures—rather than expanding it into osteoarthritis with intact cuff is present in the AOANJRR's data.


avocet

reverse avocet


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References

1. Australian Orthopaedic Association National Joint Replacement Registry. Hip, Knee and Shoulder Arthroplasty: 2025 Annual Report. Adelaide: AOA; 2025. Available from: https://aoanjrr.sahmri.com/annual-reports-2025. Data period 1 September 1999 – 31 December 2024.

2. Suissa S. Immortal time bias in pharmacoepidemiology. Am J Epidemiol. 2008;167(4):492–499. doi:10.1093/aje/kwm324. PMID: 18056625.

3. Khan AZ, Zhang X, Macarayan E, et al. Five-year mortality rates following elective shoulder arthroplasty and shoulder arthroplasty for fracture in patients over age 65. JBJS Open Access. 2024;9(2):e23.00133. doi:10.2106/JBJS.OA.23.00133. PMID: 38685966.

4. Torrens C, Martínez R, Santana F. Patients lost to follow-up in shoulder arthroplasty: descriptive characteristics and reasons. Clin Orthop Surg. 2022;14(1):112–118. doi:10.4055/cios21034. PMID: 35251548.

5. Parada SA, Flurin PH, Wright TW, Zuckerman JD, Elwell JA, Roche CP, Friedman RJ. Comparison of complication types and rates associated with anatomic and reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2021;30(4):811–818. doi:10.1016/j.jse.2020.07.028. PMID: 32763380.

6. O’Malley O, Davies A, Rangan A, Sabharwal S, Reilly P. Is there a difference in thresholds for revision between shoulder arthroplasty types? A National Joint Registry study. PLoS One. 2025;20(8):e0330975. doi:10.1371/journal.pone.0330975. PMID: 40857270.

7. Patterson DC, Chi D, Parsons BO, Cagle PJ. Acromial spine fracture after reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2019;28(4):792–801. doi:10.1016/j.jse.2018.08.033. PMID: 30497925.

8. Mahendraraj KA, Abboud J, Armstrong A, et al. How common are acromial and scapular spine fractures after reverse shoulder arthroplasty? A systematic review. Bone Joint J. 2019;101-B(6):627–634. doi:10.1302/0301-620X.101B6.BJJ-2018-1187.R1. PMID: 31154841.

9. Kim HM, Chung J, Jeong CW, Yoon JR. Is acromial fracture after reverse total shoulder arthroplasty a negligible complication? A systematic review. Clin Orthop Surg. 2019;11(4):427–435. doi:10.4055/cios.2019.11.4.427. PMID: 31788166.

10. Papadonikolakis A, Neradilek MB, Matsen FA 3rd. Failure of the glenoid component in anatomic total shoulder arthroplasty: a systematic review of the English-language literature between 2006 and 2012. J Bone Joint Surg Am. 2013;95(24):2205–2212. doi:10.2106/JBJS.L.00552. PMID: 24352774.

11. Pottinger P, Butler-Wu S, Neradilek MB, Merritt A, Bertelsen A, Jette JL, Warme WJ, Matsen FA 3rd. Prognostic factors for bacterial cultures positive for Propionibacterium acnes and other organisms in a large series of revision shoulder arthroplasties performed for stiffness, pain, or loosening. J Bone Joint Surg Am. 2012;94(22):2075–2083. doi:10.2106/JBJS.K.00861. PMID: 23172325.

12. Al-Asadi M, Rajapaksege N, Abdel Khalik H, Abesteh J, Athwal GS, Khan M. Outcomes and complications of failed anatomic shoulder arthroplasty revised with reverse arthroplasty: a systematic review. J Shoulder Elbow Surg. 2025;34(7):1832–1840.

13. Tobin JG, Thomas SK, Elwell JA, Roche CP, Rogalski BL, Eichinger JF, Friedman RJ. Anatomic total shoulder arthroplasty revised to reverse total shoulder arthroplasty: clinical and radiographic outcomes compared to primary reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2025;34(6):1525–1531. PMID: 39694226.

14. Young AA, Walch G, Pape G, Gohlke F, Favard L. Secondary rotator cuff dysfunction following total shoulder arthroplasty for primary glenohumeral osteoarthritis: results of a multicenter study with more than five years of follow-up. J Bone Joint Surg Am. 2012;94(8):685–693. doi:10.2106/JBJS.J.00727. PMID: 22419408.

15. Olson JJ, Galetta MD, Keller RE, Oh LS, O’Donnell EA. Systematic review of prevalence, risk factors, and management of instability following reverse shoulder arthroplasty. JSES Rev Rep Tech. 2022;2(3):261–268. doi:10.1016/j.xrrt.2022.02.009. PMID: 37588866.

16. Rojas J, Choi K, Joseph J, Srikumaran U, McFarland EG. Aseptic glenoid baseplate loosening after reverse total shoulder arthroplasty: a systematic review and meta-analysis. JBJS Rev. 2019;7(5):e7. doi:10.2106/JBJS.RVW.18.00132. PMID: 31145263.


Thursday, April 30, 2026

Since the surgeon is the method, how can surgeons improve their method?


Intelligence that is not artificial

As craftsmen, each of us surgeons want to get better at our craft.

Because much of what we do turns out well for our patients, our greatest opportunity for improvement comes from studying the instances in which the outcomes are adverse for them.

One way to do this is to keep an eye on the world's best population-based resource, the Australian Orthopaedic Association's National Joint Replacement Registry.

These data may inform the implants we use

the use of implant modifications


or the type of adverse outcomes we may encounnter



A complementary approach is presented in a recent JBJS article: Learning From Surgical Failures. The essence of this approach is asking the couterfactual question: what might have been done differently to lower the risk of this complication?

For example, one could consider the cases of failed pyrocarbon implants shown below and ask: "what could have been done differently in each case?"



While this kind of analysis is invaluable, the degree to which it applies to each of our own practices is uncertain.

Personal continuous quality improvement (PCQI)
An approach to learning from our own failures is presented in How a surgeon can learn from their own adverse outcomes - an example of intrapractice analysis in reverse shoulder arthroplasty. As illustrated in that blog post, this approach to introspection is straightforward.

For each adverse outcome in each of our own practices: (1) identify the mode of failure (e.g. displaced acromial stress fracture), (2) identify the important parameters of our treatment (e.g. position of the reverse total shoulder components), (3) compare these parameters in the case to those in similar patients in our practice who did not have the complication (controls), and (4) note the difference between the case and controls and consider adjusting our surgical technique in the direction of the controls (e.g. making sure that the distance between the glenosphere center of rotation to the acromion is greater than the distance between the glenosphere center of rotation to the greater tuberosity).



Each of us can be in a state of perpetual beta, continuing to ask the question,

"How can I get better?"


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Thursday, April 23, 2026

Reducing periprosthetic infection risk in shoulder arthroplasty: what the current evidence supports


A Bit of Background
A shoulder periprosthetic joint infection (PJI) is among the most significant complications a patient, a surgeon, or a health system can face. 


It is difficult to diagnose, difficult to eradicate, and disproportionately likely to be caused by Cutibacterium—an organism that lives in the pilosebaceous units of the normal dermis, beyond the reach of any antiseptic applied to the skin surface and that the host’s immune system may not recognize as “foreign.”








Reported PJI rates depend on case mix and follow-up duration, ranging from 0.4% to 3% for primary anatomic total shoulder arthroplasty (aTSA), 1% to 10% for primary reverse shoulder arthroplasty (RSA), and up to 15.4% for revision arthroplasty [1, 2]. 

The 2018 International Consensus Meeting (ICM) on Orthopaedic Infections established standardized diagnostic criteria, with “definite” PJI defined by a sinus tract from the skin to the prosthesis, gross intra-articular pus, or two positive tissue cultures with phenotypically identical virulent organisms; lower-tier diagnoses (“probable,” “possible,” “unlikely”) depend on a weighted point score combining serum and synovial markers, frozen-section findings, and culture results [55].  These criteria are useful but imperfect: Cutibacterium is a low-virulence organism that can present without classic infection findings, and the culture-based criteria depend on assumptions about specimen-handling contamination that vary widely across institutions.

Cutibacterium can be isolated from healthy shoulders. So we need to consider an “infection” as “bacteria doing harm.” Whether Cutibacterium are doing harm in a shoulder arthroplasty—a periprosthetic infection—depends primarily on the interaction between it and the host in the environment of the prosthetic joint.  Is this similar to the situation of E. Coli in the gut: Dr. Jekyll and Mr. Hyde?


Two pieces of recent data underscore this point. Wong and colleagues followed primary TSA patients with intraoperative cultures, finding 38% culture-positive (67% Cutibacterium)—yet none developed clinical infection [56]. Mook and colleagues similarly reported approximately 20% positive culture rates in open shoulder surgery without clear correlation to clinical infection [57]. The Hsu whole-genome sequencing study (2023 Neer Award) demonstrated that essentially all sequenced Cutibacterium strains carry the genetic capacity to cause PJI, but with very low rates of strain sharing across patients—that is, common environmental contamination is unlikely [58]. Hodakowski and colleagues, reviewing 22 studies on unexpected positive cultures (UPC) at revision surgery (76% Cutibacterium), found pooled revision rates of 5.4% in patients with UPC versus 3.4% with negative cultures—suggesting that culture positivity alone does not stratify clinically meaningful infection risk [59].

Shoulder periprosthetic infections can present in different ways.
An “obvious” presentation is one in which there is pain, swelling, erythema, draining sinus, intraarticular pus, elevated serum inflammatory markers, and cultures that rapidly turn positive. While obvious infections can be caused by Cutibacterium, methicillin-resistant staphylococcus and methicillin-sensitive staphylococcus are common offenders.

A “stealth” presentation is one in which the patient’s expected post-arthroplasty course becomes complicated by otherwise unexplained pain and stiffness after a “honeymoon” recovery. Stealth infections are commonly associated with Cutibacterium.


Looking at the data
Given the stakes, it is not surprising that a great deal of time, money, and effort is being spent on interventions that claim to reduce PJI risk. What is worth asking is what the supporting evidence actually shows.

It helps to distinguish two questions about any proposed intervention: (1) Does it reduce a surrogate for PJI—skin-surface colony counts, dermal culture positivity, intraoperative field culture positivity, or bacterial load on instruments? (2) Does it address the clinical outcome the patient cares about—periprosthetic infection, revision for infection, or poorer comfort and function?

The surrogate-to-outcome link is biologically plausible but unproven. Direct evidence shows that intraoperative culture positivity at primary TSA does not predict clinical PJI or inferior patient-reported outcomes [1], and the Wong, Mook, and Hodakowski data noted above point in the same direction [56–59].

Another confounding finding is that the Cutibacterium positive culture rate for a sterile swab or sponge exposed to the air in a shoulder OR is 5 to 15% [33, 34]; sterile-specimen studies have reported false-positive rates as high as 13% [57]. A positive culture for a shoulder tissue specimen may therefore reflect contamination on its path from the patient to the OR environment to the lab. 

Surgeons should consider periodically testing the culture results for sterile samples in their ORs to guide the interpretation of their surgical-specimen culture results.

Approaches to lowering infection risk
The one intervention with robust shoulder-specific outcome data: weight-based IV cefazolin
A single-institution review of 7,713 primary shoulder arthroplasties over two decades reported that cefazolin, compared with non-cefazolin alternatives (vancomycin, clindamycin), was associated with a 69% reduction in all-cause PJI and a 78% reduction in Cutibacterium PJI over 15-year follow-up [17]. The findings of this observational, retrospective analysis were congruent with a separate analysis of 139,032 primary shoulder arthroplasties [18], providing the strongest shoulder-specific outcome evidence in the entire infection-prevention literature. The mechanism is consistent with Cutibacterium’s susceptibility to beta-lactams and with the tissue concentrations cefazolin achieves when given inside the guideline window.

When vancomycin is used (usually for self-reported penicillin allergy), the protective effect depends on complete infusion before incision: a fourfold increase in PJI risk has been reported when vancomycin infusion-to-incision was less than 30 minutes [19]. A large randomized trial in total joint arthroplasty found no benefit to adding IV vancomycin to cefazolin, and in the knee subgroup vancomycin addition was associated with a higher surgical site infection (SSI) rate; the shoulder subgroup (n = 30) was too small to support inference [30].
Self-reported penicillin allergy is rarely a barrier in practice. Modern cephalosporin manufacturing has eliminated the cross-contamination that drove earlier estimates of cross-reactivity, and a 2024 total-joint-arthroplasty study reported a 0.1% reaction rate among patients with self-reported severe IgE-mediated beta-lactam allergy who received cefazolin prophylaxis, with no severe reactions and no use of epinephrine [60]. A test-dose protocol with multidisciplinary monitoring is reasonable for these patients to enable cefazolin prophylaxis.

IV cefazolin reduces but does not eliminate deep-tissue inoculation. Cutibacterium is still recoverable from deep tissues at primary arthroplasty despite prophylaxis and standard skin preparation [5]. A 2024 prospective genomic study of 90 primary reverse shoulder arthroplasties showed that the Cutibacterium recovered from deep tissues after cefazolin and chlorhexidine gluconate (CHG) skin preparation was genotypically identical to the organism present on the skin, consistent with skin-to-deep-tissue inoculation [20]. Falconer and colleagues similarly documented surgical field contamination despite prophylaxis [21]. Adding doxycycline to cefazolin did not further reduce culture positivity in a randomized trial [22].

Patient-side risk factors with shoulder-specific supporting data
A 2022 systematic review and meta-analysis by Seok and colleagues quantified risk-factor odds ratios across primary shoulder arthroplasty [61]. Reported associations include male sex (OR 1.71), younger age (~5% per-year decrement in adjusted risk), acute trauma (OR 1.74), liver disease (OR 1.70), revision arthroplasty (OR 4.76), prior nonarthroplasty shoulder surgery (OR 2.40), diabetes mellitus (OR 1.32), iron-deficiency anemia (OR 2.73), alcohol use disorder (OR 2.47), and rheumatoid arthritis (OR 1.59). Several of these—anemia, alcohol use, and glycemic control—are modifiable; others identify a higher-risk patient who deserves shared decision-making about expected outcomes. As with all meta-analyses pooling retrospective database studies, caveats about confounding and case-mix apply.

Glycemic control in patients with diabetes
A shoulder-specific analysis of patients with diabetes mellitus identified a perioperative HbA1c threshold of 8.0 as an inflection point above which wound-complication and deep-infection rates rise significantly [49]. The absolute infection rate remains low even above this threshold, and HbA1c alone has limited discrimination as a predictive test—but the data support preoperative HbA1c screening in patients with diabetes and consideration of glycemic optimization before elective surgery.

Timing of corticosteroid injection. 

Shoulder injection within 3 months of arthroplasty is associated with increased postoperative infection risk in a Medicare analysis [50]; a subsequent national-database study of reverse shoulder arthroplasty found the increased PJI risk concentrated in patients injected within 4 weeks of surgery [51]. Scheduling arthroplasty ≥4 weeks—and ideally ≥3 months—after any ipsilateral glenohumeral corticosteroid injection is a reasonable risk-reduction step.

Operative time. 
A 33,987-case NSQIP analysis showed an increasing odds of SSI as operative time lengthened, with an inflection above 180 minutes [52]. Operative time is a modifiable factor to the extent that surgical volume, implant selection, team familiarity, and case complexity permit.

Soft-tissue envelope. 
Body mass index alone has had inconsistent associations with shoulder PJI in the literature, possibly because soft-tissue distribution around the shoulder varies independently of BMI. Wu and colleagues developed a “concentric circle” radiographic method to quantify soft-tissue thickness around the shoulder and reported that increased envelope size correlates with longer surgical time, longer length of stay, and higher postoperative infection rate after RSA [62]. The measurement is simple, the dataset is retrospective, and the threshold for action is undefined—but the geometric concept is biologically reasonable. A low BMI (<20) may be as risky as a high one (>35).





Testosterone supplementation. 
Higher serum testosterone—including testosterone supplementation—has been associated with increased Cutibacterium burden on the skin and in surgical wounds, and with higher PJI risk [63]. Whether discontinuing supplementation alters this association is not known, but it is worth discussing with patients on testosterone therapy.

Other items often cited without shoulder-specific PJI-outcome data. 
Smoking cessation, preoperative anemia correction, nutritional optimization, OR personnel traffic reduction, intraoperative normothermia, appropriate hair removal, glove changes at key moments, and excellent wound closure are all reasonable, low-harm elements of a perioperative protocol. They are supported to varying degrees by extrapolated evidence from other surgical fields and by surrogate-endpoint orthopaedic data. None has a shoulder-specific randomized controlled trial showing a reduction in PJI. Recommending them is sensible; describing them as “evidence-based for shoulder PJI reduction” overstates the case.

Preoperative decolonization
Chlorhexidine gluconate (CHG) applied on the skin surface
Home CHG showers are widely used. Their shoulder-specific support is weaker than often assumed. Standard surgical preparation does not eradicate Cutibacterium from the dermis [3], home CHG washes lower skin loads of most bacteria but are specifically less effective against Cutibacterium [4], and the organism can still be isolated from deep cultures at primary shoulder arthroplasty despite prophylaxis [5]. A randomized trial in male shoulder arthroplasty patients comparing home 4% CHG washes to 10% benzoyl peroxide soap found neither agent eliminated Cutibacterium from the skin surface or the incised dermal edge [6]. Cutibacterium repopulates the shoulder skin surface from the sebaceous-gland reservoir within 60 minutes [2].

Standard surgical skin preparation
The contemporary preference for chlorhexidine–alcohol (ChloraPrep) over iodine-based or povidone-iodine alternatives derives in part from a randomized trial by Saltzman and colleagues comparing ChloraPrep, DuraPrep, and povidone-iodine scrub [64]. ChloraPrep had the lowest overall positive-culture rate (7%) versus DuraPrep (18%) and povidone-iodine scrub (31%); none of the three preparations showed a significant difference for Cutibacterium specifically. As with home washes, surface preparation does not address the deep dermal reservoir.

Benzoyl peroxide (BPO) applied on the skin surface
The BPO shoulder literature now comprises multiple randomized trials. Sabetta and colleagues first reported in 2015 that adding topical 5% BPO cream to standard skin preparation reduced Cutibacterium recovered during shoulder surgery [53]. The 2018 Neer Award trial randomized 80 shoulder-surgery patients to 5% BPO or 4% CHG for three consecutive days; the BPO-treated shoulder had fewer positive cultures than the contralateral untreated control (P = 0.0003), while the CHG-treated shoulder did not differ from its control [7]. A separate small volunteer trial showed a similar BPO surface effect [8]. Scheer and colleagues later reported in a 100-patient randomized trial that BPO reduced Cutibacterium positivity across all phases of open shoulder surgery, from skin incision through wound closure [9]. A 2022 randomized trial by Symonds and colleagues compared BPO and BPO with topical clindamycin (BPO-C) against control, reporting culture-rate reductions of 74% and 82%, respectively; despite these reductions, 22% of patients in the active arms still had positive preincision cultures, and many had positive intraoperative cultures [65].
The picture is not uniformly positive. Heckmann and colleagues showed that topical clindamycin, BPO, and the combination each failed to eliminate Cutibacterium from the dermis in randomized treatment quadrants on the upper back [54]. The Hsu trial on the shoulder was also negative [6]. Taken together, BPO has the most consistent surrogate-endpoint signal of any topical agent in this space, but it reduces rather than eliminates surface colonization and has no shoulder-arthroplasty trial demonstrating reduction in clinical PJI.

Hydrogen peroxide (H2O2)
3% hydrogen peroxide is bactericidal against Cutibacterium at clinically achievable contact times [10]. A nonrandomized controlled trial of 61 primary shoulder arthroplasties reported reduced triple-site (skin + dermis + joint) culture positivity with the addition of an H2O2 wipe to standard preparation [11], and a two-year follow-up of that cohort noted a non-significant trend toward fewer revisions and fewer Cutibacterium infections [12]. Against these: a randomized controlled trial applying H2O2 to the dermis after skin incision showed no difference in culture positivity (20% vs. 16%, p > 0.99) [13], and a 2024 randomized volunteer study found no additional benefit to H2O2-followed-by-CHG over CHG alone, with 78% of shoulders in both arms repopulating from the sebaceous reservoir within 60 minutes [14]. The collective evidence for H2O2 is split, with two studies suggesting a surrogate-endpoint benefit and two showing none; no shoulder-arthroplasty trial has demonstrated a clinical PJI benefit.

Nasal Staphylococcus aureus screening and decolonization
S. aureus is not the dominant shoulder-arthroplasty pathogen. Meta-analytic data from hip and knee arthroplasty cohorts suggest screen-and-decolonize protocols lower SSI rates [15]. The largest randomized trial enrolled 613 arthroplasty patients—only 14 (2%) of whom had shoulder arthroplasty—and found zero PJIs in either arm at 2 years, rendering the trial inconclusive [16].

Intraoperative antimicrobial measures
Discard the incision scalpel
Levy and colleagues sampled scalpel blades immediately after skin incision under standard preparation and reported Cutibacterium-positive cultures on approximately 12% of blades [66]. Discarding the scalpel after the skin incision is a low-cost, low-harm step that addresses one plausible inoculation pathway. As with most adjuncts in this space, it has not been shown in a randomized trial to reduce clinical PJI.

Dilute povidone-iodine joint irrigation
In hip and knee arthroplasty, an early report noted a reduction in acute deep PJI from 0.97% with saline lavage to 0.15% with 0.35% dilute povidone-iodine lavage [23]; a randomized trial in aseptic revision TJA showed a reduction in PJI from 3.4% (saline) to 0.4% (dilute povidone-iodine) (p = 0.038) [24]. Larger cohorts have not replicated this, and a 2025 multicenter randomized trial in high-risk primary THA and TKA found no significant reduction in 3-month PJI or wound-complication rates for dilute povidone-iodine, topical vancomycin powder, or their combination compared with saline [25].
Shoulder-specific data are sparser and focus on microbial surrogates. An observational study of 187 isolates recovered during reverse shoulder arthroplasty reported substantial reduction in recoverable Cutibacterium and coagulase-negative staphylococci after 3 minutes of 0.35% povidone-iodine irrigation [26]. No shoulder-arthroplasty RCT has demonstrated a reduction in clinical PJI attributable to dilute povidone-iodine irrigation. The practice is nonetheless endorsed by WHO, CDC, and ICM guidelines based predominantly on hip, knee, and spine data.

Subcutaneous povidone-iodine lavage
A distinct approach—povidone-iodine applied to the subcutaneous layer after skin incision, rather than joint-space lavage before closure—was tested in a 120-patient randomized, single-blinded trial. Subcutaneous povidone-iodine applied after deltoid fascia exposure significantly reduced Cutibacterium surgical-field culture positivity compared with no-additional-preparation control [35].

Subcutaneous chlorhexidine gluconate lavage
Two randomized trials published in 2025 tested 0.05% chlorhexidine gluconate as an intraoperative adjunct to reduce Cutibacterium contamination in primary shoulder arthroplasty. The results were mixed. One reported a pooled deep-culture odds ratio of 2.21 favoring CHG over saline (n = 126, single surgeon) [31]. The other reported no difference (n = 56, single surgeon); the CHG arm was numerically (but not statistically significantly) worse (10.08% vs. 5.77%) [32]. In a dermal biopsy subgroup, the CHG arm was 13% positive and the control arm was 0% (p = 0.115) [32]. The results are inconclusive.

It would be of interest to know how subcutaneous CHG compares head-to-head with subcutaneous povidone-iodine.

Topical (intrawound) vancomycin powder
Meta-analyses of predominantly retrospective hip and knee arthroplasty studies have reported reductions in PJI with intrawound vancomycin powder [27, 28]. In a prospective multicenter RCT in high-risk primary THA and TKA, topical vancomycin powder (alone or with dilute povidone-iodine) produced no statistically significant reduction in 3-month PJI compared with saline [25]. Shoulder-specific data consist of a single retrospective cohort: 422 shoulder arthroplasties that received intrawound vancomycin powder embedded in a collagen sponge compared with 405 historical controls. The study reported a reduction in PJI without an increase in aseptic wound complications [29]. The comparison is to historical rather than concurrent controls. No prospective, randomized trial in shoulder arthroplasty has tested intrawound vancomycin powder for the outcome of PJI.

Microbial sealant
A small comparison of cyanoacrylate microbial sealant added to iodine-impregnated drapes versus drapes alone showed numerically lower positive culture rates (7% vs. 18% overall, 7% vs. 13% Cutibacterium) but no statistically significant difference [67]. Like other intraoperative adjuncts, the surrogate-endpoint signal is modest and the clinical-PJI signal absent.

Dual-drape setup in revision surgery
A two-layer draping technique—removing the outer drape after the débridement portion of a revision case before component implantation—has been examined in lower-extremity arthroplasty, with one study reporting a 75% infection-control rate in DAIR procedures using a dual setup versus 47.5% with a single setup [68]. There are no shoulder-specific data, but the rationale (reducing inoculation from a contaminated outer field at the moment of clean implantation) is plausible and the technique is low-cost.

Operating-room environment
No widely used OR environment measure for shoulder PJI prevention has high-quality, shoulder-specific outcome evidence demonstrating a reduction in clinical PJI. Most data extrapolate from hip and knee arthroplasty or rely on surrogate endpoints.

Surgical drapes
Adhesive drapes—iodine-impregnated or not—reduce wound contamination in a meta-analysis (OR 0.49; 95% CI 0.34–0.72), but the two studies reporting SSI found zero infections in both arms, leaving the clinical infection benefit indeterminate [36]. WHO conditionally recommends against plastic adhesive incise drapes—with or without antimicrobial properties—for SSI prevention [37]. No shoulder-specific draping study has demonstrated PJI reduction.

Surgical hoods and helmet systems
The distinction between older Charnley-type body exhaust suits and modern positive-pressure surgical helmet systems matters. Older systems showed reduced air and wound contamination in most studies; modern helmet systems have not [38]. A 2025 systematic review found that helmet systems frequently harbor microbes and that their exhaust fans can contaminate the sterile field—some systems exhaust air laterally at the level of the surgical wound [39, 40]. Simulated studies have shown surgical helmets can actually increase particle and microbial emission rates compared with standard surgical clothing [41]. The CDC 2017 guidelines classified space suits as an “unresolved issue” [42]. The most directly relevant shoulder-specific evidence is a 2024 New Zealand Joint Registry analysis of 16,000 primary shoulder arthroplasties, which found no difference in all-cause revision or revision for deep infection between surgical helmet systems and conventional gowns [43].

Laminar airflow and closed-incision NPWT
Major guidelines recommend against laminar airflow for arthroplasty SSI prevention [37, 44]. A single shoulder-arthroplasty RCT of a localized laminar flow device (n = 43) demonstrated reduced airborne CFUs near the wound but no infections occurred in either group [45]. Closed-incision negative pressure wound therapy has broad SSI-reduction evidence across surgical specialties [46–48], but no trial has specifically evaluated it for shoulder arthroplasty PJI.

Closure, drains, and adjunctive pharmacology
Wound closure technique is largely surgeon preference, with limited shoulder-specific data. A recent international Delphi study on knee arthroplasty closure recommended barbed sutures, triclosan-coated suture, mesh-adhesive skin closure, silver-impregnated dressings for standard-risk patients, and closed-incision NPWT for high-risk patients—but no analogous shoulder-specific consensus exists [69].

Closed-suction drains have not been shown to alter shoulder PJI rates. A randomized trial by Trofa and colleagues found no difference in postoperative hemoglobin, transfusion rates, length of stay, or cost between drain and no-drain groups, although it was not powered to detect differences in PJI [70]. The contemporary use of tranexamic acid (TXA) addresses one historical purpose of drains. TXA itself has not been shown to reduce shoulder PJI directly, but a cost-effectiveness analysis suggests its use would be warranted at a PJI reduction threshold as low as 0.009%, given its low cost and wide safety margin [71].

Perioperative intravenous dexamethasone, frequently used for postoperative nausea and pain control, has not been associated with increased wound complications or PJI in shoulder arthroplasty in a 2024 retrospective cohort study; patients receiving dexamethasone had lower rates of medical complications (sepsis, urinary tract infection, acute kidney injury) and equivalent infection-related outcomes [72].

Putting all this together
Weight-based IV cefazolin, administered within the guideline window, is the one intervention with robust shoulder-specific outcome data for PJI reduction [17, 18]. When vancomycin is required, complete infusion before incision matters [19]. Self-reported penicillin allergy is rarely a barrier to cefazolin in modern practice [60]. Beyond that, the evidence base consists almost entirely of either extrapolation from hip and knee arthroplasty or surrogate endpoints that have a known and unresolved dissociation from clinical PJI [1, 33, 34, 56–59].
Several patient-side measures are supported by shoulder-specific data on associated infection risk: perioperative HbA1c screening and optimization in patients with diabetes [49]; deferring elective arthroplasty ≥4 weeks (ideally ≥3 months) after any ipsilateral corticosteroid injection [50, 51]; minimizing operative time [52]; recognizing the higher-risk patient profile (revision, prior shoulder surgery, anemia, alcohol use, rheumatoid disease) defined by the Seok meta-analysis [61]; and considering the soft-tissue envelope as an independent risk factor [62].

Smoking cessation, nutritional optimization, anemia correction, normothermia, traffic reduction, and careful wound closure are reasonable—but are not “evidence-based for shoulder PJI reduction” in the strong sense of that phrase.

Multiple inexpensive, low-harm adjuncts—BPO, H2O2, subcutaneous povidone-iodine, dilute povidone-iodine joint lavage, intrawound vancomycin, subcutaneous CHG, scalpel discard, microbial sealant, dual-drape setup in revisions—reduce surrogate endpoints with varying consistency.

Nevertheless, because shoulder PJI is serious and difficult to treat, prevention is the preferred strategy. Surgeons should consider adding such low-harm, low-cost adjuncts on biological-plausibility grounds, even though robust evidence supporting their efficacy in reducing clinical PJI is lacking. The companion 2025 JAAOS reviews by Berger, Garrigues, Chalmers, and Singh—written by authors with no disclosed financial conflicts of interest with commercial companies related to the subject matter—offer a useful complementary descriptive map of the field [73, 74].  




Lots to consider!


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