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## Meet the editor

Nahum Rosenberg, MD, Ph.D., MOrthop, MBA, FRCS, is an orthopedic consultant surgeon with more than 30 years of experience. He graduated with an MD from the Faculty of Medicine, Technion Israel Institute of Technology (Technion-IIT) in 1990. He obtained a Ph.D. from the University of Portsmouth, UK. He completed his residency in orthopedic surgery at Rambam Medical Center, Israel, in 1997. Dr. Rosenberg has devoted a

great deal of time to basic research, which helped him earn a MOrthop (Distinct) degree from Tel Aviv University, Israel, in 1996. Between 1998 and 1999, he was appointed as a Nuffield Fellow in orthopedic surgery at Oxford University, UK. He was also a clinical fellow at Mercy Private Hospital, in Australia. In 2002, he was hired by the University of Nottingham, UK, as a clinical fellow in orthopedic surgery (upper limb surgery). In 2018, he completed an MBA in Biomedicine at the College of Management Academic Studies, in Israel. Dr. Rosenberg has worked as a senior orthopedic surgeon at the Rambam Health Care Campus since 2003. In 2007, he was appointed assistant clinical professor in the Faculty of Medicine, Technion-IIT. Dr. Rosenberg actively participates on the editorial boards of ten journals on orthopedic surgery. He served on the International Society of Arthroscopy, Knee Surgery, and Orthopedic Sports Medicine's (ISAKOS) Shoulder Committee. He has 80 peer-reviewed scientific articles, 5 books, and 150 presentations at international scientific meetings to his credit.

### Contents


Preface

Tendons are the biological and mechanical interface between muscles and bones. Their physiological role is to transfer the force of the muscle contraction to joint movements. As such, tendons have semi-elastic properties due to their connective tissue content and therefore are prone to inflammatory, degenerative, and structural failure that can cause

Tendon-related disabilities (tendinopathies) can significantly impact a person's daily functions. Tendinopathies can result from various causes, such as acute injury, systemic disease, or overuse. The following are the most prevalent causes of disabling pathology

• Tendinitis: This is an inflammation of the tendon, usually caused by overuse and repetitive strain or systemic inflammatory disease. The most common anatomic sites prone to tendinitis are the shoulder, elbow, wrist, knee, and ankle. The clinical manifestations of tendinitis involve pain, swelling, and limited mobility.

• Tendinosis: This is a chronic degeneration of the tendon that occurs following microtrauma. It can also be caused by aging or other medical conditions.

• Tear or separation: This can be caused by a sudden injury or by overuse. Tendon rupture can result in severe pain, swelling, and loss of function in the affected

• Tenosynovitis: This is inflammation of the synovial membrane surrounding the tendon. Tenosynovitis can result in pain, swelling, and limited mobility. It is

This book highlights recent advances in the current understanding of the mechanical and inflammatory structural pathologies involving the tendons. It also discusses the biochemical characteristics and mechanics of tendons and examines traumatic and degenerative causes (e.g., acute tears and microtrauma) of impairment. Furthermore, it presents pharmacological approaches for inflammatory conditions involving

> **Nahum Rosenberg**  Specialists Center,

> > Haifa, Israel

National Insurance Institute,

Tendinosis can cause pain and weakness in the affected areas.

most prevalent in the hand and wrist.

disabling effects, primarily pain, and impaired joint function.

related to tendons:

limb.

tendons.

## Preface

Tendons are the biological and mechanical interface between muscles and bones. Their physiological role is to transfer the force of the muscle contraction to joint movements. As such, tendons have semi-elastic properties due to their connective tissue content and therefore are prone to inflammatory, degenerative, and structural failure that can cause disabling effects, primarily pain, and impaired joint function.

Tendon-related disabilities (tendinopathies) can significantly impact a person's daily functions. Tendinopathies can result from various causes, such as acute injury, systemic disease, or overuse. The following are the most prevalent causes of disabling pathology related to tendons:


This book highlights recent advances in the current understanding of the mechanical and inflammatory structural pathologies involving the tendons. It also discusses the biochemical characteristics and mechanics of tendons and examines traumatic and degenerative causes (e.g., acute tears and microtrauma) of impairment. Furthermore, it presents pharmacological approaches for inflammatory conditions involving tendons.

> **Nahum Rosenberg**  Specialists Center, National Insurance Institute, Haifa, Israel

**1**

Section 1

Introduction

Section 1 Introduction

#### **Chapter 1**

### Introductory Chapter: Tendons – Trauma, Inflammation, Degeneration, and Treatment

*Nahum Rosenberg*

#### **1. Introduction**

*"When a joint becomes painful, swollen, and inflamed, it is impossible not to consider the ligaments and tendons, as they are the immediate cause of these symptoms." Citation attributed to Hippocrates.*

Tendons are specialized connective tissues essential for transferring forces from muscle contraction to the bones, enabling joint movement and mobility. Due to the semi-stiff nature of the tendons, forces may be effectively transferred from the muscle to the bone. Tendons' mechanical strength makes it possible to withstand mechanical forces.

The collagen fibers within the tendon have a very well-organized structure, which accounts for their strength. On the other hand, tendons display some viscoelastic activity that is dependent on the rate and length of loading. This characteristic enables tendons to adjust over time to variations in mechanical loading. As a result, tendons resist structural failure even under repeated strain. Its resistance to fatigue results from the tendon cells' capacity to repair and remodel the tendon according to its stress–strain characteristics, expressed by the stress–strain curve (**Figure 1**) [1, 2]. This curve determines the tendon's stiffness and toughness and present the maximum force the tendon can withstand before failing. A tendon's structural and mechanical characteristics may alter over time due to degeneration or damage, according to changes in the stress–strain curve.

#### **Figure 1.** *The stress–strain curve of a tendon – A simplified schematic representation.*

These biomechanical features are made possible by the peculiar structure of tendons. A sheath of connective tissue (such as the endotenon) surrounds the collagen fiber bundles that make up tendons at the microscopic level, where they are arranged into fascicles. The endotenon has a vascular and nerve supply that allows the tendon to receive nutrients and react to external stimuli.

The basic structural element of tendons is collagen fibers (the primary type is type I collagen). The parallel bundles they form give the tendon its strength and stiffness. Moreover, tendons include elastin fibers that provide some semi-flexibility and allow them to stretch slightly in response to stress (toe region on the stress–strain curve). Tenocytes, which are fibroblasts in the tendon tissue, is crucial to preserving the tendon's form and functionality. The collagen and elastic fibers of the tendon are produced and maintained by these cells. In addition, tenocytes can adapt the tendon to changes prompted by the stresses of a contracting muscle because of their mechanosensing characteristics.

A. Toe region – the tendon can withstand stress of low magnitude with minimal strain (up to ~2%). This region is due to the straightening and reorientation of the crimped collagen fibers within the tendon. B: Linear region – elastic deformation (a strain of ~2–4%) when the tendon returns to its original shape once the stress is removed. This region is due to the stretching of the collagen fibers within the tendon. C: Microscopic failure region- the tendon beyond the plastic deformation (a strain of ~4–8%) and incapable of returning to its original shape once the stress is removed. This region is due to the rupture of the collagen fibers within the tendon. D: Total structural rupture of the tendon (a strain above ~8%).

The distinctive structure of tendons is created by type I collagen, which makes long, thin fibers grouped in parallel bundles. Other forms of collagen, such as type III collagen, are also in minor quantities in the tendon tissue. The tendon's structure and function are supported by type III collagen, which is present in lesser levels and is less rigid than type I collagen.

As a result, the tendon is made up of fascicles that are packed with multiple parallel collagen fibers. A matrix of proteoglycans and glycosaminoglycans holds these fibers together while also acting as a shock absorber and lubricant thanks to the presence of synovia-like material. Collagen molecules repeating units are arranged staggered to form the collagen fibers. The tensile strength of the tendon is provided by this arrangement [3, 4].

The myotendinous junction is created at the tendon-muscle interface, where the collagen fibers of the tendon are continuous with the muscle fibers.

The fibrocartilaginous enthesis is created at the tendon–bone junction, where the collagen fibers of the bone and the tendon are continuous. The enthesis is a unique area with numerous discrete zones with various compositions and architecture. A highly organized structure called the fibrocartilaginous enthesis enables effective force transmission from the tendon to the bone. The multiple zones of the enthesis are designed to withstand the various mechanical stresses at the interface, such as compressive forces in the highly mineralized fibrocartilage zone and tensile forces in the tendon zone due to the well-aligned collagen fibers.

Tendon collagen content varies according to environmental and endogenous factors, such as age, systemic conditions, and specific anatomical location.

Thus tendon is a complex structure dependent on material and biochemical factors; therefore, it might be susceptible to mechanical failure, acute or degenerative, and pathological inflammatory conditions of connective tissue disorders. This makes *Introductory Chapter: Tendons – Trauma, Inflammation, Degeneration, and Treatment DOI: http://dx.doi.org/10.5772/intechopen.110708*

the tendon a source of numerous disabling conditions expressed by pain and movement disorders [5].

This book addresses and discusses several unique and clinically important tendons-related issues. This text should be an important information source for clinicians treating musculoskeletal pathology.

### **Author details**

Nahum Rosenberg Specialists Center, National Insurance Institute, Haifa, Israel

\*Address all correspondence to: nahumrosenebrg@hotmail.com

© 2023 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Robi K, Jakob N, Matevz K, Matjaz V. Chapter 2. The physiology of sports injuries and repair processes. In: Hamlin M, Draper N, Kathiravel Y, editors. Current Issues in Sports and Exercise Medicine. London, UK: Intech Open; 2013. pp. 43-86. DOI: 10.5772/54234

[2] Maganaris CN, Chatzistergos P, Reeves ND, Narici MV. Sec. Exercise Physiology. Frontiers in Physiology. 28 Feb 2017;**8**:1-11. DOI: 10.3389/ fphys.2017.00091

[3] Thorpe CT, Screen HRC. Tendon structure and composition. In: Ackermann P, Hart D, editors. Metabolic Influences on Risk for Tendon Disorders. Advances in Experimental Medicine and Biology. Vol. 920. Cham: Springer; 2016. DOI: 10.1007/978-3-319-33943-6\_1

[4] Kannus P. Structure of the tendon connective tissue. Scandinavian Journal of Medicine & Science in Sports. 2000;**10**(6):312-320. DOI: 10.1034/j.1600- 0838.2000.010006312.x

[5] Zabrzyński J, Łapaj Ł, Paczesny Ł, Zabrzyńska A, Grzanka D. Tendon function-related structure, simple healing process and mysterious ageing. Folia Morphologica. 2018;**77**(3):416-427. DOI: 10.5603/FM.a2018.0006. Epub 2018 Jan 18

Section 2
