Plantaris-related midportion Achilles Tendinopathy

“85% of the [general] population have a plantaris. It exists. It is a stiff tendon and can cause an inflammatory response between the Achilles.” -Jarrod Antflick

Jarrod Antflick closes the Decision Making and Management module with a set of cases that illustrate how experienced clinicians navigate diagnostic uncertainty. Across five distinct scenarios, he shows how careful observation, mechanistic reasoning, and patient‑specific pattern recognition shape the actions of a high‑level practitioner.

A central tenet of his lecture is that one size does not fit all. Diagnostic precision is imperative for any intervention that hopes to consistently produce change.

In two of these cases, Jarrod makes a passionate argument for addressing a sometimes‑contentious comorbidity: plantaris-related midportion Achilles tendinopathy. 

Plantaris Tendon

The plantaris originates near the lateral supracondylar line of the femur and courses distally before inserting medial to the Achilles tendon (AT) on the calcaneus [1]. It has been a long held belief that the plantaris muscle is a vestigial remnant of our evolutionary past. However, recent research speculates that the plantaris, rather than having direct locomotor function, might serve a more somatosensory role. Its high spindle density may help monitor tension or positional changes within the Achilles tendon complex and influence how load is distributed during eccentric tasks [3].

Regardless of the specific functional role, the muscle displays substantial anatomical variability between individuals. Across existing classification systems, the plantaris has been categorized into six or more anatomical types, defined by differences in proximal origin, spatial relationship to Achilles tendon, and distal insertion on or around the calcaneus [1,2].

A research group led by Lukasz Olewnik has provided detailed descriptions of these variants and have expanded upon how their structure may contribute to different clinical presentations. The plantaris has been implicated in vascular and neural entrapment cases, and, importantly for this discussion, has been theoretically associated with the pain and dysfunction seen in mid-portion Achilles tendinopathy [1,2].

Clinical Relevance

The plantaris has been proposed as a contributor to midportion Achilles tendon symptoms due to its close anatomical relationship with the AT. Its proximity has led to hypotheses about compressive irritation, and its substantially higher tensile stiffness relative to the Achilles has been used to argue for differential excursion between the two tissues. This scenario could impart shear forces at their interface and contribute to pain or degenerative change. These remain speculative mechanistic pathways, but they provide a plausible framework for why the two tissues may exist [1].

Regardless of whether these mechanisms are causal, co‑existing pathology is well supported. Alfredson’s group has shown that in patients with midportion Achilles tendinopathy undergoing surgery, the plantaris tendon often displays degenerative changes and elevated local acetylcholine activity, a pattern that resembles the reactive tissue profile seen in the adjacent Achilles [4,5].

The same group found surgically excising the plantaris tendon (and scraping the ventromedial Achilles tendon) resulted in significantly improved AT structure and function (increases in type I and II UTC echotypes, reductions in type III and IV echotypes, and improvements in VISA‑A scores) [4]. These successful outcomes have been reinforced by similar studies done by Bedi (14 of 15 individuals receiving the same surgery displayed improved subjective reports and enhanced UTC markers of structure) and Calder (16 patients who had previously failed conservative management demonstrated significant improvements in pain and subjective outcomes after plantaris removal, regardless of the presence of plantaris tendinopathy) [6,7].

More recent work suggests the plantaris can even be an independent driver of symptoms. In 14 of 81 individuals presenting for surgical management, Alfredson identified isolated plantaris‑driven pain with no Achilles involvement [8].

Treatment

Evidence for conservative management of plantaris‑related symptoms is extremely limited. The only substantial publication addressing this topic is a textbook chapter co‑authored by Jarrod [9]. The expert consensus presented there is pragmatic. Begin with conservative approaches such as relative unloading, training modification, and targeted exercise. Consider injections directed at the plantaris–Achilles interface when symptoms persist and reserve surgery for a smaller subset of cases if all else fails.

This framework is helpful, but understanding how often plantaris involvement occurs and how differently it responds to treatment is essential for clinical decision making.

To properly orient ourselves, we need to know the prevalence of plantaris pathology, how frequently its treatment trajectory diverges from isolated Achilles injury, and when those divergences should prompt adjustments in loading parameters or consideration of alternative interventions.

How sensitive should we be to the existence of plantaris involvement?

When plantaris involvement is present, how much do treatment responses diverge from isolated Achilles cases, and what adjustments are warranted?

What timelines should we expect in these cases, and at what point should alternative or non‑conservative approaches enter the decision tree?

Data released by Pollock in a retrospective study of elite UK track and field athletes helps begin this discussion [10]. Across four years and 214 athletes, the group documented 33 plantaris injuries in 30 athletes, with sprinters accounting for the majority. Twenty-two of the thirty had simultaneous Achilles tendinopathy, and fifty additional cases involved isolated Achilles pathology without plantaris involvement.

The most striking observation was that more than half of the plantaris-related cases ultimately required surgical intervention.

These findings may reinforce Alfredson’s suggestion that plantaris pathology regularly resists typical rehabilitative strategies [8]. They contend that standard loading programs can worsen symptoms in this context, meaning an incorrect or incomplete diagnosis can result in ineffective rehabilitation.

It should be noted, this conjecture needs to be tested. Unfortunately, Pollock’s dataset provides little detail about individual case circumstances, and it is entirely plausible that conservative care could have succeeded if not constrained by elite sport demands or Olympic timelines.

More robust data will be needed to clarify these assertions. Still, even if surgery is frequently utilized, early outcomes are encouraging.

A 2025 systematic review and meta‑analysis by Wen and colleagues concluded that Achilles tendon scraping with plantaris tendon removal has shown encouraging preliminary results with improved post‑operative PROs, excellent return to sport rates, and low complication rates [11].

Think Horses not Zebras

Based on what we’re just discussed, you’d probably feel justified assuming plantaris pathology is a relatively widespread concern impacting a large percentage of patients walking through your clinic.

Epistemic caution is warranted.

The majority of data presented here has come from small, retrospective studies. This has not been done out of a convenience sample for this post, rather, it reflects the general dearth of evidence regarding this condition. Despite being hypothesized about over 20 years ago, we still rely heavily on anatomical models, small case series, and highly selected surgical cohorts to inform how the plantaris may impact Achilles tendinopathy. 

For clarity, this is not to imply any wrongdoing or malice on the part of these groups. This point is merely intended to draw attention to the importance of the scientific process. Replication is important. Different eyes examining the same problem set, with large sample sizes, in various demographics, allow for a refined perspective and clearer understanding.

To highlight the fragility of the current explanatory model, Khullar presents data that muddies the established narrative [12]. In a retrospective observational study, the group examined the MRIs of 100 cases of individuals experiencing mid-portion Achilles tendinopathy.

Within their subjects, only 10 displayed signs of a co-existent pathological plantaris, and of those 10, only 1 matched locations between the sites of Achilles and plantaris degeneration [12].

This raises two main points of contention.

1) The true prevalence of plantaris involvement is yet-to-be-determined.

In the majority of evidence provided, we’re looking at a highly filtered subject pool. With the exception of Pollock’s study, we’re examining cohorts with chronic tendon pain that have already resisted typical management strategies and/or examining tendons exclusively from a group that has confirmed mid-portion Achilles tendinopathy.

What this means is that we’re likely underestimating the percentage of individuals who have isolated Achilles pathology and we are left in the dark regarding the prevalence of isolated plantaris-related midportion Achilles tendinopathy (as in both cases, we’re still selecting for a cohort that experienced persistent symptoms serious enough to receive high level imaging).

2) Compression is not a slam-dunk factor.

In Khullar’s study, 90% of the cases where there were concomitant structural findings, the location of pathology was in vastly different sites [12]. Unless there is reason to believe compressive forces differentially impact the Achilles tendon to a greater extent than the plantaris, odds are this is not a primary factor.

These findings remind us that plantaris involvement may be the exception rather than the rule. It would be prudent to adhere to typical practice guidelines rather than assuming you’re surrounded by zebras in a field commonly inhabited by horses. Do not rush to injections or surgical intervention before due diligence. 

Open-Minded but Disciplined

Alluding back to our discussion on extracorporeal shockwave therapy, it would be intellectually dishonest to come to strong conclusions at this point. The data informing our perspective is limited and it is important to avoid premature closure of thought on these topics.

A disciplined clinical process helps maintain appropriate boundaries.

In practice, this means continually cycling through the OODA loop: observing what is in front of you, orienting that information against the best available evidence, deciding on the next step, and acting in accordance with that framework.

Importantly, doing so affords the agility to update your position as new information emerges. This iterative process ensures that your management evolves in response to the athlete rather than in service of a preconceived narrative.

Applied Clinical Reasoning in Practice

Uncertainty is inevitable when navigating individual cases in clinical practice. Those blind spots are magnified when the evidence base is thin, as it is with Plantaris-related midportion Achilles tendinopathy.

In this context, Jarrod’s presentation is even more impactful. He shows how clinicians can work through atypical situations when standard patterns do not fully explain what is happening. His case examples provide insight into management of plantaris-related pathology: weighing the clinical presentations, the timelines, and the external considerations.

In each, the athletes had limited response to typical interventions and their careers were at risk of being hindered or cut short. Jarrod relied on disciplined clinical reasoning to identify atypical presentations and guide appropriate escalation when standard approaches failed.

The first involved an athlete who returned for a playoff push after receiving a hyaluronic acid injection between his plantaris and Achilles. The second involved a world‑champion track and field athlete who had considered retirement before a plantarisectomy allowed her to continue.

Fortunately their cases are illustrations of a decision-making process done well rather than a cautionary “what if” tale. By orienting clinical observations, treatment responses, and the expanding evidence base, Jarrod was able to act on the true driver of symptoms and select interventions that produced meaningful outcomes. 

He did not skip steps or abandon common best practice. His strong foundational knowledge allowed him to identify how each athlete’s presentation required alternative approaches. Rather than prescriptions, his cases should be viewed as examples of how a clinician can remain grounded in evidence, responsive to the athlete, and disciplined in the face of uncertainty.

Decision Making and Management: Conclusion

The goal of our final section has been to establish sound processes and refine orientation, not to dictate practice. Enhanced scope of knowledge leads to more accurate decisions, faster recognition of what matters, and fewer detours into conjecture. When managing the athletes in front of us, that kind of disciplined openness is what keeps our process anchored yet responsive and effective.

A clearer decision process strengthens management. The work in this subtopic has centered on how we interpret presentations, how we adjust when patterns shift, and how we choose the next step with intention rather than habit.

When those elements align, management becomes a direct extension of reasoning instead of a collection of prefabricated interventions.

Debrief written by: Jason Eure, PT, DPT, OCS, CSCS

Closing the Series, Looking Ahead

With this installment, the inaugural sixteen-part series is complete.

Across the run, we moved from the foundational science of tendon biology and adaptation, through the practical work of evaluation and diagnosis, and into the frameworks that shape management and decision making.

Neal Millar, Falk Mersmann, and Stephanie Cone grounded us in the science. Ruth Chimenti and Seth O'Neill sharpened how we evaluate. Scot Morrison, Jarred Boyd, and Jarrod Antflick worked through how we decide and manage. Each approached the Achilles from a different angle, and much of the value lived in the friction between those perspectives. The goal was never to hand you a set of answers. It was to sharpen the questions worth asking.

From here, we shift our attention forward.

The 2027 Summit turns to the knee, with the patellar, quadriceps, and distal hamstring tendons taking center stage. Different structures, different demands, and a fresh set of questions to work through together. More information on specific dates (April/May 2027), speakers, and registration is coming soon. If you haven't subscribed to this newsletter yet, we highly recommend doing so to be the first to know.

To the readers who followed all sixteen parts, and to everyone who supported the Summit through its inaugural year: thank you. None of this works without you.

We're looking forward to building the next chapter together.

REFERENCES

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2. Olewnik Ł, Landfald IC, Łapot M, LaPrade RF. Vascular and Neural Compression Syndromes Associated with Plantaris Muscle Variants: A Classification-Based Review. J Clin Med. 2026 Apr 15;15(8):3006. doi: 10.3390/jcm15083006. PMID: 42074805; PMCID: PMC13116904.

3. Olewnik Ł, Landfald IC, Gonera B, Szabert-Kajkowska A, Triantafyllou G, Piagkou M. The Plantaris Muscle Is Not Vestigial: Developmental, Comparative, and Functional Evidence for Its Sensorimotor Role. Biology (Basel). 2025 Jun 13;14(6):696. doi: 10.3390/biology14060696. PMID: 40563947; PMCID: PMC12189277.

4. Masci L, Spang C, van Schie HT, Alfredson H. Achilles tendinopathy-do plantaris tendon removal and Achilles tendon scraping improve tendon structure? A prospective study using ultrasound tissue characterisation. BMJ Open Sport Exerc Med. 2015 May 2;1(1):e000005. doi: 10.1136/bmjsem-2015-000005. PMID: 27900118; PMCID: PMC5117009.

5. Spang C, Alfredson H, Ferguson M, Roos B, Bagge J, Forsgren S. The plantaris tendon in association with mid-portion Achilles tendinosis: tendinosis-like morphological features and presence of a non-neuronal cholinergic system. Histol Histopathol. 2013 May;28(5):623-32. doi: 10.14670/HH-28.623. Epub 2013 Feb 4. PMID: 23378267.

6. Bedi HS, Jowett C, Ristanis S, Docking S, Cook J. Plantaris Excision and Ventral Paratendinous Scraping for Achilles Tendinopathy in an Athletic Population. Foot Ankle Int. 2016 Apr;37(4):386-93. doi: 10.1177/1071100715619989. Epub 2015 Dec 4. PMID: 26637273.

7. Calder JD, Stephen JM, van Dijk CN. Plantaris Excision Reduces Pain in Midportion Achilles Tendinopathy Even in the Absence of Plantaris Tendinosis. Orthop J Sports Med. 2016 Dec 13;4(12):2325967116673978. doi: 10.1177/2325967116673978. PMID: 28203584; PMCID: PMC5298419.

8) Alfredson H, Waldén M, Roberts D, Spang C. Tendinopathic Plantaris but Normal Achilles Tendon Found in About One-Fifth of Patients Not Responding to Conservative Achilles Tendon Management – Results from a Prospective WALANT Surgical Case Series on 105 Tendons. Open Access J Sports Med. 2024;15:41-45. https://doi.org/10.2147/OAJSM.S456389

9) Wever, S., Antflick, J., Calder, J. (2023). The Effect of the Plantaris Tendon on Achilles Tendinopathy. In: Adams, S.B. (eds) The Achilles Tendon. Springer, Cham. https://doi.org/10.1007/978-3-031-45594-0_3

10) Pollock N, Dijkstra P, Calder J, Chakraverty R. Plantaris injuries in elite UK track and field athletes over a 4-year period: a retrospective cohort study. Knee Surg Sports Traumatol Arthrosc. 2016 Jul;24(7):2287-92. doi: 10.1007/s00167-014-3409-3. Epub 2014 Nov 2. PMID: 25362249.

11) Wen J, Alam M, Sedighi R, Syed B, Khalil R, Shehabat M, Joy B, Razick D, Razick A, Frezza E. Achilles Tendon Scraping With Plantaris Tendon Removal for Achilles Tendinopathy: A Systematic Review and Meta-analysis. Foot Ankle Orthop. 2025 Jun 26;10(2):24730114251346791. doi: 10.1177/24730114251346791. PMID: 40585348; PMCID: PMC12202896.

12) Khullar S, Gamage P, Malliaras P, Huguenin L, Prakash A, Connell D. Prevalence of Coexistent Plantaris Tendon Pathology in Patients with Mid-Portion Achilles Pathology: A Retrospective MRI Study. Sports (Basel). 2019 May 22;7(5):124. doi: 10.3390/sports7050124. PMID: 31121856; PMCID: PMC6571766.