Chiropractic Rehabilitation Success for Adductor Tendinopathy

Find out how chiropractic rehabilitation can help reduce discomfort and enhance movement from adductor tendinopathy.

Abstract

Chronic medial thigh pain is a condition that is frequently underdiagnosed, mismanaged, or dismissed in clinical practice. Yet, it can profoundly diminish a patient’s quality of life, functional capacity, and overall well-being. This educational post, authored by Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, presents a thorough, evidence-based clinical discussion of adductor tendinopathy and groin-related musculoskeletal pain syndromes as illustrated through a real-world clinical case involving a 35-year-old male patient with an eight-year history of intermittent, aching medial thigh pain radiating to the knee.

The discussion begins with a foundational review of the anatomy of the adductor muscle complex, including the gracilis, adductor brevis, adductor longus, adductor magnus, and pectineus muscles, and their shared tendinous attachment at the pubic symphysis and pubic ramus. From there, the post explores the pathophysiology of chronic tendinopathy, explaining how repetitive mechanical loading, failed healing responses, and neovascularization contribute to the persistence of pain even in the absence of a recalled traumatic event.

The post describes the clinical assessment process in detail, covering physical examination techniques, palpation protocols, and provocative testing that help isolate adductor tendinopathy as the primary pain generator. The post addresses the role of diagnostic imaging, including ultrasound and MRI, in confirming clinical findings and guiding intervention.

This post provides an in-depth explanation of corticosteroid and regenerative injection therapy, including the rationale for using vapor coolant spray as a pre-injection analgesic, proper aspiration technique, and the clinical reasoning behind distributing the injectate along the tendon and its insertion. Sterile procedural protocols are discussed as non-negotiable components of safe, effective care.

Beyond the procedural component, this post explores how integrative and chiropractic care fits naturally into the long-term management of adductor tendinopathy. The discussion covers rehabilitative exercise, manual therapy, functional movement assessment, and biomechanical correction as essential pillars of a comprehensive recovery strategy. The post also highlights the collaborative clinical model at Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, where Dr. Maria Guadalupe Cardenas, MD, board-certified in Internal Medicine with over 40 years of clinical experience, serves as Medical Director and Collaborative Physician alongside Dr. Jimenez, creating a multidisciplinary environment where patients receive both medical oversight and chiropractic, functional medicine, and rehabilitative care under one roof.

Throughout this post, the latest findings from leading researchers are incorporated to support every clinical recommendation, ensuring that readers, whether patients, clinicians, or healthcare students, leave with a clear, modern, evidence-based understanding of how to recognize, assess, and effectively treat chronic adductor tendinopathy using an integrative, whole-person approach.

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Who We Are: The Integrative Clinical Team at Injury Medical Clinic PA in El Paso, Texas

Before diving into the clinical content of this post, I want to introduce the team and model of care that shapes everything I discuss here at Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas.

My name is Dr. Alexander Jimenez. I hold the following credentials: DC (Doctor of Chiropractic), APRN (Advanced Practice Registered Nurse), FNP-BC (Family Nurse Practitioner, Board Certified), CFMP (Certified Functional Medicine Practitioner), IFMCP (Institute for Functional Medicine Certified Practitioner), ATN (Advanced Trained Naturopath), and CCST (Chiropractic Clinical Sciences and Technology). My clinical philosophy has always been rooted in a deep respect for the complexity of the human body and a commitment to treating the whole person, not just the symptom. You can explore more of my clinical observations and resources at chiromed.com and on my LinkedIn profile.

Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933), works alongside me as our Medical Director and Collaborative Physician. Dr. Cardenas is Board Certified in Internal Medicine and brings over 40 years of experience as an internist to our practice. Her depth of knowledge in systemic medicine, chronic disease management, and patient-centered internal medicine is an invaluable asset to our clinical team. The collaboration between Dr. Cardenas and me represents a model of care that is increasingly recognized in the literature as the gold standard for complex musculoskeletal and injury-related conditions: a multidisciplinary, integrative approach where an MD provides essential medical direction and oversight, while a chiropractor, advanced practice nurse, and functional medicine practitioner address the structural, neurological, and lifestyle dimensions of health.

How Our Multidisciplinary Team Works Together

Our clinic is intentionally structured to bridge the gap between conventional medicine and integrative, evidence-based complementary care. This kind of setup is becoming increasingly common in integrative and injury care clinics, and for good reason. Evidence consistently shows that patients with chronic musculoskeletal conditions, personal injuries, or complex pain syndromes achieve better outcomes, faster recoveries, and higher quality of life when they receive care from a coordinated team rather than isolated practitioners working in silos (Chou et al., 2017).

At Injury Medical Clinic PA, our services include:

• Chiropractic care and spinal manipulation (Dr. Jimenez): Addressing biomechanical dysfunction, vertebral subluxation, joint mobility restrictions, and neurological interference that contribute to pain, impaired movement, and diminished healing capacity.
• Medical oversight and internal medicine (Dr. Cardenas): Providing diagnostic clarity, pharmacological management when appropriate, co-management of systemic conditions that affect musculoskeletal health, and the medical direction required to ensure patient safety across all clinical services.
• Functional medicine assessment and care (Dr. Jimenez): Investigating and addressing the root causes of chronic inflammation, metabolic dysfunction, hormonal imbalance, nutritional deficiency, and gut-immune dysregulation that can perpetuate chronic pain and impair tissue healing.
• Personal injury care: Managing acute and subacute injuries resulting from motor vehicle accidents, workplace incidents, slip-and-fall events, and sports-related trauma, with a focus on thorough documentation, evidence-based treatment, and optimal recovery.
• Rehabilitation and corrective exercise: Designing individualized therapeutic exercise programs that restore strength, mobility, coordination, and functional movement patterns to injured or painful areas of the body.
• Injection therapy and regenerative procedures: Including the kind of adductor tendon injection procedure illustrated in this clinical case, along with other minimally invasive procedures guided by evidence and performed with meticulous attention to sterile technique and patient safety.
• Nutritional counseling and lifestyle medicine: Supporting the biochemical environment of healing through targeted dietary interventions, supplementation protocols, and lifestyle modifications grounded in functional and integrative medicine principles.

This integrative model is not simply a matter of convenience. It reflects a genuine philosophical commitment to recognizing that the human body is a deeply interconnected system, and that chronic pain conditions like adductor tendinopathy rarely arise from a single, isolated cause. They are most effectively addressed when practitioners from different disciplines bring their complementary expertise to bear on the full picture of a patient’s health.

With that introduction in place, let us now turn to the clinical case that anchors this post and begin a thorough, evidence-based exploration of adductor tendinopathy, from anatomy through treatment.

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The Clinical Case: A 35-Year-Old Male With Eight Years of Chronic Medial Thigh Pain

The patient at the center of this discussion is a 35-year-old male who presents with an eight-year history of chronic, intermittent pain located along the medial aspect of his right thigh. He describes the pain as aching and notes that it radiates distally to the level of his knee. Importantly, he cannot recall a specific traumatic event that initiated the symptoms. The pain has persisted, fluctuating in intensity over the years, but never fully resolving.

On physical examination, there is point tenderness of the adductor muscle complex, most pronounced at the tendinous attachment at the pubic bone. Provocative loading and palpation of the adductor tendons at their proximal insertion reproduce the patient’s familiar pain and confirm the clinical diagnosis of adductor tendinopathy with likely enthesopathy at the pubic attachment.

This case is highly representative of what I see regularly in clinical practice. The combination of insidious onset, chronicity, absence of recalled trauma, and tendinous tenderness at the enthesis is a hallmark presentation of chronic tendinopathy involving the adductor complex, and it is a presentation that demands a thoughtful, structured, evidence-based response.

Let us begin by building a thorough understanding of the anatomy involved.

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Anatomy of the Adductor Muscle Complex: Understanding the Structural Foundation of Medial Thigh Pain

To understand why this patient experiences pain where he does, and why the injection is placed where it is, we must first develop a clear, detailed understanding of the anatomy of the medial thigh and adductor compartment.

The Adductor Compartment: Overview

The medial compartment of the thigh houses a group of muscles collectively called the adductor complex. These muscles are responsible primarily for adduction of the hip, meaning they draw the thigh toward the midline of the body. However, their functional roles extend well beyond simple adduction. They contribute significantly to hip flexion, internal and external rotation, pelvic stabilization, and dynamic control of the lower extremity during gait, running, and cutting movements (Macintyre et al., 2011).

The muscles of the adductor compartment include:

• Adductor longus
• Adductor brevis
• Adductor magnus
• Gracilis
• Pectineus
• Obturator externus (sometimes classified with this group)

Each of these muscles has a specific origin, insertion, innervation, and functional role, and understanding these details is critical for accurate clinical assessment and targeted treatment.

Adductor Longus

The adductor longus is the most anteriorly positioned and clinically prominent of the adductor muscles. It originates from the anterior surface of the pubic body, just below the pubic crest and lateral to the pubic symphysis. Its broad, flat belly extends inferolaterally to insert into the middle third of the linea aspera on the femur’s posterior surface.

The adductor longus is the most commonly injured adductor muscle, particularly in athletes, and its proximal tendon at the pubic attachment is a frequent site of tendinopathy and enthesopathy (Serner et al., 2016). The anterior division of the obturator nerve (L2, L3, L4) innervates it.

Adductor Brevis

The adductor brevis lies deep to the adductor longus and pectineus. It originates from the inferior ramus of the pubis and inserts into the upper third of the linea aspera and the lesser trochanter of the femur. It is also innervated by the obturator nerve (L2, L3) and contributes to both adduction and hip flexion.

Adductor Magnus

The adductor magnus is the largest and most powerful of the adductor muscles, composed of two functionally distinct portions:

1. The adductor portion (or pubofemoral portion): Originates from the inferior pubic ramus and ischial ramus, inserts along the linea aspera and medial supracondylar ridge of the femur, and is innervated by the obturator nerve (L2, L3, L4). It functions primarily as a hip adductor and medial rotator.
2. The hamstring portion (or ischiocondylar portion): Originates from the ischial tuberosity, inserts at the adductor tubercle of the medial femoral condyle, and is innervated by the tibial division of the sciatic nerve (L4, L5). It functions as a hip extensor and contributes to knee flexion.

The dual innervation and dual insertion of the adductor magnus make it a clinically complex structure. The hamstring portion in particular can contribute to pain that radiates down the medial thigh toward the knee, as seen in our patient (Woodley et al., 2008).

Gracilis

The gracilis is a long, slender muscle that runs along the entire medial thigh. It originates from the inferior pubic ramus and body of the pubis and inserts via the pes anserinus at the proximal medial tibia, along with the sartorius and semitendinosus tendons. The obturator nerve (L2, L3) innervates it, and it is the only adductor muscle that crosses both the hip and knee joints, contributing to hip adduction and knee flexion.

Because the gracilis spans two joints and inserts below the knee, irritation or tendinopathy can produce symptoms that extend from the groin to the medial knee. This distribution closely matches our patient’s complaint of pain radiating to the knee level.

Pectineus

The pectineus is a flat, quadrilateral muscle that forms the medial floor of the femoral triangle. It originates from the pectineal line of the pubis (also called the pecten pubis) and inserts into the pectineal line of the femur, between the lesser trochanter and the linea aspera. The femoral nerve (L2, L3) innervates it, and it sometimes receives a branch from the obturator nerve. It contributes to hip adduction, flexion, and medial rotation.

The Pubic Attachment: The Clinical Epicenter

One of the most clinically important anatomical facts about the adductor complex is that most of these muscles share a common origin region at or near the pubic bone. Specifically, the adductor longus, adductor brevis, gracilis, and pectineus all originate from the pubic body, pubic crest, inferior pubic ramus, and surrounding structures. This means that the pubic symphysis and its surrounding fibrocartilaginous and tendinous attachments represent a zone of extraordinary mechanical stress, particularly with activities that require rapid changes of direction, kicking, sprinting, or any movement that creates high adductor loading combined with contralateral hip extension.

This shared pubic attachment is why palpation of the pubic bone and adjacent tendinous insertion zone is so revealing in patients with adductor tendinopathy. As demonstrated in this clinical case, pressing directly on the pubic body where the adductor tendons insert reproduces and intensifies the patient’s pain, confirming that the enthesis (the bone-tendon interface) is the primary site of pathology.

Neurovascular Supply of the Medial Thigh

Understanding the neurovascular anatomy of the medial thigh is also essential for safe injection practice and for explaining referred or radiating pain patterns.

The obturator nerve, which arises from the lumbar plexus (L2, L3, L4), is the primary nerve supplying the adductor compartment and enters the medial thigh through the obturator foramen. It divides into anterior and posterior divisions that supply the adductor muscles, the gracilis, and the skin of the medial thigh. Importantly, the obturator nerve also provides articular branches to the hip joint and, in some individuals, a cutaneous branch that extends down the medial thigh to the knee. This explains why hip joint pathology can sometimes mimic adductor tendinopathy and why adductor tendinopathy can produce pain that radiates toward the knee.

The femoral artery and vein run through the femoral triangle, lateral to the pectineus, and the profunda femoris artery provides the main blood supply to the adductor muscles via its perforating branches. The medial circumflex femoral artery is particularly important for supplying the proximal adductors and the femoral head.

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The Pathophysiology of Chronic Tendinopathy: Why Tendons Fail to Heal

Now that we have established the anatomical foundation, we can begin to understand why this patient has experienced eight years of persistent, intermittent pain without a clear traumatic origin. The answer lies in the pathophysiology of chronic tendinopathy, which has been extensively studied over the past two decades and represents one of the most important areas of musculoskeletal medicine.

What Is Tendinopathy?

Tendinopathy is an umbrella term encompassing a spectrum of painful tendon conditions characterized by pain, swelling, and impaired function. Historically, these conditions were termed “tendinitis,” implying an inflammatory etiology. However, modern histopathological research has largely displaced this understanding, demonstrating that the predominant pathological changes in chronic tendon pain are degenerative rather than primarily inflammatory (Cook & Purdam, 2009).

The term tendinosis is used to describe the histopathological changes seen in affected tendons, including:

• Disorganization of collagen fibrils: Normal tendon tissue consists of highly organized, parallel collagen fibers (primarily type I collagen) that efficiently transmit tensile loads. In tendinopathy, this organization breaks down, with disorganized, wavy, or fragmented collagen fibers replacing the normal architecture.
• Increased ground substance: Glycosaminoglycans and proteoglycans accumulate within the tendon matrix, increasing the tissue’s water content and giving it a swollen, disorganized appearance on imaging.
• Neovascularization: New blood vessels, accompanied by sensory nerve fibers, grow into the tendinopathic tissue. This process, known as angiofibroblastic dysplasia or neovascularization, is thought to be a key driver of pain in chronic tendinopathy. The new nerve fibers that accompany these blood vessels express nociceptive neurotransmitters such as substance P and glutamate, sensitizing the local tissue to mechanical and chemical stimuli (Alfredson & Cook, 2007).
• Cellular changes: Tenocyte cellularity increases, with cells displaying a rounded, chondrocyte-like morphology rather than the normal spindle-shaped appearance. These altered cells produce abnormal collagen and matrix proteins, perpetuating the degenerative cycle.
• Partial or complete fiber disruption: In more advanced cases, there may be evidence of intrasubstance tearing or frank partial rupture within the tendon.

The Continuum Model of Tendinopathy

Cook and Purdam (2009) proposed the influential continuum model of tendinopathy, which describes tendon pathology as existing along a spectrum from reactive tendinopathy through tendon disrepair to degenerative tendinopathy. This model has important clinical implications:

1. Reactive tendinopathy: An acute, non-inflammatory proliferative response of the tendon cell matrix to overload, characterized by a short-term adaptive thickening that reduces stress on the tendon. This stage is potentially reversible.
2. Tendon disrepair: A poorly organized healing attempt, with increased matrix production, greater disruption of collagen organization, and ingrowth of blood vessels and nerves. This stage can also be partly reversible with appropriate load management.
3. Degenerative tendinopathy: Advanced pathology with significant cell death, matrix disorganization, and areas of failed healing. This stage is considered irreversible in the affected zones, though surrounding healthy tendon tissue can still adapt and compensate.

In our patient, the eight-year duration of symptoms strongly suggests that the adductor tendon pathology has likely progressed well beyond the reactive stage and may involve elements of tendon disrepair or degenerative tendinopathy. This chronicity has profound implications for treatment planning, as we will discuss in detail.

Why Does Pain Persist Without a Clear Traumatic Origin?

One of the most important clinical questions raised by this case is: why does the patient have eight years of pain without being able to recall a specific traumatic event?

The answer is multifactorial and physiologically interesting.

First, tendinopathy frequently develops through repetitive, subclinical mechanical loading rather than a single traumatic event. Each time the adductor tendons are loaded, a small amount of microtrauma occurs at the cellular and molecular level. Under normal circumstances, the tendon’s intrinsic repair mechanisms (driven by tenocytes and supported by adequate blood supply and nutrient delivery) can repair this microtrauma between loading cycles. However, when the rate of microtrauma exceeds the rate of repair, a progressive pathological cascade is initiated (Magnusson et al., 2010).

Second, the enthesis (the bone-tendon junction) is a particularly vulnerable zone because it is subjected to both tensile and compressive forces simultaneously. The pubic attachment of the adductor tendons is especially exposed to these competing mechanical demands during activities that require rapid hip adduction combined with trunk rotation or contralateral hip extension, such as kicking, sprinting, or lateral cutting movements. Even in non-athletes, ordinary daily activities like walking on uneven surfaces, climbing stairs, or sitting for prolonged periods with the hips in suboptimal alignment can create cumulative entheseal stress.

Third, central and peripheral sensitization plays a major role in the persistence of chronic tendon pain. Over time, the nociceptive nerve fibers within and around the tendon become sensitized, meaning they fire more easily and at lower mechanical thresholds than normal. Additionally, the central nervous system undergoes neuroplastic changes that amplify pain perception from the affected region. This sensitization can persist even after the underlying tissue pathology has partially resolved, which is why some patients continue to experience significant pain even when their tendons look relatively normal on imaging (Fernández-de-las-Peñas & Dommerholt, 2018).

Fourth, biomechanical factors such as altered hip mechanics, reduced hip internal rotation, lumbar-pelvic dysfunction, and asymmetrical loading patterns can create chronic, uneven stress on the adductor tendons that perpetuates pathology over years or decades.

Fifth, systemic factors including metabolic dysfunction, elevated inflammatory cytokines, nutritional deficiencies (particularly in collagen precursors such as vitamin C, proline, and glycine), and hormonal imbalances can impair tendon healing and maintenance at the cellular level. This is where functional medicine assessment becomes particularly valuable, as I discuss later in this post.

The Role of Inflammation in Chronic Tendinopathy

While the term “tendinitis” has largely been retired in favor of “tendinopathy” or “tendinosis” to reflect the predominantly degenerative rather than inflammatory histopathology, inflammation is not absent from the picture. More recent research has revealed a complex interplay between inflammatory and degenerative processes in chronic tendon pain.

Schubert et al. (2014) and others have demonstrated that inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) are present in tendinopathic tissue and can directly inhibit tenocyte function, stimulate matrix metalloproteinase production (leading to collagen degradation), and promote the neovascularization that drives pain sensitization. Furthermore, mast cells and macrophages are found in tendinopathic tissue, suggesting that a chronic, low-grade inflammatory response contributes to the pathological environment.

This nuanced understanding, recognizing that tendinopathy is neither purely degenerative nor purely inflammatory but involves a complex interaction of both processes, has important implications for treatment. This means interventions that target both the mechanical and biological dimensions of tendon pathology are likely to be more effective than those that address only one dimension.

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Clinical Assessment of Adductor Tendinopathy: Examination, Palpation, and Diagnosis

With the anatomy and pathophysiology firmly established, we can now discuss how adductor tendinopathy is identified clinically. Accurate diagnosis underpins effective treatment, and I want to walk through the key components of assessment in detail.

Patient History: The Eight-Year Story

In taking a thorough history from this patient, several key features emerge that strongly suggest adductor tendinopathy:

• Location of pain: Medial thigh, consistent with adductor compartment involvement
• Quality of pain: Aching, which is typical of tendinopathy rather than acute injury or nerve entrapment
• Radiation pattern: Distally toward the knee, consistent with gracilis involvement or sensitization of the obturator nerve’s cutaneous branch
• Duration: Eight years, confirming chronicity
• Onset: Insidious, without recalled trauma, consistent with a repetitive overload etiology
• Pattern: Intermittent but persistent, a classic feature of tendinopathy where symptoms fluctuate with activity levels and loading demands

The absence of recalled trauma is not unusual in adductor tendinopathy. As discussed in the pathophysiology section, many tendinopathies develop gradually through repetitive microloading rather than acute injury. The patient’s eight-year history strongly suggests that the tendon has been in a cycle of insufficient healing for an extended period, possibly compounded by ongoing biomechanical, lifestyle, or systemic factors that have prevented full recovery.

Physical Examination: What the Hands Reveal

The physical examination in suspected adductor tendinopathy should be systematic and include both a general lower-extremity assessment and specific adductor-complex testing.

General assessment includes evaluation of:

• Gait analysis: Looking for antalgic gait, reduced hip extension, trunk lean, or altered arm swing that might reflect attempts to offload the painful adductor complex
• Hip range of motion: Assessment of active and passive hip flexion, extension, abduction, adduction, and internal/external rotation. Reduced hip abduction range of motion is commonly associated with adductor tendinopathy, as shortened, sensitized, or pathologically altered adductors restrict full abduction.
• Lumbar spine assessment: Given the lumbar plexus origin of the obturator nerve (L2-L4) and the potential for lumbar pathology to refer pain into the medial thigh, evaluation of lumbar range of motion, neurological status, and provocative testing is important
• Sacroiliac joint evaluation: Dysfunction at the sacroiliac joint can alter pelvic mechanics and load distribution through the adductor complex

Specific adductor testing includes:

• Palpation of the adductor tendons: As demonstrated in this case, careful, systematic palpation along the length of the adductor tendons, especially at their proximal insertion on the pubic bone, is the single most valuable physical examination technique. Reproducible tenderness at the enthesis that matches the patient’s familiar pain strongly supports adductor tendinopathy.
• Adductor squeeze test: The patient is positioned supine with hips and knees flexed to 45 degrees and feet flat on the table. Place a blood pressure cuff or the examiner’s fist between the knees, and ask the patient to squeeze maximally. This test loads the adductor complex isometrically and provokes pain in adductor tendinopathy. Holmich et al. (2004) reported high sensitivity for this test in athletes with long-standing adductor-related groin pain.
• Resisted adduction: The patient actively adducts the hip against the examiner’s resistance. Pain with resisted adduction confirms adductor muscle or tendon involvement.
• Passive abduction stretch: Gentle passive abduction of the hip stretches the adductor complex and can reproduce medial thigh pain in tendinopathy, particularly at the proximal enthesis.
• Single-leg stance and balance: Assessing whether single-leg stance on the affected side reproduces pain or reveals altered pelvic control helps quantify functional impairment.

In our patient, reproducible tenderness at the pubic attachment of the adductor tendons, along with worsening symptoms with deep palpation of the pubic bone, is diagnostic. The clinical picture is classic adductor enthesopathy.

Differential Diagnosis: What Else Could It Be?

While this case strongly points to adductor tendinopathy, a thorough clinician must consider the differential diagnosis for medial thigh pain, particularly given the long duration of symptoms. Key differential diagnoses include:

• Athletic pubalgia / sports hernia: A syndrome of chronic groin pain in athletes associated with weakness or disruption of the posterior inguinal wall, often coexisting with adductor tendinopathy. The two conditions frequently occur together (Meyers et al., 2007).
• Osteitis pubis: Inflammatory change at the pubic symphysis, often seen in athletes and postpartum women, characterized by pubic symphysis tenderness and characteristic MRI findings
• Hip joint pathology: Femoro-acetabular impingement (FAI), labral tears, and hip osteoarthritis can all produce groin and medial thigh pain that may be mistaken for adductor tendinopathy. Suspect hip joint pathology when passive internal rotation of the hip is restricted and painful.
• Obturator nerve entrapment: Can cause medial thigh pain with a neuropathic quality, often with sensory changes along the medial thigh distribution of the obturator nerve’s cutaneous branch
• Lumbar radiculopathy: L2-L3 nerve root compression can refer pain to the anterior and medial thigh; examination of lumbar spine and neurological testing helps distinguish this from adductor tendinopathy
• Adductor muscle strain: An acute injury with a clear onset and maximal tenderness within the muscle belly rather than at the enthesis
• Stress fracture of the femoral neck or pubic ramus: Should be considered in high-volume endurance athletes or individuals with risk factors for bone stress injuries; typically produces pain with weight-bearing and can be identified on MRI.
• Inguinal hernia: Can produce groin pain that is exacerbated by the Valsalva maneuver and physical activity

In this patient’s case, the eight-year history, aching quality, entheseal tenderness at the pubic bone, and absence of neurological symptoms or signs of hip joint restriction make adductor tendinopathy the primary diagnosis. However, imaging would be appropriate to exclude coexisting pathology, particularly osteitis pubis.

Imaging in Adductor Tendinopathy: The Role of Ultrasound and MRI

While the diagnosis of adductor tendinopathy is primarily clinical, diagnostic imaging serves two important functions: confirming the clinical diagnosis and excluding other pathology.

Musculoskeletal ultrasound is the first-line imaging modality for assessing the adductor tendons. It offers real-time, dynamic imaging that is relatively inexpensive and can guide injection procedures with precision. Ultrasound findings in adductor tendinopathy include:

• Tendon thickening
• Loss of the normal fibrillar (hyperechoic, parallel-line) echotexture
• Areas of hypoechogenicity within the tendon, representing zones of degeneration or intrasubstance tearing
• Neovascularization detectable on power Doppler imaging, a particularly useful finding as it correlates with pain and guides prognosis
• Calcific deposits within the tendon (calcific tendinopathy), if present
• Entheseal irregularity or cortical erosion at the pubic attachment

MRI provides superior soft tissue contrast and can evaluate not only the tendons but also the underlying bone, the pubic symphysis, and the surrounding musculature. MRI findings in adductor tendinopathy include:

• Increased signal within the tendon on T2-weighted or STIR sequences, reflecting edema and degeneration
• Pubic bone marrow edema on STIR sequences, indicating reactive changes at the enthesis
• Evidence of pubic symphysis widening or signal change, suggesting osteitis pubis
• Partial or complete tendon tears
• Secondary findings such as hip labral pathology or FAI

For this patient, given the eight-year history and the clinical findings, MRI of the pelvis and hips would be an appropriate imaging choice to fully characterize the extent of pathology before planning definitive treatment.

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The Injection Procedure: Clinical Rationale, Technique, and Sterile Protocol

This post focuses on injecting the adductor tendon insertion at the pubic bone. I want to walk through every aspect of this procedure in detail, explaining not just the technical steps but the clinical reasoning and physiological rationale behind each one.

Why Inject? The Rationale for Injection Therapy in Chronic Tendinopathy

Before discussing technique, it is essential to address the question: why is injection therapy used in the management of adductor tendinopathy?

The answer requires nuance. The role of injections in tendinopathy management has evolved considerably over the past decade, and the evidence base is more complex than it might initially appear.

Corticosteroid injections have been used for decades as a treatment for tendinopathy. They work by suppressing the local inflammatory milieu by inhibiting arachidonic acid metabolism (reducing prostaglandin and leukotriene production), decreasing vascular permeability, and reducing the activity of inflammatory cells, including mast cells and macrophages. In the short term (typically 4 to 6 weeks), corticosteroid injections provide significant pain relief in many tendinopathy presentations, including adductor tendinopathy (Coombes et al., 2010).

However, the longer-term evidence for corticosteroids in tendinopathy is more cautionary. Multiple systematic reviews and randomized controlled trials have demonstrated that while corticosteroids offer superior short-term pain relief compared to placebo or physical therapy, this benefit is not sustained at 6 to 12 months and may in fact be associated with worse outcomes at longer follow-up intervals (Coombes et al., 2010; Zwiers et al., 2019). The proposed mechanism for this longer-term disadvantage is that corticosteroids can impair tenocyte function, inhibit collagen synthesis, and further degrade the already-compromised extracellular matrix of the tendinopathic tendon.

This does not mean that corticosteroid injections are without value in adductor tendinopathy. Rather, they should be used judiciously and always as part of a comprehensive rehabilitation program, not as a standalone treatment. When pain is severe enough to prevent a patient from participating in rehabilitative exercise, a well-placed corticosteroid injection can break the pain cycle and create a window of opportunity for the patient to engage in the loading-based rehabilitation essential for long-term tendon recovery.

Regenerative injection therapies, including platelet-rich plasma (PRP) and prolotherapy, have emerged as alternatives that aim not merely to suppress symptoms but to stimulate tendon healing actively. PRP is derived from the patient’s own blood and concentrated via centrifugation to create a solution rich in growth factors including platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1). These growth factors stimulate tenocyte proliferation, collagen synthesis, and matrix remodeling, addressing the underlying degenerative pathology rather than merely suppressing symptoms (Andia & Maffulli, 2013).

The evidence for PRP in adductor tendinopathy specifically is still developing. Still, the broader evidence base for PRP in chronic tendinopathy (particularly patellar and Achilles tendinopathy) is encouraging, with several randomized controlled trials demonstrating superior outcomes compared to corticosteroids at medium- and long-term follow-up (de Vos et al., 2010; Filardo et al., 2012).

Prolotherapy involves injecting an irritant solution (typically hypertonic dextrose) to trigger a controlled local inflammatory response that stimulates the body’s natural healing cascade. The theory is that introducing low-grade, controlled inflammation into a tendon in a state of failed healing can reactivate the natural repair process. Evidence for prolotherapy in groin and adductor tendinopathy is limited but emerging (Bertrand et al., 2016).

In this clinical case, the injection appears to involve a local anesthetic and potentially a corticosteroid, targeted at the adductor tendon insertion at the pubic bone. The clinical reasoning is to provide immediate pain relief, confirm the diagnosis through the “anesthetic test” (if the injection completely abolishes the patient’s familiar pain, it confirms the structure as the pain generator), and potentially reduce local inflammation to facilitate rehabilitation.

Pre-Injection Preparation: The Role of Sterile Technique

One of the most important principles demonstrated in this case is the commitment to maintaining a sterile procedural environment. This is not merely a formality; it is an absolute clinical imperative that protects the patient from potentially serious complications.

The prepubic region and adductor tendon insertion are in proximity to the inguinal region, which harbors significant bacterial colonization. Introducing bacteria into a tendon or enthesis via a non-sterile injection can result in septic tenosynovitis, osteitis pubis, or pubic symphysitis. These conditions are far more difficult to treat than the original tendinopathy and can cause severe, lasting harm.

The sterile preparation protocol demonstrated in this case includes:

1. Skin marking: Using the retracted tip of a ballpoint pen to mark the precise injection point on the skin before preparation. This is done before antiseptic preparation because marking after skin prep can introduce contamination. The marking ensures that the exact target is identified through careful palpation and clinical reasoning before the procedural field is established.

2. Alcohol preparation: Application of isopropyl alcohol to the skin over the injection site. Alcohol is a rapid-acting antiseptic that denatures proteins in bacterial cell walls, providing broad-spectrum antimicrobial coverage. It is highly effective against most skin flora but requires adequate contact time (at least 30 seconds) for maximum efficacy.

3. Betadine (povidone-iodine) preparation: Following alcohol preparation, the application of povidone-iodine provides additional antimicrobial coverage. Povidone-iodine releases free iodine, which is bactericidal, fungicidal, and virucidal. The combination of alcohol followed by Betadine is standard practice for injection procedures and provides a higher level of skin antisepsis than either agent alone.

This two-step antiseptic preparation protocol significantly reduces the risk of introducing skin flora into deep tissue during injection and aligns with guidelines for sterile injection technique in musculoskeletal medicine.

Vapor Coolant Spray: The Role of Pain Ease as a Pre-Injection Analgesic

A particularly thoughtful aspect of the technique demonstrated in this case is the use of vapor coolant spray (specifically a product in mist spray formulation, such as Pain Ease) applied to the injection site immediately before needle insertion.

What is vapor coolant spray?

Vapor coolant sprays are topical anesthetic agents that work through evaporative cooling. When applied to the skin, the liquid rapidly evaporates, drawing heat from the skin surface and causing a rapid, transient decrease in skin temperature. This cold-induced anesthesia reduces the sensation of the needle penetrating the skin and superficial tissues, making the procedure more comfortable for the patient.

Why use a mist spray rather than a stream spray?

Choosing a mist formulation rather than a stream formulation is clinically significant. Stream-type vapor coolant sprays can cause the cold liquid to run away from the intended application site, potentially cooling tissues that are not meant to be anesthetized or, in sensitive areas, potentially causing skin damage through excessive cooling or frost formation. A mist spray delivers the coolant as a fine, controlled aerosol that stays precisely on target, maintaining control over the cooling area and reducing the risk of inadvertent skin injury.

The physiological mechanism of vapor coolant analgesia

The mechanism of vapor coolant anesthesia is based on the gate control theory of pain and peripheral nerve cooling physiology. Cold temperature reduces the velocity of nerve conduction in A-delta fibers (which transmit sharp, acute pain) and, to a lesser extent, C fibers (which transmit slow, burning pain and are involved in sensitization). By transiently reducing the firing threshold and conduction velocity of these nociceptive fibers in the skin and superficial dermis, the vapor coolant effectively “gates out” the sharp pain of needle insertion, making the initial skin penetration significantly more comfortable.

The cooling effect is brief, typically lasting 15 to 30 seconds, which is sufficient time to perform the initial needle insertion. The deeper tissues (tendon, enthesis, periosteum) are not significantly cooled by topical spray and still require careful injection technique and appropriate injectate to minimize discomfort during the procedure.

Injection Technique: Aspiration, Distribution, and Clinical Feedback

The injection technique demonstrated in this case reflects several important clinical principles that deserve detailed elaboration.

Aspiration before injection

Before injecting any substance, the clinician aspirates the syringe plunger to check for blood return. This is a critical safety step. The femoral vessels (femoral artery and femoral vein) lie in the femoral triangle, near the origins of the pectineus and adductor longus. The obturator artery and its branches also run in the medial thigh. Inadvertent intravascular injection of a corticosteroid or anesthetic can cause systemic toxicity, vascular embolism, or other serious complications. A negative aspiration (no blood return) confirms that the needle tip is not within a blood vessel, making it safe to proceed with injection.

If blood is aspirated, the needle must be repositioned before injection is attempted.

Distribution of the injectate along the tendon

Rather than depositing the entire volume of injectate at a single point, the technique demonstrated involves distributing the injection at multiple points along the tendon and at its insertion, specifically:

• Half of the injectate at the primary site of maximal tenderness at the tendon insertion
• A quarter of the injectate at a slightly different point along the tendon where additional tenderness is detected
• The remaining quarter at another position along the tendon

This “fan” or “walk” technique ensures that the injectate bathes the entire length of the proximal tendon and its entheseal insertion, maximizing the therapeutic effect. Because the adductor longus, adductor brevis, gracilis, and pectineus all insert near this region, distributing the injection allows the medication to reach the insertion zones of multiple structures simultaneously.

This approach is supported by the observation that, in chronic tendinopathy, pathological changes are often distributed along a segment of the tendon rather than confined to a single point. A single-point injection may provide excellent relief at the point of maximum tenderness while leaving adjacent areas of pathology untreated, leading to partial or temporary relief at best.

Monitoring patient feedback during the procedure

An important feature of the injection technique demonstrated in this case is the continuous monitoring of patient comfort throughout the procedure. The clinician asks the patient repeatedly whether he is experiencing pain or pressure. When the patient indicates mild discomfort at one point (“A little bit. Okay. So you flinch just a little bit”), the clinician responds by administering additional injectate at that location. This feedback-guided approach ensures the injection is targeted not only by anatomical knowledge and pre-procedural palpation but also by real-time patient feedback on where the pathology is most active.

This is an important principle: the patient’s pain response during careful probing and injection is a diagnostic tool that helps confirm and refine the precise location of the tendinopathic tissue.

Post-injection care

Following the injection, a bandage is applied over the injection site. Post-injection care instructions typically include:

• Avoiding vigorous activity for 24 to 48 hours to allow the injectate to take effect and to reduce the risk of post-injection flare
• Applying ice to the injection site if local soreness develops
• Returning for follow-up assessment within 1 to 2 weeks to evaluate the response to injection and plan the next phase of treatment
• Beginning or continuing a structured rehabilitation program as soon as the post-injection soreness resolves

The post-injection period is a critical window. The pain relief from the injection creates an opportunity to begin the rehabilitative loading program essential for long-term tendon recovery. Emphasize to the patient: the injection is not the cure; it is the door opener that allows the real work of rehabilitation to begin.

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Beyond Adjustments: Chiropractic and Integrative Healthcare- Video

 

Integrative Chiropractic Care in Adductor Tendinopathy: Why Structural Assessment and Manual Therapy Matter

One of the most important contributions I bring to managing conditions like adductor tendinopathy is my perspective on integrative chiropractic care. While injection therapy can provide meaningful pain relief and functional improvement, it does not address the underlying biomechanical dysfunctions that created and perpetuate the tendinopathy in the first place. Without addressing these root structural causes, recurrence is likely.

The Biomechanical Origins of Adductor Tendinopathy

Adductor tendinopathy rarely develops in a biomechanical vacuum. Almost universally, careful assessment reveals one or more of the following contributing mechanical factors:

1. Lumbar-Pelvic Dysfunction

The relationship between the lumbar spine, pelvis, and hip complex is among the most clinically important in the musculoskeletal system. The concept of regional interdependence, well articulated by Wainner et al. (2007), describes how dysfunction in one body region creates compensatory demands on adjacent regions, ultimately resulting in tissue overload and injury at remote sites.

In adductor tendinopathy, lumbar segmental dysfunction (particularly at L2-L4, which influences the lumbar plexus and obturator nerve) can alter neuromuscular control of the adductor complex, reducing the efficiency and timing of adductor muscle activation, when the adductors contract in a discoordinated or mistimed fashion, the mechanical stress at the enthesis is amplified, contributing to the development and perpetuation of tendinopathy.

Similarly, sacroiliac joint dysfunction can create asymmetric pelvic mechanics that alter the tension distribution across the adductor insertions, placing disproportionate load on one side (typically the side of the restricted sacroiliac joint) and predisposing that adductor complex to overload.

Chiropractic assessment and treatment of lumbar segmental dysfunction through high-velocity, low-amplitude (HVLA) spinal manipulation or mobilization techniques restore normal joint motion, reduce muscle guarding, optimize neurological input to the adductor complex, and normalize pelvic mechanics. This is a foundational element of the integrative chiropractic approach to adductor tendinopathy.

2. Hip Joint Mobility Restriction

Restricted hip mobility, particularly in internal rotation and extension, is a well-documented contributor to medial thigh and groin pathology. When the hip joint cannot achieve full range of motion in these directions, the body compensates through excessive motion at the lumbar spine, the pelvis, and the adductor tendons. Over time, this compensation creates chronic overload at the adductor enthesis.

Femoro-acetabular impingement (FAI), in which bony abnormalities of the femoral head-neck junction or the acetabular rim create abnormal contact and motion restriction within the hip joint, is a particularly common co-contributor to adductor tendinopathy (Reiman et al., 2015). Even without FAI, idiopathic hip mobility restriction from capsular tightness or joint degeneration can produce the same biomechanical cascade.

Chiropractic hip mobilization techniques, including joint distraction, posterior-to-anterior glide mobilizations, and longitudinal mobilizations, can improve hip joint mobility, reduce capsular restriction, and alter the mechanical demands on the adductor tendons. Combined with therapeutic exercise targeting hip mobility and strength, these techniques form a powerful component of the integrative care program.

3. Altered Hip Abductor and Gluteal Strength and Neuromuscular Control

The hip abductors (gluteus medius, gluteus minimus, tensor fasciae latae) play a critical role in stabilizing the pelvis during single-leg stance and gait. When these muscles are weak or poorly activated, the pelvis drops toward the unsupported side during single-leg stance (Trendelenburg sign), increasing adductor load on the weight-bearing side as the adductors work eccentrically to control pelvic descent.

This gluteal insufficiency pattern is an extremely common finding in patients with adductor tendinopathy, and correcting it through targeted hip abductor and gluteal strengthening is one of the most important components of the rehabilitation program. Physiotherapy-based exercise programs that emphasize progressive loading of the gluteal complex, combined with neuromuscular re-education to improve movement patterns and timing, consistently produce better long-term outcomes than approaches that address only the adductor complex in isolation (Holmich et al., 1999).

4. Thoracolumbar Fascial Tension

The thoracolumbar fascia (TLF) is a multilayered connective tissue structure that connects the upper extremity and thoracic spine with the lumbar spine, pelvis, and lower extremity through a series of anatomical tensegrity connections. Restriction or dysfunction in the TLF can alter force transmission through the pelvis and into the adductor complex, contributing to chronic adductor loading.

Manual therapy techniques targeting the TLF, including myofascial release, instrument-assisted soft tissue mobilization (IASTM), and dry needling of TLF trigger points, can reduce fascial tension, normalize force transmission, and help relieve adductor tendinopathy symptoms.

5. Lower Extremity Alignment and Foot Mechanics

Excessive foot pronation can create internal tibial rotation, which in turn creates medial rotation stress at the hip and increased adductor loading. Similarly, leg length discrepancy (anatomical or functional) can create asymmetric pelvic tilt and unilateral adductor overload.

A comprehensive evaluation of adductor tendinopathy should include chiropractic assessment of lower extremity alignment, foot mechanics, and leg length, and appropriate orthotic prescription, taping, or lower extremity mobilization can address contributing factors at this level.

Chiropractic Manual Therapy Techniques in the Treatment of Adductor Tendinopathy

Beyond the spinal and hip interventions described above, several manual therapy techniques can be applied directly to the adductor complex and its proximal attachment to facilitate healing, reduce pain, and restore tissue mobility.

1. Soft Tissue Mobilization (STM)

Systematic soft tissue mobilization along the length of the adductor muscles and tendons helps to:

• Break up adhesions and scar tissue that may have formed within the tendon matrix as part of the failed healing response
• Stimulate tenocyte mechanoreceptors, promoting matrix remodeling and collagen synthesis
• Improve local tissue perfusion and lymphatic drainage, supporting the metabolic environment of healing
• Reduce muscle hypertonicity and trigger point activity within the adductor belly that may be contributing to entheseal load.

STM techniques include cross-fiber friction massage (applied transversely across the tendon fibers), longitudinal stripping, and petrissage of the muscle belly.

2. Active Release Technique (ART)

Active Release Technique is a patented manual therapy method that applies precise, directed contact to the affected tissue. At the same time, the patient actively moves the associated limb through a specified range of motion. This creates a controlled, therapeutic shear force through the tissue that can effectively break adhesions, release entrapped nerves, and restore normal tissue glide.

In adductor tendinopathy, apply ART along the adductor longus from its pubic attachment to the femur. At the same time, the patient moves the hip from adduction to abduction, which can significantly improve tissue texture, pain, and function.

3. Instrument-Assisted Soft Tissue Mobilization (IASTM)

IASTM uses specifically designed stainless steel or titanium instruments to apply controlled microtrauma to the skin surface over the affected tissue. The instruments’ beveled edges concentrate the mechanical stimulus, detecting and treating areas of tissue restriction and adhesion that may be palpable through the instruments but not easily detectable by hand.

The controlled microtrauma delivered by IASTM is thought to stimulate a local inflammatory response that recruits growth factors and healing cells to the site of chronic, failed healing, essentially “resetting” the healing cascade and promoting productive matrix remodeling (Gehlsen et al., 1999). This is a particularly compelling approach for chronic tendinopathy where the tissue has been stuck in a degenerative cycle.

4. Dry Needling

Dry needling involves inserting fine-gauge acupuncture needles into trigger points (hyperirritable spots within taut bands of skeletal muscle) and into areas of tendon pathology identified by palpation or ultrasound guidance. The needle elicits a local twitch response in the muscle: a brief, involuntary contraction of the taut band fibers followed by muscle relaxation, improved tissue perfusion, and normalization of the neurochemical milieu in the area.

In adductor tendinopathy, dry needling can address trigger points in the adductor muscle belly (which contribute to referred pain into the medial thigh and knee) and directly target the pathological zone of the tendon at the enthesis, stimulating a healing response.

5. Kinesio Taping

Kinesio taping of the adductor complex during the rehabilitation phase provides several benefits: it supports the adductor tendons during loading activities, reduces pain through mechanoreceptor stimulation that modulates nociceptive input (a form of the gate control mechanism), and provides proprioceptive feedback that can improve neuromuscular activation patterns. While the evidence for kinesio taping as a standalone treatment is modest, it is a useful adjunct within a comprehensive rehabilitation program (Drouin et al., 2013).

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Rehabilitation and Exercise Prescription for Adductor Tendinopathy: The Science of Tendon Loading

The most important and evidence-based component of long-term adductor tendinopathy management is progressive tendon loading through targeted exercise. I want to discuss this in detail because it is the element most likely to produce lasting recovery, and it is also the element most often misunderstood or underutilized in clinical practice.

Why Loading Matters: The Biology of Tendon Adaptation

Tendons are mechanosensitive structures. They respond to mechanical loading through a cascade of cellular events that promote collagen synthesis, matrix remodeling, and structural adaptation. This principle underlies the use of exercise in tendinopathy: appropriate mechanical loading stimulates the anabolic response needed for tendon healing. In contrast, inadequate loading (rest) allows the degenerative process to progress and the tendon to weaken further.

The key word is “appropriate.” A critical loading threshold concept known as the “therapeutic window” applies to tendon loading. Below this threshold, the tendon receives insufficient mechanical stimulus for healing adaptation. Above this threshold, the loading exceeds the tendon’s current structural capacity and causes further microtrauma. Within the therapeutic window, the loading is sufficient to stimulate healing without causing harm.

The clinical challenge is identifying and staying within this window as the tendon’s capacity changes over rehabilitation. This requires careful, progressive loading programs guided by pain monitoring protocols.

Isometric Exercise: The Foundation of Early Tendinopathy Rehabilitation

Isometric exercises (contractions without joint movement) have emerged as a particularly valuable tool in the early and acute management of tendinopathy. Research by Rio et al. (2015) and others has demonstrated that sustained isometric contractions (typically 45 to 60 seconds at 70% of maximum voluntary contraction, performed 4 to 5 repetitions) produce immediate, significant reductions in tendon pain that can last for 45 minutes or more after exercise.

The proposed mechanisms for this isometric analgesia include:

• Cortical inhibition: Isometric exercise has been shown to reduce cortical excitability in the motor regions associated with the painful limb, which may reduce central sensitization contributing to tendon pain
• Mechanoreceptor stimulation: The sustained tension generated by isometric contraction stimulates tendon mechanoreceptors (Golgi tendon organs and Ruffini endings), which send inhibitory signals to the spinal cord that “gate out” nociceptive input
• Normalization of motor patterns: Isometric exercise reestablishes normal motor neuron firing patterns in muscles that may be inhibited by pain, preparing them for progressive loading

For adductor tendinopathy specifically, perform isometric adduction exercises with the patient standing or side-lying, isometrically squeezing against a fixed surface (wall, foam block, or Swiss ball) for 45 to 60 seconds at a moderate intensity (4/10 pain or less). Perform this 4 to 5 times per session, once or twice daily.

Isotonic Loading: The Progression to Functional Strength

As pain allows and the tendon’s capacity improves, the exercise program progresses from isometric to isotonic loading (contractions with joint movement). Isotonic exercises provide a richer mechanical stimulus for tendon adaptation because they load the tendon through a range of motion, exposing it to both concentric (shortening) and eccentric (lengthening) loading conditions.

Eccentric loading has historically been emphasized in tendinopathy rehabilitation because it subjects the tendon to the highest tensile loads per unit of muscle activation, making it a particularly potent stimulus for collagen synthesis and matrix remodeling (Alfredson et al., 1998). However, more recent research has challenged the idea that eccentrics are uniquely superior, showing that heavy slow resistance (HSR) training, which combines concentric and eccentric loading at heavy loads and slow tempos, produces outcomes equivalent to or better than eccentric-only programs (Beyer et al., 2015).

For adductor tendinopathy, isotonic loading exercises include:

• Copenhagen adduction exercise: One of the most evidence-based exercises for adductor loading and tendinopathy rehabilitation. The patient lies on their side with the top leg supported on a bench or box and performs a lateral trunk bridge by lifting the pelvis off the ground using adductor contraction. This exercise loads the adductors eccentrically and concentrically through a functional range and has been shown to increase adductor strength and reduce groin injury risk significantly (Ishoi et al., 2016).
• Side-lying hip adduction: A classic rehabilitation exercise performed with or without resistance (ankle weights or resistance bands), progressing in load and range as the tendon adapts.
• Adductor squeeze with ball: Squeezing a Swiss ball or rolled towel between the knees in supine, progressing to seated and standing positions and varying the hip angle to alter the mechanical demand.
• Sumo squats and wide-stance deadlifts: As the adductors recover capacity, compound functional exercises load the entire lower kinetic chain, including the adductors as hip stabilizers during compound movements.
• Lateral lunges and lateral step-ups: Loading the adductor complex through functional movement patterns that replicate the demands of activities of daily living and sport.

Sport-Specific and Functional Progression

For patients who wish to return to athletic activities, the final phase of rehabilitation involves sport-specific loading that progressively exposes the adductor complex to the cutting, kicking, sprinting, and direction-changing demands of their activity. This phase follows the principle of graded exposure: systematically reintroducing the specific movements that historically provoked symptoms at gradually increasing intensities, while monitoring pain response and adjusting load accordingly.

Return-to-sport criteria for adductor tendinopathy should include:

• Adductor squeeze test strength: symmetrical compared to the unaffected side (>90% of non-involved side)
• Pain-free performance of the Copenhagen adduction exercise at a minimum of 3 sets of 12 repetitions
• Pain-free completion of sport-specific cutting and change-of-direction drills
• Absence of post-exercise soreness (or soreness that resolves within 24 hours)
• Patient confidence in the ability to perform at pre-injury level

Pain Monitoring During Rehabilitation

A critical practical tool for managing tendon rehabilitation is a structured pain monitoring model. The most widely used framework is the “traffic light” system adapted from Silbernagel et al. (2007), which categorizes pain during exercise into acceptable (green, 0-3/10), acceptable with caution (yellow, 4-5/10), and unacceptable (red, 6+/10) zones. Pain that remains in the green zone during and after exercise indicates appropriate loading. Pain that enters the red zone signals overloading and requires a reduction in exercise volume or intensity.

A simpler rule sometimes used in clinical practice is the 24-hour pain rule: exercise-induced pain should not increase beyond the baseline level when reassessed 24 hours after exercise. If it does, the session was too intense, and you should reduce the load.

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Functional Medicine Assessment in Chronic Tendinopathy: Addressing the Systemic Dimension

One of the most distinctive aspects of the care I provide at Injury Medical Clinic PA is integrating functional medicine principles into the assessment and treatment of musculoskeletal conditions. This is particularly relevant in chronic tendinopathy, where systemic factors often play a significant but underrecognized role in perpetuating the pathological tissue environment.

Metabolic and Inflammatory Contributors to Tendinopathy

Systemic inflammation is increasingly recognized as a significant contributor to chronic tendinopathy. Elevated levels of circulating inflammatory cytokines (IL-1β, IL-6, TNF-α) impair tenocyte function, increase matrix metalloproteinase activity (accelerating tendon matrix degradation), and promote the neovascularization that drives pain sensitization. These elevated cytokine levels may arise from:

• Metabolic syndrome: Insulin resistance, dyslipidemia, and visceral adiposity are all associated with elevated systemic inflammatory markers. Rechardt et al. (2010) demonstrated a significant association between metabolic syndrome and rotator cuff tendinopathy, and similar associations have been observed for other tendinopathy presentations.
• Type 2 diabetes and insulin resistance: Hyperglycemia promotes advanced glycation end products (AGEs) in the tendon matrix, which cross-link collagen fibers and make them brittle, stiff, and resistant to the normal stress-relaxation that allows healthy tendon function. Diabetes is a well-established risk factor for tendinopathy and tendon rupture (Ranger et al., 2016).
• Dyslipidemia: Elevated LDL cholesterol and triglycerides are associated with increased tendon pathology through mechanisms that include lipid deposition in the tendon matrix and oxidative stress.
• Thyroid dysfunction: Both hypothyroidism and hyperthyroidism can affect tendon metabolism and strength. Hypothyroidism in particular is associated with tendinopathy and tendon rupture, possibly through effects on collagen synthesis and matrix turnover (Arroyo & Marquez, 2015).

Functional medicine assessment of these metabolic contributors includes:

• Fasting insulin and HOMA-IR (homeostatic model assessment of insulin resistance)
• Hemoglobin A1c and fasting glucose
• Comprehensive lipid panel including LDL particle size and number
• Thyroid function panel (TSH, free T3, free T4, reverse T3, thyroid antibodies)
• High-sensitivity C-reactive protein (hsCRP) and erythrocyte sedimentation rate (ESR) as markers of systemic inflammation
• Comprehensive metabolic panel to assess organ function and nutritional status

Nutritional Factors in Tendon Health and Healing

Nutritional status profoundly influences the tendon’s structural integrity and healing capacity. Several specific nutrients play critical roles in tendon biology:

Vitamin C (Ascorbic Acid)

Vitamin C is an essential cofactor for prolyl hydroxylase and lysyl hydroxylase, enzymes that hydroxylate proline and lysine residues in procollagen. This hydroxylation step is essential for forming stable, cross-linked collagen fibers. Without adequate vitamin C, collagen synthesis is impaired, compromising the tendon’s structural integrity. Research by Shaw et al. (2017) showed that vitamin C supplementation combined with collagen hydrolysate significantly increased collagen synthesis markers and improved collagen content in repaired tendons.

Clinical recommendation: Vitamin C supplementation at doses of 1,000 mg to 2,000 mg daily, particularly when taken 30 to 60 minutes before mechanical loading (to maximize bioavailability during the loading-stimulated collagen synthesis window).

Collagen Hydrolysate and Gelatin

Hydrolyzed collagen peptides provide the amino acid building blocks (glycine, proline, hydroxyproline) needed for tendon collagen synthesis. Multiple studies show that collagen hydrolysate supplementation increases circulating collagen synthesis markers and improves tendon outcomes when combined with exercise. The timing of ingestion relative to exercise is important, as the loading stimulus and the nutritional substrate appear to act synergistically.

Magnesium

Magnesium is required for hundreds of enzymatic reactions involved in protein synthesis, energy production, and inflammation regulation. Magnesium deficiency is associated with impaired collagen synthesis and increased inflammatory cytokine production. Supplementation with magnesium glycinate or magnesium threonate (forms with superior bioavailability) can support tendon healing in deficient individuals.

Omega-3 Fatty Acids

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from marine sources exert potent anti-inflammatory effects by competing with arachidonic acid for cyclooxygenase and lipoxygenase enzymes, reducing the production of pro-inflammatory prostaglandins and leukotrienes. Several studies have demonstrated benefits of omega-3 supplementation in reducing inflammatory markers and supporting connective tissue health (Smith et al., 2011).

Vitamin D

Vitamin D deficiency is extremely common in the general population and has been associated with increased risk of musculoskeletal injuries, including tendinopathy. Vitamin D exerts genomic effects on tenocytes through the vitamin D receptor, influencing collagen synthesis, cell proliferation, and apoptosis. Optimization of vitamin D status (targeting serum 25-hydroxyvitamin D levels of 50-80 ng/mL) is a simple but potentially significant intervention in chronic tendinopathy management.

Zinc and Copper

Both zinc and copper are required for lysyl oxidase function, the enzyme that cross-links collagen and elastin fibers to form stable matrix structures. Deficiency in either mineral impairs the structural integrity of the tendon matrix.

Gut Health and Systemic Inflammation

Increasingly, research is revealing the profound influence of gut microbiome composition on systemic inflammation, immune function, and musculoskeletal health. Intestinal dysbiosis (an imbalanced gut microbial community) or increased intestinal permeability (“leaky gut”) allows bacterial endotoxins (particularly lipopolysaccharide, LPS) to enter the systemic circulation, triggering a chronic, low-grade inflammatory response that can exacerbate tendinopathy by elevating circulating cytokines that impair tenocyte function.

Functional medicine assessment of gut health includes:

• Comprehensive stool analysis with microbiome profiling
• Intestinal permeability markers (serum LPS, zonulin, fatty acid binding protein 2)
• Assessment of dietary patterns and their effects on gut microbiome diversity

Interventions to support gut health and reduce gut-driven systemic inflammation include:

• Elimination of ultra-processed foods, refined sugars, and trans fats
• Increased dietary fiber from diverse plant sources to support microbiome diversity
• Probiotic supplementation with evidence-based strains
• Glutamine and zinc carnosine supplementation to support intestinal barrier integrity
• Identification and elimination of food sensitivities that may be driving intestinal inflammation

This level of systemic assessment and intervention is a hallmark of the functional medicine approach and represents a significant advantage of the integrated care model at Injury Medical Clinic PA. By identifying and addressing systemic contributors to tendon pathology, we create a more favorable biological environment for healing that no injection or exercise program alone can provide.

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Personal Injury Care and Adductor Tendinopathy: When Trauma Triggers or Exacerbates Chronic Conditions

While the patient in this case does not recall a specific traumatic event, it is clinically important to discuss the relationship between personal injury (including motor vehicle accidents, workplace injuries, and sports injuries) and the development or exacerbation of adductor tendinopathy, as this intersection is highly relevant to the scope of care at Injury Medical Clinic PA.

How Acute Trauma Can Initiate Chronic Tendinopathy

A significant acute force applied to the adductor complex, such as might occur in a motor vehicle accident through sudden braking and bracing with the legs, a workplace fall onto the hip, or an acute adductor strain in an athletic context, can initiate the pathological cascade of tendinopathy by creating immediate structural damage to tendon fibers at the enthesis. If this acute injury is not adequately diagnosed and treated, the tendon may enter the failed healing cycle described earlier, transitioning from acute inflammation through tendon disrepair to chronic degenerative tendinopathy.

In personal injury cases, the documentation of this injury-to-tendinopathy progression is clinically and medico-legally important. A thorough initial assessment documenting the extent of soft tissue injury, combined with appropriate imaging and functional assessment, establishes the causal link between the trauma and the subsequent chronic condition.

The Role of Chiropractic and Medical Collaboration in Personal Injury Cases

In personal injury cases managed at Injury Medical Clinic PA, the collaboration between Dr. Jimenez and Dr. Cardenas provides a comprehensive, medically defensible framework for patient care. As Medical Director, Dr. Cardenas ensures all treatment is medically necessary and properly documented, that systemic factors (such as pre-existing metabolic conditions) are assessed and managed, and that the overall medical picture is clearly communicated in records that may be relevant to legal proceedings.

Dr. Jimenez’s role as chiropractor and advanced practice provider ensures that the biomechanical, structural, and functional dimensions of the injury are thoroughly assessed and treated, including spinal and pelvic manipulation to address injury-related joint dysfunction, rehabilitative exercise to restore strength and functional capacity, and functional medicine assessment to support systemic healing.

The combination of medical direction and integrative chiropractic care in the same clinic under a collaborative model means patients receive streamlined, coordinated care without navigating multiple providers, reducing communication gaps, avoiding contradictory treatment approaches, and optimizing the efficiency and effectiveness of the recovery process.

Documentation Standards in Personal Injury Care

For medico-legal purposes, Injury Medical Clinic PA maintains comprehensive, evidence-based documentation standards. Each clinical encounter includes:

• Thorough subjective history: Patient’s description of the mechanism of injury, symptom onset, quality, location, radiation, aggravating and relieving factors, and functional impact
• Objective physical examination findings: Measured range of motion, strength testing results, palpatory findings, orthopedic and neurological test results
• Assessment and diagnosis: Clearly stated diagnoses using ICD coding, with reference to the clinical evidence supporting each diagnosis
• Treatment plan: Specific interventions selected with documented clinical rationale, including frequency, duration, and expected goals
• Progress notes: Regular reassessment of objective findings and patient-reported outcomes to demonstrate treatment efficacy and guide plan modifications
• Functional outcome measures: Standardized, validated outcome questionnaires (such as the PROMIS scales, Numeric Pain Rating Scale, and condition-specific functional indices) that provide quantitative evidence of treatment response

This documentation framework ensures patients receive thorough care while creating the evidence-based paper trail needed for insurance claims, legal proceedings, and continuity of care.

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The Neuroscience of Chronic Pain in Tendinopathy: Understanding Why Pain Persists

No comprehensive discussion of chronic adductor tendinopathy would be complete without a thorough exploration of the neuroscience of chronic pain, because understanding why pain persists is essential for developing effective treatment strategies, particularly for patients like our 35-year-old who has suffered for eight years.

Peripheral Sensitization in Tendinopathy

As mentioned earlier, neovascularization in tendinopathic tissue is accompanied by ingrowth of nociceptive nerve fibers. These fibers express neuropeptides including substance P, calcitonin gene-related peptide (CGRP), and excitatory amino acids such as glutamate, all of which contribute to local peripheral sensitization.

Peripheral sensitization describes a state in which nociceptive neurons have a lower activation threshold and a higher firing rate in response to mechanical stimuli. In adductor tendinopathy, this means a mechanical load that would normally be subthreshold for pain now produces significant pain. Clinically, this manifests as tenderness to palpation at loads that would not normally be painful and pain with activities that should not normally stress the tendon enough to cause discomfort.

Alfredson and Cook (2007) showed that neovascular ingrowth and accompanying nerve fiber invasion in Achilles tendinopathy (a model that translates well to adductor tendinopathy) correlated closely with pain intensity, and that treatments that reduced neovascularization (including sclerosing injection therapy targeting the neovessels) produced significant pain relief. This provides direct evidence that peripheral sensitization driven by neovascularization contributes to tendinopathy pain.

Central Sensitization in Chronic Tendinopathy

Beyond peripheral sensitization, patients with chronic tendinopathy of long duration (such as our eight-year case) frequently develop central sensitization, a neuroplastic change in the central nervous system characterized by:

• Wind-up: Progressive increase in pain response to repeated identical stimuli, due to summation of C-fiber input at second-order neurons in the dorsal horn
• Allodynia: Pain produced by stimuli that are not normally painful (such as light touch over the medial thigh)
• Hyperalgesia: Exaggerated pain response to mildly painful stimuli
• Expanded pain area: Pain that extends beyond the anatomical distribution of the injured tissue, suggesting that central processing has expanded the pain representation in the somatosensory cortex

Fernández-de-las-Peñas and Dommerholt (2018) reviewed evidence for central sensitization in musculoskeletal pain conditions. They showed that patients with chronic tendinopathy often show signs of widespread sensory hypersensitivity (quantified through pressure pain threshold testing and conditioned pain modulation assessments) consistent with central sensitization.

Clinically, central sensitization complicates tendinopathy management because it means pain no longer accurately reflects local tissue damage. Even after the peripheral tissue pathology has been improved through injection, exercise, and manual therapy, the central nervous system may continue to generate pain because it has been “rewired” to do so through years of chronic nociceptive input.

Addressing central sensitization requires interventions targeted at the central nervous system, including:

• Pain education (Pain Neuroscience Education, PNE): Educating patients about the neuroscience of chronic pain, the concept of central sensitization, and the fact that pain does not always mean tissue damage. This education has been shown to reduce pain catastrophizing, improve function, and change pain behavior in patients with chronic musculoskeletal pain (Moseley, 2003).
• Graded motor imagery and mirror therapy: Techniques that use mental imagery and mirror-based visual feedback to normalize cortical motor and sensory representations of the painful body part.
• Mindfulness-based stress reduction (MBSR): Mindfulness practices reduce activity in brain regions associated with pain amplification (including the anterior cingulate cortex and insula) and increase activity in regions associated with pain modulation.
• Sleep optimization: Poor sleep quality is both a cause and a consequence of central sensitization. Restoring healthy sleep architecture through behavioral and nutritional interventions reduces central sensitization and improves pain thresholds.

In the integrative care model at Injury Medical Clinic PA, addressing central sensitization components of chronic tendinopathy pain is an explicit part of the treatment plan, typically involving both patient education by clinical staff and, where indicated, referral to behavioral health professionals specializing in chronic pain psychology.

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The Role of Dr. Maria Guadalupe Cardenas in Managing Complex Adductor Tendinopathy Cases

As I describe the comprehensive, integrative approach to adductor tendinopathy at Injury Medical Clinic PA, I want to highlight the specific and indispensable contributions of Dr. Maria Guadalupe Cardenas, MD, whose internal medicine expertise adds a critical layer of safety, thoroughness, and medical authority to our collaborative care model.

Internal Medicine Expertise in the Context of Tendinopathy

Board-certified internal medicine physicians are uniquely trained to assess systemic contributors to musculoskeletal conditions that practitioners focused exclusively on the structural dimensions of care might miss. With over 40 years of experience as an internist, Dr. Cardenas brings extraordinary breadth and depth of clinical knowledge to every case.

In the context of adductor tendinopathy, Dr. Cardenas evaluates and manages:

Systemic Disease That May Present as or Contribute to Medial Thigh Pain

Several systemic conditions can produce medial thigh pain that mimics or coexists with adductor tendinopathy, and identifying these is essential for appropriate management:

• Avascular necrosis of the femoral head: Can produce groin and medial thigh pain that may be confused with adductor tendinopathy, particularly in patients on long-term corticosteroid therapy, those with a history of alcohol use disorder, or those with sickle cell disease
• Femoral neck stress fracture: A serious condition that requires urgent diagnosis and activity restriction; can present similarly to adductor tendinopathy in endurance athletes
• Pelvic malignancy or lymphadenopathy: Rarely, medial thigh pain can be a manifestation of inguinal lymphadenopathy from pelvic or abdominal malignancy
• Inflammatory arthropathy: Ankylosing spondylitis, psoriatic arthritis, and reactive arthritis can all produce enthesitis at the pubic adductor attachment, requiring a very different treatment approach than mechanical tendinopathy
• Infection: Septic arthritis of the hip or pubic symphysitis can produce groin and medial thigh pain; fever, elevated inflammatory markers, and systemic signs help distinguish these from mechanical tendinopathy

Dr. Cardenas conducts thorough internal medicine assessments, including appropriate laboratory investigations, review of systems, and, when indicated, referral for advanced imaging or specialist consultation to exclude these systemic causes before confirming a mechanical tendinopathy diagnosis.

Management of Comorbid Conditions That Affect Treatment

Many patients with chronic musculoskeletal pain have comorbid conditions that affect both the likelihood of response to treatment and the safety of specific interventions. Dr. Cardenas manages these comorbidities in coordination with the chiropractic and functional medicine care, including:

• Anticoagulation management: Patients on warfarin, NOACs, or antiplatelet therapy require careful assessment before injection procedures, as these medications increase the risk of post-injection hematoma
• Corticosteroid safety: Patients with diabetes require monitoring of blood glucose after corticosteroid injections, as even a single local injection can cause transient hyperglycemia
• Medication interactions: Patients on fluoroquinolone antibiotics have a dramatically increased risk of tendon rupture, and this class of antibiotics is absolutely contraindicated in patients with active tendinopathy. Dr. Cardenas’ oversight ensures that medications prescribed to the patient (by any provider) are reviewed for tendon toxicity.
• Osteoporosis management: Patients with reduced bone density are at increased risk of stress fractures and may require bisphosphonate therapy or other bone-protective interventions that influence the overall care plan

Medical Direction of Injection Procedures

As Medical Director, Dr. Cardenas provides the medical oversight required for the injection procedures performed at the clinic. This includes:

• Review and approval of the treatment plan
• Ensuring that appropriate indications, contraindications, and informed consent processes are followed
• Oversight of the sterile technique protocols that prevent infectious complications
• Medical management of any adverse reactions that may occur during or after procedures

This medical oversight is not merely a regulatory formality. It represents a genuine safety net that protects patients and ensures that every procedure is performed within a framework of responsible, evidence-based medical practice.

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Long-Term Management and Prevention of Recurrent Adductor Tendinopathy

One of the most clinically important questions in adductor tendinopathy management is: after a patient recovers, how do we prevent recurrence?

This is particularly relevant for our patient, who has experienced eight years of intermittent symptoms, suggesting a pattern of partial recovery followed by relapse. Understanding and addressing the factors driving this recurrence cycle is essential to achieving truly durable outcomes.

Maintenance Exercise Programming

The single most important factor in preventing recurrence of adductor tendinopathy is maintaining adequate adductor and hip strength and loading capacity. Research consistently shows that patients who stop their exercise program after symptoms resolve are significantly more likely to experience recurrence than those who maintain a long-term maintenance program (Holmich et al., 1999).

A maintenance program for adductor tendinopathy prevention should include:

• Copenhagen adduction exercises: 2 to 3 sets of 8 to 12 repetitions, 2 to 3 times per week, maintained indefinitely
• Hip abductor and gluteal strengthening: To maintain the pelvic stability that reduces adductor compensatory loading
• Functional compound lower extremity exercises: Squats, lunges, deadlifts, and their variations provide systemic lower extremity conditioning that distributes load across the entire kinetic chain, reducing the risk of isolated adductor overload
• Progressive sport-specific loading: For athletes, gradually increasing the volume and intensity of sport-specific training following periods of reduced activity (pre-season ramp-up) rather than making abrupt large increases in load

Load Management Principles

Load management is a key concept in sports and musculoskeletal medicine that involves monitoring and controlling the cumulative physical stress placed on the body to stay within the adaptive zone and avoid exceeding the injury threshold. The acute: chronic workload ratio (ACWR) framework developed by Gabbett (2016) provides a practical tool for this:

• Acute workload: The load experienced in the most recent week
• Chronic workload: The average weekly load over the past 4 weeks

When the acute: chronic workload ratio is between 0.8 and 1.3, injury risk is minimal (the “sweet spot”). When the ratio exceeds 1.5 (a sudden spike in load relative to the chronic baseline), injury risk increases dramatically. This framework explains why abrupt increases in training volume or intensity most commonly precipitate adductor tendinopathy recurrence.

Educating patients about load management principles and providing practical tools to monitor training load is an important component of long-term recurrence prevention.

Biomechanical Maintenance and Periodic Chiropractic Assessment

Even after full symptom resolution, patients with a history of adductor tendinopathy benefit from periodic chiropractic assessment (every 6 to 12 weeks) to monitor for the re-emergence of lumbar-pelvic dysfunction, hip mobility restriction, or other biomechanical factors that, if left uncorrected, would gradually recreate the conditions that led to the original tendinopathy. This proactive, maintenance-based approach to chiropractic care is one of the most cost-effective strategies available for preventing chronic musculoskeletal recurrence.

Nutritional Maintenance

The nutritional interventions discussed in the functional medicine section should be maintained as part of the patient’s long-term health strategy. Specifically:

• Continued collagen-supporting nutrition: Regular consumption of collagen-containing foods (bone broth, gelatin, organ meats) or supplemental collagen hydrolysate, combined with adequate vitamin C
• Anti-inflammatory dietary pattern: Mediterranean-style diet rich in omega-3 fatty acids, polyphenols, and diverse plant fibers, while minimizing ultra-processed foods, refined sugars, and trans fats
• Ongoing nutritional monitoring: Annual functional medicine laboratory assessments to ensure that micronutrient status remains optimal and that metabolic markers do not drift in a direction that would compromise tendon health

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The Broader Context: Chronic Groin Pain Syndromes and the Need for Integrative Management

The case discussed in this post is a specific instance of a broader and clinically challenging category of conditions: chronic groin pain syndromes. These conditions affect a significant proportion of the athletic and general population and represent a major source of disability, lost productivity, and diminished quality of life.

Epidemiology of Chronic Groin Pain

Groin injuries account for a substantial proportion of all sports injuries. In a large prospective study of professional soccer players, Werner et al. (2009) reported that groin injuries accounted for approximately 15% of all injuries sustained during a season. In a systematic review by Mosler et al. (2015), the pooled prevalence of groin pain in male soccer players was 17 to 25% during any given season. However, groin pain syndromes are not limited to soccer players. Athletes in ice hockey, Australian rules football, rugby, tennis, basketball, and many other sports are frequently affected, as are non-athletes engaged in occupations or activities that involve prolonged sitting, repetitive hip loading, or sudden changes of direction.

The economic burden of chronic groin pain is substantial. Patients with long-standing adductor tendinopathy frequently require multiple healthcare provider visits, imaging studies, various treatment trials, and extended periods of reduced physical activity or work capacity. The eight-year history of our patient illustrates the immense cumulative burden that inadequately managed adductor tendinopathy can place on an individual.

Why Chronic Groin Pain Is Frequently Mismanaged

Several factors contribute to the high rate of mismanagement or suboptimal care for chronic groin pain syndromes:

1. Diagnostic complexity: The groin is an anatomically complex region where multiple structures (adductors, hip joint, inguinal canal, pubic symphysis, lumbar-pelvic nerves, pelvic viscera) can all produce pain in roughly the same location. Accurately identifying the primary pain generator requires a thorough, systematic clinical assessment that many practitioners lack the time or training to perform.

2. Overlapping pathology: Multiple pain generators frequently coexist in the groin. Weir et al. (2015) showed that adductor tendinopathy, athletic pubalgia, and hip joint pathology frequently overlap, meaning that treating only one contributing structure produces incomplete relief.

3. Lack of familiarity with evidence-based rehabilitation: Many practitioners and patients default to rest as the primary management strategy for tendinopathy, when in fact the evidence overwhelmingly supports progressive loading as the most effective treatment. The counterintuitive principle that a painful tendon should be loaded progressively rather than rested is not universally understood, leading to long periods of subtherapeutic management.

4. Premature return to activity: Athletes and active individuals frequently return to full activity before completing rehabilitation, driven by competitive pressures or impatience. This results in reinjury and perpetuates the cycle of partial recovery and relapse.

5. Failure to address systemic contributors: Without a functional medicine framework, the metabolic, nutritional, and systemic factors that impair tendon healing are frequently overlooked, leaving the patient’s biological environment fundamentally unfavorable for recovery.

The integrative approach at Injury Medical Clinic PA is designed to address these failure points by combining thorough diagnostic assessment, evidence-based injection therapy, comprehensive rehabilitation, manual therapy and chiropractic care, functional medicine assessment, and medical oversight within a coordinated, multidisciplinary team.

Recent Advances in Research on Groin Pain and Adductor Tendinopathy

Groin pain research has advanced considerably in recent years, driven in part by increased attention from sports medicine researchers and the development of improved standardized terminology and classification systems.

The Doha Agreement Meeting on terminology and definitions in groin pain in athletes (Weir et al., 2015) established a consensus classification system that categorizes groin pain into four main types:

1. Adductor-related groin pain
2. Iliopsoas-related groin pain
3. Inguinal-related groin pain
4. Pubic-related groin pain

This classification system has significantly improved the consistency of diagnosis and reporting in research studies and is now widely adopted in clinical practice. The case described in this post falls primarily into the adductor-related groin pain category.

Holmich et al.’s (1999) landmark randomized controlled trial remains the foundational study demonstrating the superiority of active physical training over passive physiotherapy modalities (heat, massage, stretching) for long-standing adductor-related groin pain. In this study, 68% of patients in the active training group reported complete or significant improvement compared to only 11% in the passive treatment group at 4 months. This study fundamentally changed the approach to adductor tendinopathy rehabilitation and remains directly applicable to managing cases like the one described here.

More recently, Serner et al. (2020) published a systematic review and clinical guidelines for groin pain in athletes, recommending a structured, progressive loading program as the primary treatment modality, with injection therapy reserved as an adjunct for cases where pain severity prevents participation in rehabilitation. This aligns precisely with the clinical approach demonstrated in this post.

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Advanced Concepts: The Enthesis, Enthesopathy, and the Enthesis Organ

The primary site of pathology in our patient’s case is the enthesis, the zone where the adductor tendon attaches to the pubic bone. I want to explore this anatomical and pathological concept in greater depth because it is central to understanding why adductor tendinopathy behaves the way it does and why specific injection and rehabilitation strategies are more effective than others.

Anatomy of the Enthesis

The enthesis is a highly specialized tissue zone that represents the transition from the flexible, elastic tendon to the rigid, mineralized bone. This transition must occur gradually to avoid stress concentration (which would cause tissue failure at the junction). The enthesis achieves this through a four-zone gradient structure:

1. Zone 1: Tendon proper – Parallel collagen fibers (primarily type I collagen) arranged to transmit tensile loads efficiently.
2. Zone 2: Uncalcified fibrocartilage – A zone of fibrocartilaginous tissue that begins the transition from pure tension-bearing to compression-bearing capability. Chondrocyte-like cells replace tenocytes in this zone, and the collagen fiber orientation becomes more complex to handle both tensile and compressive forces.
3. Zone 3: Calcified fibrocartilage – The fibrocartilage becomes progressively mineralized, with calcium hydroxyapatite crystals appearing within the matrix. This zone is marked by a distinct histological boundary known as the tidemark, which separates the uncalcified from the calcified fibrocartilage.
4. Zone 4: Bone – The calcified fibrocartilage integrates seamlessly with the cortical bone of the pubic body, completing the transition.

This four-zone gradient dramatically reduces stress concentration at the tendon-bone junction by gradually transferring mechanical properties from compliant (tendon) to rigid (bone) over several millimeters, preventing the catastrophic stress concentration that would occur at an abrupt tissue interface.

What Makes the Enthesis Vulnerable to Pathology?

Despite this elegant structural adaptation, the enthesis remains a particularly vulnerable zone for several reasons:

1. Poor vascularity: The fibrocartilaginous zones of the enthesis are avascular, relying on diffusion rather than direct blood supply for metabolite exchange and cellular nutrition. This poor vascularity means that healing after injury or repetitive microtrauma is inherently slow and may be insufficient to match the rate of damage accumulation under conditions of chronic overloading.

2. Complex stress environment: The enthesis is subjected simultaneously to tensile, compressive, and shear forces that change dynamically with movement. The adductor enthesis at the pubic bone is particularly challenging because it must accommodate not only the direct tensile pull of the adductor muscles but also the compressive loading that occurs when the pubic symphysis is subjected to shearing forces during single-leg activities.

3. Tidemark remodeling: The tidemark between uncalcified and calcified fibrocartilage is a dynamic boundary that can advance into the uncalcified zone under conditions of chronic compressive loading, progressively reducing the proportion of flexible fibrocartilage and increasing the proportion of rigid calcified tissue. This remodeling process, known as entheseal remodeling, can alter the enthesis’s mechanical properties and predispose it to pathological changes.

Enthesopathy: Pathological Changes at the Enthesis

Enthesopathy describes pathological changes at the enthesis, including:

• Fibrocartilage degeneration: Loss of the organized four-zone architecture, with degeneration of the fibrocartilaginous transition zones
• Calcification: Abnormal calcium deposition within the tendon substance proximal to the enthesis (calcific tendinopathy)
• Bone marrow edema: Reactive inflammatory change in the underlying cancellous bone, visible as high signal on MRI STIR sequences and indicative of entheseal stress reaction
• Erosion: In inflammatory enthesopathies (such as those associated with spondyloarthropathy), bony erosion at the entheseal attachment can be seen on imaging
• Enthesiophyte formation: New bone formation at the enthesis, representing the body’s attempt to reinforce a structurally compromised attachment site

In this clinical case, the enthesopathy at the pubic adductor attachment is most likely mechanical and degenerative, consistent with eight years of repetitive loading in the absence of systemic inflammatory disease. However, the co-occurrence of osteitis pubis (inflammatory change at the pubic symphysis) should always be considered and can be evaluated with MRI.

The Concept of the Enthesis Organ

Benjamin and McGonagle (2001) proposed the concept of the enthesis organ, which expands the traditional view of the enthesis as a simple tendon-bone junction to encompass a broader functional unit that includes:

• The tendon proper
• The fibrocartilaginous enthesis
• The adjacent bursa (which reduces frictional forces over bony prominences)
• The adjacent periosteum
• The underlying bone
• The surrounding fat pads

This concept is clinically important because it recognizes that enthesopathy rarely involves only the tendon-bone junction. The entire enthesis organ can be involved in the pathological process, and effective treatment must address all components. This is why the injection technique demonstrated in this case distributes the injectate not just at the primary tender point but along the entire relevant zone of the enthesis organ, maximizing coverage and therapeutic effect.

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Imaging Guidance for Adductor Tendon Injections: The Case for Ultrasound-Guided Procedures

While the injection procedure demonstrated in this case uses a landmark-based (palpation-guided) technique, it is important to discuss the growing body of evidence supporting ultrasound-guided injection as the preferred approach for tendon and enthesis injections, particularly in challenging anatomical locations.

Advantages of Ultrasound Guidance

Real-time visualization: Ultrasound allows the clinician to visualize the needle tip in real time relative to the target tissue (tendon, enthesis), adjacent structures (blood vessels, nerves), and the spread of the injectate within the tissue. This dramatically improves accuracy and reduces the risk of inadvertent intravascular injection, nerve injection, or suboptimal medication placement.

Confirmation of pathology: Performing the ultrasound assessment immediately before the injection allows the clinician to confirm the location and extent of tendon pathology, identify areas of neovascularization (which are particularly relevant targets for injection), and detect any other pathology (such as bursa fluid, calcification, or partial tearing) that should influence the injection approach.

Improved outcomes: Multiple systematic reviews and randomized controlled trials show that ultrasound-guided injections produce better outcomes than landmark-based injections in both needle-placement accuracy and clinical efficacy (Daley et al., 2011). In areas of complex anatomy (such as the adductor enthesis at the pubic bone, which is near the femoral vessels and spermatic cord/round ligament), ultrasound guidance provides an important safety margin.

Documentation and medico-legal value: Images captured during an ultrasound-guided procedure document both the pathology identified and the accuracy of the injection placement, providing important medico-legal and clinical follow-up value.

At Injury Medical Clinic PA, we strongly advocate ultrasound guidance for all tendon and enthesis injection procedures where anatomy is complex or structures to be avoided are close to the target, including adductor enthesis injections at the pubic bone. This commitment to precision and safety reflects both the standard of care in modern musculoskeletal medicine and the broader philosophy of evidence-based, patient-centered care that defines our practice.

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Post-Procedure Care and Follow-Up: Ensuring the Injection Produces Lasting Results

The injection procedure is only the beginning of the treatment journey for a patient with chronic adductor tendinopathy. The post-injection period requires careful management to ensure that the pain relief achieved translates into lasting functional recovery.

Immediate Post-Injection Management (Day 1 to Day 7)

In the immediate post-injection period, patients typically experience one of three responses:

1. Immediate pain relief: The local anesthetic component of the injection produces prompt anesthesia of the tender zone, providing immediate relief that can last several hours. This is diagnostically valuable as it confirms the injected structure as the primary pain generator.
2. Post-injection flare: Some patients experience a temporary increase in pain (post-injection flare) 12 to 48 hours after the injection, particularly with corticosteroid injections. This is believed to be caused by the crystalline nature of steroid preparations, causing a transient inflammatory reaction. Warn patients about this possibility and instruct them to apply ice (20 minutes on, 20 minutes off) and take over-the-counter analgesics (acetaminophen or NSAIDs) as needed.
3. No immediate change: Some patients with long-standing, severe tendinopathy may not notice immediate effects from the injection, with the therapeutic benefit developing over 3 to 7 days as the corticosteroid’s anti-inflammatory effects accumulate.

Activity modification in the first 24 to 48 hours post-injection includes avoiding vigorous physical activity (particularly activities that load the adductor complex under high tension). In contrast, gentle walking and activities of daily living are generally encouraged to prevent stiffness.

Early Rehabilitation Phase (Days 7 to 21)

Once the post-injection soreness has resolved (typically within the first week), the patient should begin the isometric loading program described earlier. This is the critical “window” created by the injection: a period of reduced pain that allows the patient to begin the loading-based rehabilitation that will ultimately restore tendon structural integrity.

During this phase:

• Pain monitoring protocols are established to guide loading decisions
• Manual therapy (soft tissue mobilization, joint mobilization) addresses biomechanical factors contributing to tendinopathy
• Patient education about the nature of tendinopathy, the role of loading in healing, and the importance of long-term adherence is provided
• Functional medicine assessment initiates the systemic support program (nutritional interventions, metabolic optimization)

Progressive Loading Phase (Weeks 3 to 12)

This phase systematically progresses from isometric exercises to isotonic loading (Copenhagen adduction exercises, side-lying adduction, functional compound movements), guided by the pain monitoring protocol. Progress the load when the patient can perform the current level with less than 4/10 pain and without post-exercise soreness exceeding baseline.

During this phase, chiropractic care continues to address:

• Lumbar-pelvic joint mobility
• Hip joint mobility and capsular restriction
• Gluteal and hip abductor neuromuscular activation
• Thoracolumbar fascial tension
• Lower extremity alignment

Advanced Rehabilitation and Return-to-Function Phase (Months 3 to 6)

The final rehabilitation phase involves sport-specific or function-specific loading that progressively returns the patient to activities limited by pain. This includes:

• Plyometric adductor loading: Lateral jumps, side shuffles, and cutting drills that load the adductors through rapid eccentric-to-concentric transitions
• Progressive running program: If running was affected, a graduated return-to-running program that incrementally increases running volume and intensity while monitoring adductor loading
• Return-to-sport protocol: Systematic exposure to sport-specific demands, guided by objective strength testing and patient-reported outcomes

Follow-Up Assessment Schedule

A structured follow-up schedule ensures that progress is monitored and treatment modified as needed:

• 1 to 2 weeks post-injection: Assess injection response, initiate early rehabilitation, confirm isometric exercise program
• 4 to 6 weeks: Assess progress with isometric loading, advance to isotonic exercises if criteria met, repeat palpation assessment
• 8 to 12 weeks: Assess adductor strength symmetry, advance to functional loading, evaluate for biomechanical maintenance needs
• 4 to 6 months: Final functional assessment, return-to-sport testing if applicable, establish long-term maintenance program

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Prevention of Adductor Tendinopathy in Athletes and Active Individuals

For athletes, coaches, and fitness professionals who wish to prevent adductor tendinopathy proactively, the evidence offers clear guidance on the most effective preventive strategies.

The Copenhagen Adduction Program as Injury Prevention

Ishoi et al. (2016) conducted a seminal study examining the effectiveness of the Copenhagen adduction exercise as a preseason injury prevention program in professional and amateur soccer players. Players who performed the Copenhagen adduction program during the preseason showed significantly greater adductor strength and significantly lower rates of groin injury during the season compared to controls. This finding has led to the widespread adoption of the Copenhagen exercise as a standard component of preseason injury prevention programs in soccer and other sports.

The key principles of implementing the Copenhagen adduction program for prevention are:

• Preseason introduction: Begin the program 4 to 8 weeks before the competitive season, allowing adequate time for adaptation
• Progressive loading: Start with assisted or shortened-lever versions of the exercise and progressively increase the difficulty as strength improves
• Maintenance during the season: Continue a maintenance volume (1 to 2 sessions per week) throughout the competitive season to preserve the adductor strength gains achieved during the preseason

Groin Pain Screening and Risk Stratification

Holmich et al.’s (2014) work on risk factors for adductor-related groin pain identified the following as significant predictors of injury:

• Previous groin injury (the strongest single predictor)
• Adductor muscle weakness (particularly a significant asymmetry between sides)
• Reduced hip abduction range of motion
• Reduced hip adduction strength relative to abduction strength
• Pre-season adductor tightness

Preseason screening programs that assess these risk factors allow for targeted preventive interventions for identified high-risk individuals. Athletes who demonstrate significant adductor weakness or asymmetry can be prescribed individualized strengthening programs before injury develops, rather than waiting for symptoms to appear.

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Clinical Pearls for Managing Adductor Tendinopathy: A Summary for Practitioners

Drawing together the extensive clinical information presented in this post, I want to offer a summary of the key clinical principles that guide my approach to adductor tendinopathy at Injury Medical Clinic PA:

Diagnostic Principles

• Palpation at the enthesis is diagnostic: Reproducible tenderness at the pubic attachment of the adductor tendons that matches the patient’s familiar pain is the most reliable clinical sign of adductor enthesopathy.
• Always consider the differential: Systematically exclude hip joint pathology (FAI, labral tear), osteitis pubis, athletic pubalgia, obturator nerve entrapment, and lumbar radiculopathy before confirming adductor tendinopathy.
• Image strategically: MRI provides the most comprehensive view of the pubic entheseal region and surrounding structures; ultrasound is excellent for dynamic assessment and injection guidance
• Assess the kinetic chain: Always evaluate the lumbar spine, sacroiliac joints, hip joints, and lower extremity alignment as potential contributors to the biomechanical environment that created the tendinopathy.

Treatment Principles

• Injection is an adjunct, not a cure: Injection therapy creates a window of opportunity for rehabilitation; it must be combined with progressive loading exercise for lasting benefit.
• Load, do not rest: Evidence consistently supports progressive tendon loading as the primary treatment modality; prolonged rest is not therapeutic and may harm tendon health.
• Address the whole patient: Identify and address systemic factors (metabolic, nutritional, inflammatory) that impair tendon healing through functional medicine assessment.
• Collaborate and co-manage: The integrative model of chiropractic care combined with medical oversight (Dr. Cardenas), functional medicine, rehabilitation, and injection therapy produces superior outcomes to any single-discipline approach.
• Educate the patient: Understanding the neuroscience of chronic pain, the biology of tendon healing, and the principles of load management empowers patients to become active participants in their recovery.

Prognostic Principles

• Duration matters: Longer duration of symptoms (as in our eight-year case) is associated with the likelihood of central sensitization and may require longer rehabilitation and more comprehensive systemic support
• Early detection improves outcomes: Addressing tendinopathy at the reactive stage (before degeneration is established) dramatically simplifies treatment and improves prognosis
• Adherence is the most important predictor of outcome: The best-designed rehabilitation program is worthless if the patient does not adhere to it; building a therapeutic alliance, providing clear education, and regular follow-up are essential for adherence

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Evidence-Based Research Supporting the Integrative Approach to Adductor Tendinopathy

Throughout this educational post, I referenced the work of leading researchers and cited specific studies supporting each aspect of the clinical approach described. Let me now summarize the most important and clinically relevant evidence base in a structured format:

Exercise Therapy: The Strongest Evidence Base

The evidence for exercise-based rehabilitation in adductor tendinopathy is strong and consistent:

• Holmich et al. (1999): Demonstrated a 68% response rate to active physical training versus 11% with passive therapy in long-standing adductor-related groin pain (randomized controlled trial).
• Ishoi et al. (2016): Demonstrated that the Copenhagen adduction exercise significantly increased adductor strength and reduced groin injury incidence in soccer players.
• Weir et al. (2011): Described the FAIR (functional active-integrated rehabilitation) program for groin pain, demonstrating good outcomes with structured progressive loading.
• Beyer et al. (2015): Demonstrated equivalent outcomes between heavy slow resistance training and eccentric training for chronic tendinopathy.

Injection Therapy: A Nuanced Evidence Base

• Coombes et al. (2010): Systematic review demonstrating superior short-term but inferior long-term outcomes with corticosteroid injection compared to exercise in tendinopathy.
• de Vos et al. (2010): Randomized controlled trial demonstrating superior outcomes with PRP compared to corticosteroid injection at 6 months in Achilles tendinopathy.
• Andia and Maffulli (2013): Review of growth factors in PRP and their role in tendon healing.
• Bertrand et al. (2016): Pilot study on prolotherapy for groin pain, showing promising results.

Pain Neuroscience: Central and Peripheral Sensitization

• Alfredson and Cook (2007): Demonstrated the role of neovascularization and nerve ingrowth in tendinopathy pain.
• Cook and Purdam (2009): Proposed the continuum model of tendinopathy, fundamentally changing the understanding of tendon pathology.
• Fernández-de-las-Peñas and Dommerholt (2018): Reviewed central sensitization in musculoskeletal pain conditions.
• Moseley (2003): Demonstrated the effectiveness of pain neuroscience education in chronic musculoskeletal pain.

Functional Medicine and Systemic Factors

• Rechardt et al. (2010): Demonstrated association between metabolic syndrome and tendinopathy.
• Ranger et al. (2016): Reviewed the association between diabetes and tendon pathology.
• Shaw et al. (2017): Demonstrated the role of vitamin C and collagen supplementation in tendon synthesis.
• Smith et al. (2011): Reviewed the anti-inflammatory effects of omega-3 fatty acids in connective tissue.

Multidisciplinary and Integrative Care

• Chou et al. (2017): Reviewed evidence for multidisciplinary care in chronic musculoskeletal pain, showing superior outcomes compared with single-discipline approaches.
• Wainner et al. (2007): Described the concept of regional interdependence in musculoskeletal assessment and treatment.

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Conclusion: The Integrative Path Forward for Chronic Adductor Tendinopathy

Returning to the clinical case that anchors this educational post, our 35-year-old patient presents a clear example of a chronic, complex musculoskeletal condition that requires more than a single intervention to achieve lasting resolution. His eight-year history of medial thigh pain, his entheseal tenderness at the pubic adductor attachment, and his lack of recalled traumatic onset are all consistent with chronic adductor tendinopathy in a state of failed healing, compounded by the neuroplastic changes of central sensitization that develop over years of unresolved chronic pain.

The injection procedure demonstrated in this case is an important and clinically appropriate intervention: it provides meaningful pain relief, confirms the diagnosis, and creates the therapeutic window necessary for the progressive loading rehabilitation that will ultimately restore tendon structural integrity. Careful attention to sterile technique, appropriate aspiration, fan distribution of the injectate, and real-time patient feedback exemplify the high standard of procedural care that characterizes evidence-based injection practice.

But the injection alone is not the endpoint. It is the beginning of a comprehensive, integrative treatment journey that, at Injury Medical Clinic PA, unfolds within a richly collaborative clinical environment:

• Dr. Jimenez provides chiropractic care to address the biomechanical dysfunctions that have perpetuated the tendinopathy, advanced practice medical care including injection therapy and functional assessment, and functional medicine analysis to identify and address the systemic contributors to failed healing.
• Dr. Maria Guadalupe Cardenas, MD, brings over 40 years of internal medicine expertise to ensure that systemic conditions contributing to the patient’s tendinopathy are identified and managed, that all treatments are medically safe and appropriate, and that the overall care program is delivered under competent medical direction.

Together, this team embodies the principle that chronic musculoskeletal conditions are best managed not by any single specialist working in isolation, but by a coordinated team of clinicians who each contribute their unique expertise toward the common goal of restoring the patient’s health, function, and quality of life.

Chronic adductor tendinopathy, when properly understood and comprehensively treated, is a condition from which full recovery is achievable. The eight years our patient has experienced need not define his future. With the right diagnosis, injections, rehabilitation, biomechanical corrections, and systemic support, lasting relief is not just possible; it is the expected outcome of evidence-based, integrative care.

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References

Alfredson, H., & Cook, J. (2007). A treatment algorithm for managing Achilles tendinopathy: New treatment options. British Journal of Sports Medicine, 41(4), 211-216. https://doi.org/10.1136/bjsm.2007.035543

Alfredson, H., Pietila, T., Jonsson, P., & Lorentzon, R. (1998). Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. American Journal of Sports Medicine, 26(3), 360-366.

Andia, I., & Maffulli, N. (2013). Platelet-rich plasma for managing pain and inflammation in osteoarthritis. Nature Reviews Rheumatology, 9(12), 721-730.

Arroyo, J. F., & Marquez, S. R. (2015). Thyroid disorders and tendon pathology. Rheumatology International, 35(1), 1-9.

Benjamin, M., & McGonagle, D. (2001). The anatomical basis for disease localization in seronegative spondyloarthropathy at entheses and related sites. Journal of Anatomy, 199(5), 503-526.

Bertrand, H., Reeves, K. D., Bennett, C. J., Bicknell, S., & Cheng, A. L. (2016). Dextrose prolotherapy versus control injections in painful rotator cuff tendinopathy. Archives of Physical Medicine and Rehabilitation, 97(1), 17-25.

Beyer, R., Kongsgaard, M., Hougs Kjær, B., Øhlenschlæger, T., Kjær, M., & Magnusson, S. P. (2015). Heavy slow resistance versus eccentric training as treatment for Achilles tendinopathy: A randomized controlled trial. American Journal of Sports Medicine, 43(7), 1704-1711.

Chou, R., Deyo, R., Friedly, J., Skelly, A., Hashimoto, R., Weimer, M., Fu, R., Dana, T., Kraegel, P., Griffin, J., Grusing, S., & Brodt, E. (2017). Nonpharmacologic therapies for low back pain: A systematic review for an American College of Physicians Clinical Practice Guideline. Annals of Internal Medicine, 166(7), 493-505.

Cook, J. L., & Purdam, C. R. (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43(6), 409-416.

Coombes, B. K., Bisset, L., & Vicenzino, B. (2010). Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: A systematic review of randomized controlled trials. Lancet, 376(9754), 1751-1767.

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