Tendinitis and Bursitis

1. Introduction

Tendinitis and bursitis represent prevalent musculoskeletal disorders characterized by localized inflammation of tendons and bursae, respectively. These conditions are significant contributors to pain, functional impairment, and healthcare utilization across diverse patient populations. While often discussed concurrently due to overlapping anatomical proximity and clinical presentation, they involve distinct structures within the musculoskeletal system. A comprehensive understanding of their pathophysiology, diagnostic criteria, and therapeutic management is essential for clinical practice, particularly in primary care, orthopedics, rheumatology, and sports medicine.

The historical understanding of these conditions has evolved from vague descriptions of “rheumatism” to a more precise delineation of specific anatomical structures. The advent of advanced imaging modalities, such as high-resolution ultrasound and magnetic resonance imaging, has refined diagnostic accuracy and illuminated the underlying pathological processes. In pharmacological contexts, the management of tendinitis and bursitis serves as a fundamental application for several major drug classes, including nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and analgesics, making their study directly relevant to therapeutic decision-making.

Learning Objectives

• Differentiate the anatomical structures, pathophysiological mechanisms, and clinical features of tendinitis and bursitis.
• Analyze the pharmacological rationale for using NSAIDs, corticosteroids, and other therapeutic agents in managing inflammation and pain associated with these conditions.
• Evaluate the evidence-based non-pharmacological and pharmacological treatment strategies, including the risks and benefits of interventional procedures like corticosteroid injections.
• Apply knowledge of tendinopathy and bursitis to develop appropriate patient-specific management plans within clinical case scenarios.
• Critically assess the role of emerging therapies and the limitations of current pharmacological approaches in promoting tissue healing.

2. Fundamental Principles

The foundational principles of tendinitis and bursitis rest upon a clear understanding of the involved anatomical structures and the biological response to injury or overuse.

Core Concepts and Definitions

Tendinitis is clinically defined as a symptomatic condition characterized by pain and impaired function, historically attributed to inflammation of a tendon and its surrounding paratenon. Contemporary evidence suggests that the pathology in chronic overuse tendon pain is more accurately described as a failed healing response, often termed tendinosis, which is characterized by collagen disorganization, increased non-collagenous matrix, and neovascularization, with a notable absence of inflammatory cells. The term tendinopathy is a broader, non-specific descriptor encompassing both painful inflammatory (tendinitis) and degenerative (tendinosis) conditions of the tendon.

Bursitis refers to the inflammation of a bursa, which is a synovium-lined, fluid-filled sac strategically located to reduce friction between adjacent moving structures such as tendons, muscles, and bones. True bursitis involves a clear inflammatory response within the bursal lining, often resulting in fluid accumulation (effusion).

Theoretical Foundations

The theoretical framework for these conditions integrates concepts from biomechanics, cell biology, and inflammation science. The primary etiological model is repetitive microtrauma or overload that exceeds the tissue’s adaptive capacity. This leads to a cycle of matrix breakdown, attempted repair, and, in cases of persistent insult, pathological remodeling. The pain mechanism is multifactorial, potentially involving biochemical mediators (e.g., glutamate, substance P), mechanical stimulation of neovessels and nerves (angiofibroblastic hyperplasia), and increased intratendinous pressure.

Key Terminology

• Enthesis: The site of tendon or ligament insertion into bone.
• Paratenon: The loose areolar connective tissue sheath surrounding tendons not enclosed within a synovial sheath.
• Tenosynovitis: Inflammation of the synovial sheath surrounding a tendon.
• Calcific Tendinitis: A condition characterized by the deposition of hydroxyapatite calcium crystals within a tendon, often the supraspinatus, which can cause acute inflammatory episodes.
• Adhesive Capsulitis: Often associated with subacromial bursitis, this is a condition of the shoulder joint capsule characterized by pain and global stiffness.

3. Detailed Explanation

The detailed pathophysiology, risk factors, and clinical manifestations of tendinitis and bursitis require systematic exploration.

Pathophysiology of Tendinopathy

The traditional view of tendinitis as a purely inflammatory condition has been revised. The pathological continuum is often described in three overlapping stages, though progression is not always linear.

1. Reactive Tendinopathy: This is a non-inflammatory, short-term adaptive thickening of the tendon in response to acute overload. It involves increased production of proteoglycans and water content within the matrix, leading to a reversible swelling that may protect the tendon from rupture.
2. Tendon Dysrepair (Failed Healing): With continued excessive loading, the attempted repair process becomes dysregulated. There is increased cellularity, prominent collagen disorganization (loss of the normal parallel fiber alignment), and significant production of non-collagenous matrix (proteoglycans and glycosaminoglycans). Neovascularization and associated nerve ingrowth (neoinnervation) often occur at this stage, which are thought to contribute to pain.
3. Degenerative Tendinopathy (Tendinosis): This late stage is characterized by areas of cell death, marked matrix disorganization, lipid accumulation, and calcification. The tendon is mechanically compromised and at higher risk for partial or complete rupture. Inflammatory cells are typically absent unless there is an acute tear or concomitant bursal involvement.

Acute inflammatory infiltrates may be present in paratenonitis (inflammation of the outer sheath) or in specific conditions like calcific tendinitis during the resorptive phase, when macrophages phagocytose calcium deposits.

Pathophysiology of Bursitis

Bursitis typically results from one of four mechanisms: acute trauma, chronic friction or pressure (overuse), systemic inflammatory disease (e.g., rheumatoid arthritis, gout), or infection (septic bursitis). The inflammatory cascade within the bursal synovium leads to vasodilation, increased vascular permeability, and cellular infiltration by neutrophils and later monocytes/macrophages. This results in bursal effusion, synovial hyperplasia, and pain. Chronic bursitis may lead to bursal wall thickening, adhesion formation, and, in some cases, villous proliferation.

Common Anatomical Sites

The prevalence of these conditions is highest in regions subject to repetitive motion or pressure.

Factors Affecting the Process

The development and progression of tendinopathy and bursitis are influenced by a complex interplay of intrinsic and extrinsic factors.

4. Clinical Significance

The clinical significance of tendinitis and bursitis extends beyond their high prevalence to their impact on patient quality of life, functional capacity, and the healthcare system. They serve as common models for applying principles of musculoskeletal pharmacotherapy.

Relevance to Drug Therapy

Pharmacological management is primarily symptomatic, aimed at reducing pain and modulating the local inflammatory environment to facilitate rehabilitation. The choice of agent is guided by the presumed underlying pathology (inflammatory vs. degenerative), acuity, severity, and patient comorbidities. The mainstay systemic therapies include oral NSAIDs and analgesics. Topical formulations, particularly NSAIDs, offer a favorable risk-benefit profile for localized conditions. Injectable corticosteroids represent a potent interventional option for bursitis and paratenonitis, but their use in intratendinous pathology is controversial due to potential detrimental effects on tendon structure and strength.

Practical Applications and Therapeutic Goals

The overarching therapeutic goals are pain relief, preservation or restoration of function, and prevention of recurrence. Pharmacotherapy is rarely used in isolation; it is typically integrated into a multimodal management plan that includes activity modification, physical therapy (eccentric strengthening is a cornerstone for tendinopathy), and biomechanical corrections. The practical application of drugs must consider the treatment phase. In the acute inflammatory phase (more common in bursitis or acute paratenonitis), anti-inflammatory agents may be more directly relevant. In the chronic degenerative phase of tendinosis, analgesics may be preferred to control pain during loading exercises that are essential for stimulating tendon remodeling and strengthening.

Clinical Examples of Pharmacological Relevance

• Acute Calcific Shoulder Tendinitis: This condition often presents with severe inflammatory pain. NSAIDs are frequently employed for their analgesic and anti-inflammatory effects during the painful resorptive phase. A subacromial corticosteroid injection may provide significant short-term pain relief to allow participation in physical therapy.
• Chronic Achilles Tendinosis: The primary pathology is degenerative. While NSAIDs may be used for short-term pain control, their long-term use is not supported for altering disease progression. Pain management with simple analgesics like acetaminophen during the initiation of eccentric heel-drop exercises is a common strategy.
• Olecranon Bursitis: Management depends on etiology. For aseptic inflammatory bursitis, aspiration of fluid combined with an intrabursal corticosteroid injection can be highly effective. If infection is suspected (septic bursitis), aspiration for culture is diagnostic, and therapy shifts entirely to appropriate antibiotics, with NSAIDs used adjunctively for symptom control.

5. Clinical Applications and Examples

The integration of diagnostic reasoning and therapeutic principles is best illustrated through clinical scenarios.

Case Scenario 1: Lateral Epicondylopathy

A 45-year-old right-handed office worker presents with a 4-month history of gradually worsening pain over the lateral aspect of the right elbow. The pain is exacerbated by gripping objects, lifting a coffee cup, and using a computer mouse. Physical examination reveals tenderness directly over the lateral epicondyle and pain reproduced with resisted wrist extension. There is no swelling or erythema.

Diagnostic Considerations: The clinical presentation is classic for lateral epicondylopathy, likely in the tendon dysrepair or degenerative stage given the chronicity. Imaging is not routinely required but ultrasound could confirm tendon thickening, hypoechogenicity, and neovascularization.

Pharmacological and Therapeutic Approach:

1. First-Line Pharmacotherapy: A topical NSAID gel (e.g., diclofenac sodium 1%) applied to the lateral epicondyle three times daily for two weeks is recommended. This provides localized analgesia with minimal systemic exposure.
2. Adjunctive Oral Therapy: If pain is severe, a short course (5-7 days) of an oral NSAID like naproxen 500 mg twice daily could be considered, with appropriate gastroprotective counseling given the patient’s age.
3. Interventional Option: If pain persists after 6-8 weeks of conservative care (including physical therapy with eccentric exercises), a percutaneous needle tenotomy or platelet-rich plasma (PRP) injection might be considered. The role of corticosteroid injection is debated; while it may provide superior short-term (≈6 week) pain relief compared to physiotherapy alone, evidence suggests poorer intermediate-term outcomes and higher recurrence rates, potentially due to inhibitory effects on tenocyte activity and collagen synthesis.

Case Scenario 2: Septic vs. Aseptic Olecranon Bursitis

A 60-year-old male with a history of gout presents with 2 days of painful swelling and redness over the tip of his left elbow. He reports no recent trauma but recalls a minor scratch in the area a week prior. The bursa is warm, fluctuant, and exquisitely tender. He is afebrile.

Diagnostic Considerations: The acute presentation with overlying skin compromise (scratch) raises strong suspicion for septic bursitis, though gouty bursitis is also possible. The critical pharmacological distinction hinges on accurate diagnosis.

Pharmacological and Therapeutic Approach:

1. Diagnostic Procedure: Aspiration of the bursal fluid is mandatory. Fluid should be sent for Gram stain, culture, cell count, and crystal analysis.
2. Management if Septic: Empirical oral antibiotic therapy covering Staphylococcus aureus (e.g., cephalexin) is initiated pending culture results. NSAIDs (e.g., indomethacin) can be used adjunctively for pain and inflammation. The bursa should be re-aspirated if it re-accumulates. Intra-bursal corticosteroid injection is absolutely contraindicated.
3. Management if Aseptic (Gouty): Therapy is directed at the crystal arthropathy. First-line treatment includes oral NSAIDs (e.g., naproxen), colchicine, or oral corticosteroids. Once the acute inflammatory episode resolves, urate-lowering therapy (e.g., allopurinol) for gout prophylaxis may be indicated. A corticosteroid injection into the bursa could be considered if oral agents are contraindicated or ineffective.

Application to Specific Drug Classes

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): NSAIDs exert their effects by inhibiting cyclooxygenase (COX) enzymes, thereby reducing the synthesis of prostaglandins (PGs), which are key mediators of pain, vasodilation, and edema. Their role in tendinopathy is primarily analgesic. Concerns exist that by inhibiting PG production, which may have anabolic signaling roles in connective tissue, NSAIDs could potentially impair long-term tendon healing, though clinical evidence for this is inconclusive. Their use in bursitis, where inflammation is more central, is well-supported.

Corticosteroids (Glucocorticoids): These potent anti-inflammatory agents work via genomic and non-genomic pathways to suppress the expression of pro-inflammatory cytokines, inhibit phospholipase A2, and reduce vascular permeability. When injected into a bursa or peritendinous space, they can rapidly reduce inflammation and pain. However, repeated intratendinous injections are associated with risks including tendon atrophy, collagen necrosis, and potential rupture. Therefore, their use is generally restricted to peritendinous applications for short-term symptom control in tendinopathy and as a primary treatment for bursitis.

Analgesics (Acetaminophen, Topical Agents): Acetaminophen is a central-acting analgesic with minimal peripheral anti-inflammatory activity. It is useful for pain management when NSAIDs are contraindicated. Topical counterirritants (e.g., capsaicin) work by depleting substance P from sensory nerve endings, inducing a localized desensitization. Topical NSAIDs offer the benefit of local drug delivery with low systemic concentrations, minimizing gastrointestinal and cardiovascular risks.

6. Summary and Key Points

• Tendinitis (more accurately, tendinopathy) and bursitis are common, often overlapping, but distinct musculoskeletal disorders involving tendons and bursae, respectively.
• The pathophysiology of chronic tendinopathy is predominantly degenerative (tendinosis), characterized by collagen disorganization and failed healing, rather than a pure inflammatory process. Acute inflammation may be present in paratenonitis, calcific tendinitis, or bursitis.
• Etiology is multifactorial, involving a combination of intrinsic (e.g., age, genetics, metabolism) and extrinsic (e.g., overuse, biomechanics) factors.
• Diagnosis is primarily clinical, based on history and targeted physical examination. Imaging (ultrasound, MRI) is reserved for atypical presentations or to guide interventions.
• Pharmacological management is symptom-focused and adjunctive to core physical therapies (e.g., eccentric exercise for tendinopathy).
• NSAIDs are effective for analgesia and reducing inflammation in bursitis; their role in chronic tendinosis is primarily for short-term pain control.
• Corticosteroid injections can provide effective short-term relief for bursitis and peritendinous pain but should be used judiciously, with caution regarding intratendinous placement due to risks of tissue weakening and rupture.
• Treatment must be etiology-specific, particularly in distinguishing septic from aseptic bursitis, as management differs fundamentally (antibiotics vs. anti-inflammatories).
• Emerging biological therapies (e.g., platelet-rich plasma, prolotherapy) are areas of active investigation but lack consistent high-level evidence to support routine use over established rehabilitative protocols.

Clinical Pearls

• The presence of warmth, erythema, and systemic symptoms should always prompt consideration of infection (septic bursitis) or an acute inflammatory crystalline arthropathy.
• For chronic mid-portion Achilles or patellar tendinopathy, a structured eccentric loading program remains the cornerstone of evidence-based treatment, with pharmacotherapy playing a supportive role in pain management.
• When considering a corticosteroid injection for shoulder pain, targeting the subacromial bursa (for impingement/bursitis) rather than the rotator cuff tendon itself may mitigate the risk of iatrogenic tendon damage.
• Patient education regarding activity modification, biomechanics, and the expected prolonged timeline for recovery from chronic tendinopathy (often 3-6 months) is crucial for adherence and realistic expectations.
• Pharmacists play a key role in counseling patients on the appropriate use, dosing, potential adverse effects (e.g., GI bleeding with NSAIDs, skin atrophy with topical steroids), and drug interactions of medications used for these conditions.

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