Management of Osteoarthritis - A holistic view E-Book
40,48 €
Mehr erfahren.
- Herausgeber: Bentham Science Publishers
- Kategorie: Fachliteratur
- Serie: Frontiers in Arthritis
- Sprache: Englisch
Frontiers in Arthritis is an ebook series devoted to publishing the latest and the most important advances in arthritis research. Each volume brings together contributions from rheumatologists ad orthopedic specialists on the diagnosis, management and treatment of arthritis. The series also puts a focus on strategies for managing pain in patients in both pre and post operative situations.
Management of Osteoarthritis - A holistic view provides information about osteoarthritis of the knee and hip. Chapters explain osteoarthritis pathology and therapy (nutritional, exercise and surgical). The volume also covers different therapies such as viscosupplementation, platelet rich plasma injections, biologicals (amniotic membranes) and surgical options aimed at alleviating pain. The book is an ideal quick reference guide for medical students and nursing staff.
Sie lesen das E-Book in den Legimi-Apps auf:
Seitenzahl: 267
Veröffentlichungsjahr: 2017
Ähnliche
Frontiers in Arthritis
(Volume 1)
Management of Osteoarthritis -A
Holistic View
Edited by
Ashish Anand
GV Montgomery Veteran Affairs Medical Center,
Jackson, Mississippi,
USA
BENTHAM SCIENCE PUBLISHERS LTD.
End User License Agreement (for non-institutional, personal use)
This is an agreement between you and Bentham Science Publishers Ltd. Please read this License Agreement carefully before using the ebook/echapter/ejournal (“Work”). Your use of the Work constitutes your agreement to the terms and conditions set forth in this License Agreement. If you do not agree to these terms and conditions then you should not use the Work.
Bentham Science Publishers agrees to grant you a non-exclusive, non-transferable limited license to use the Work subject to and in accordance with the following terms and conditions. This License Agreement is for non-library, personal use only. For a library / institutional / multi user license in respect of the Work, please contact: [email protected].
Usage Rules:
All rights reserved: The Work is the subject of copyright and Bentham Science Publishers either owns the Work (and the copyright in it) or is licensed to distribute the Work. You shall not copy, reproduce, modify, remove, delete, augment, add to, publish, transmit, sell, resell, create derivative works from, or in any way exploit the Work or make the Work available for others to do any of the same, in any form or by any means, in whole or in part, in each case without the prior written permission of Bentham Science Publishers, unless stated otherwise in this License Agreement.You may download a copy of the Work on one occasion to one personal computer (including tablet, laptop, desktop, or other such devices). You may make one back-up copy of the Work to avoid losing it. The following DRM (Digital Rights Management) policy may also be applicable to the Work at Bentham Science Publishers’ election, acting in its sole discretion:25 ‘copy’ commands can be executed every 7 days in respect of the Work. The text selected for copying cannot extend to more than a single page. Each time a text ‘copy’ command is executed, irrespective of whether the text selection is made from within one page or from separate pages, it will be considered as a separate / individual ‘copy’ command.25 pages only from the Work can be printed every 7 days.3. The unauthorised use or distribution of copyrighted or other proprietary content is illegal and could subject you to liability for substantial money damages. You will be liable for any damage resulting from your misuse of the Work or any violation of this License Agreement, including any infringement by you of copyrights or proprietary rights.
Disclaimer:
Bentham Science Publishers does not guarantee that the information in the Work is error-free, or warrant that it will meet your requirements or that access to the Work will be uninterrupted or error-free. The Work is provided "as is" without warranty of any kind, either express or implied or statutory, including, without limitation, implied warranties of merchantability and fitness for a particular purpose. The entire risk as to the results and performance of the Work is assumed by you. No responsibility is assumed by Bentham Science Publishers, its staff, editors and/or authors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products instruction, advertisements or ideas contained in the Work.
Limitation of Liability:
In no event will Bentham Science Publishers, its staff, editors and/or authors, be liable for any damages, including, without limitation, special, incidental and/or consequential damages and/or damages for lost data and/or profits arising out of (whether directly or indirectly) the use or inability to use the Work. The entire liability of Bentham Science Publishers shall be limited to the amount actually paid by you for the Work.
General:
Any dispute or claim arising out of or in connection with this License Agreement or the Work (including non-contractual disputes or claims) will be governed by and construed in accordance with the laws of the U.A.E. as applied in the Emirate of Dubai. Each party agrees that the courts of the Emirate of Dubai shall have exclusive jurisdiction to settle any dispute or claim arising out of or in connection with this License Agreement or the Work (including non-contractual disputes or claims).Your rights under this License Agreement will automatically terminate without notice and without the need for a court order if at any point you breach any terms of this License Agreement. In no event will any delay or failure by Bentham Science Publishers in enforcing your compliance with this License Agreement constitute a waiver of any of its rights.You acknowledge that you have read this License Agreement, and agree to be bound by its terms and conditions. To the extent that any other terms and conditions presented on any website of Bentham Science Publishers conflict with, or are inconsistent with, the terms and conditions set out in this License Agreement, you acknowledge that the terms and conditions set out in this License Agreement shall prevail.Bentham Science Publishers Ltd. Executive Suite Y - 2 PO Box 7917, Saif Zone Sharjah, U.A.E. Email: [email protected]
FOREWORD
Osteoarthritis is known enigma for Orthopedic Surgeons and it continues to be amongst the most important cause of chronic pain and disability. It is estimated that around 6 billion dollars/year are spent alone on management of this epidemic.
The purpose of this monograph is to offer the reader treatment options available for the management of osteoarthritis of knee and hip. If one reviews the current spectrum of literature available to, it becomes clear that there is a large body of literature in which the patient has to sort through with varying degree of scientific evidence, making anyone embarking on this Journey a difficult and conducing one. This Monograph provides an in depth analysis of the Pathology, Role of Nutrition and Exercise in treatment of arthritis there by offering a unique perspective to the Reader.
The book also provides insights into Role of injectables such as Platelet rich plasma and Viscosupplementation and elaborates on the Role of Amniofix- stem cells from the Amnion and Chorion in the treatment of Osteoarthritis. Finally, the book presents a number of surgical options for the reader that have had an established place for decades in the field of surgical arthritis such as Osteotomy, Arthroscopy and Replacement surgery.
Dr. Ashish Anand, MD has done a commendable Job in editing the manuscript. This book is a good read for Medical students, residents in training and the busy practitioner.
PREFACE
The book contains eight chapters with initial ones focusing on pathology behind osteoarthritis, Role of Nutrition in management of Osteoarthritis and Role of exercise in Management of Osteoarthritis. All of them point and educate the reader/clinician on their important role in pathogenesis as well as prevention of osteoarthritis. The Reader is encouraged to incorporate Nutrition and Exercise management in his Clinical practice.
The next chapter tells us about the Role of Viscosupplementation and Platelet Rich Plasma(PRP) in management of osteoarthritis and what the current clinical evidence is for the above two modalities.
Chapter 5 is an interesting chapter on Amniofix, which is relatively unheard of. Amniofix is an allograft tissue obtained from a Human baby and contains growth factors which have the potential for treating osteoarthritis pain when everything has failed and the patient is not interested in surgery. It may even possibly reverse the early damaging changes to the Cartilage. As time goes by, I am sure one will hear a lot about this “Novel” approach.
The second last section deals with surgical aspects of treatment of arthritis of knee in which the book dwells on the role of Arthroscopy with Cartilage Surgery, role of Osteotomy around the knee, and Current Concepts in Total Knee Replacement.
The last section deals with surgical management of arthritis of Hip-namely Role of Arthroscopy with Cartilage Surgery as well as Current Concepts in Total hip replacement.
It is my sincere hope that this book will stimulate the minds of the busy clinicians to read more about the subject and possibly also add some new tools to their armamentarium to give their patients the best possible treatment.
ACKNOWLEDGEMENTS
I always used to wonder what does work of an editor involve? All my questions were answered as I worked diligently during the preparation of this monograph. It gave me sleepless nights so that I could stick to the schedule given to me by the publishers. Interacting with the various authors and then editing their work was an excellent learning experience. I would like to thank all the authors who spent there valuable time in preparing the manuscripts and sticking to my schedule. All of us enjoyed writing this book and we sincerely hope that the reader gets the same pleasure and adds something more to his knowledge while reading this book.
I am indebted to my parents for instilling the values of hard work, perseverance and commitment as all these qualities served me in good stead during the preparation of this manuscript. I would like to thank my wife Varsha for constantly nudging me to go above and beyond. Finally, I would like to thank my two lovely daughters Advikaa and Vahita for helping me out with computer glitches and sparing me valuable time without which this book would not have seen light of the day.
List of Contributors
DEDICATION
Pathology of Osteoarthritis
Carmen Frias Kletecka*Abstract
The pathology of osteoarthritis is extremely complex and multifactorial. Recent technological advances have allowed the identification of specific genes and genetic alterations which have helped to elucidate some intricacies involved in the molecular basis of disease development and progression. Known factors and key recent discoveries in pathogenesis, plus typical gross and histologic pathologic findings are described in this chapter.
INTRODUCTION
Osteoarthritis (OA), also known as degenerative joint disease, is characterized by the progressive degradation of articular cartilage causing loss of function as a shock absorber [1]. The term OA was introduced by Archibald E. Garrod, an English physician in the 1890s [2]. The characteristic features of OA include initial softening, splitting, and fragmentation of articular cartilage followed by sclerosis of the bone underlying the articular surface cartilage (subchondral bone), bone cysts, and bony outgrowths at the joint margins (osteophytes) [3].
Etiology/Pathogenesis
OA is a multifactorial disease with a complex pathogenesis involving both environmental and genetic factors. The molecular basis of disease development
and progression encompasses chondrocyte injury, repair, and ultimately, death. Chondrocyte injury elicits an inflammatory response and lymphocyte production of pro-inflammatory mediators, including TNF and IL-B. OA chondrocytes produce IL-1, inducing the expression of MMPs, and other catabolic enzymes. Pro-inflammatory mediators and catabolic enzymes subsequently lead to cartilage destruction [6]. In most cases, OA results from aging and an unknown underlying cause. In a minority of cases, OA develops in young patients with a predisposing condition, such as a previous joint injury, congenital deformity, or systemic disease. Environmental factors include aging and biomechanical stress related to physical characteristics like body weight and joint stability. Genetic factors include both intrinsic genes and altered gene expression via epigenetic modifications. Family and epidemiological studies show that OA is associated with multiple genes and has a heritability component. Genome wide association studies identified specific genes associated with the development and progression of OA [4, 5]. Genome wide methylation studies suggest that DNA methylation plays a significant role regulating the inflammation in cartilage through epigenetic modifications and together with cytokines, growth factors and changes in matrix composition, are involved in the development of OA. One in particular reports hypomethylation leading to increased transcription of pro-inflammatory factors including TFF, IL-1 and IL-6. Furthermore, epigenetic regulation involving microRNAs play a role in skeletal development and chondrogenesis [7, 8].
GROSS PATHOLOGY
The osteoarthritic articulating joint commonly displays cartilaginous outgrowths or osteophytes and loss of normal roundness. In the early stages of OA, hyaline cartilage on the articular surface is soft and granular. With disease progression, the articular cartilage sloughs off and is partially or completely lacking over weight bearing areas and remnants are usually present at the periphery. The underlying bone will have a polished, smooth appearance or eburnation in areas where it is in direct contact with another bone (Fig. 1). The bony surface may have regenerative cartilage clusters where repair is taking place. Characteristic features seen on cross section include subchondral bone with a sclerotic appearance, subcortical cysts and wedge shaped necrosis (Fig. 2). Subcortical cysts form when synovial fluid enters the subchondral bone space through small fractures on the bone surface. Multiple loose bodies may be present within the joint space [9-12].
Fig. (1)) Femoral head with osteoarthritis. The articular surface is eburnated and there are remnants of cartilage around the periphery (Image courtesy of Reggie Thomasson, MD).MICROSCOPIC PATHOLOGY
Injury and repair related changes are seen histologically within bone and cartilage tissue. As the superficial layers of cartilage and collagen degrade, vertical and horizontal fibrillation become apparent with subsequent matrix cracking. Cartilage repair or regeneration occurs both intrinsically and extrinsically. Intrinsic repair exists within the original articular hyaline cartilage as islands composed of chondrocyte clones within the matrix. Extrinsic repair presents as a highly cellular fibrocartilage with coarse and disorganized collagen overlying remnants of articular hyaline cartilage and at the joint margin (Fig. 3).
Subchondral bone denuded of surface cartilage shows osteoblast proliferation and associated new bone formation, corresponding with areas of sclerosis seen grossly and on x-ray. Small fractures are commonly seen and may be associated with a subchondral cyst.
Fig. (2)) Cross section of femoral head with osteoarthritis showing sclerotic subchondral bone, fracture and wedge necrosis (Image courtesy of Joel France, DO). Fig. (3)) Photomicrograph of cartilage with extrinsic and intrinsic repair. Fig. (4)) Photomicrograph of synovium with hypertrophic and hyperplastic lining, stromal fibrosis, and chronic inflammation (Image courtesy of Harry Porterfield, DO).Synovium changes include stromal fibrosis of fibroadipose tissue, chronic inflammation, and both hyperplastic and hypertrophied lining (Fig. 4).
Loose bodies typically have irregular, concentric calcified rings and cartilage replication.
Conflict of Interest
The author confirms that the author has no conflict of interest to declare for this publication.
ACKNOWLEDGEMENTS
Declared none.
REFERENCES
[1]Mankin HJ, Dorfman H, Lippiello L, Zarins A. Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. II. Correlation of morphology with biochemical and metabolic data. J Bone Joint Surg Am 1971; 53(3): 523-37. [PMID: 5580011][2]Garrod AE. A treatise on rheumatism and rheumatoid arthritis. Griffin 1890.[3]Dieppe P, Kirwan J. The localization of osteoarthritis. Br J Rheumatol 1994; 33(3): 201-3. [http://dx.doi.org/10.1093/rheumatology/33.3.201] [PMID: 8156279][4]Valdes AM, Spector TD. The contribution of genes to osteoarthritis. Rheum Dis Clin North Am 2008; 34(3): 581-603. [http://dx.doi.org/10.1016/j.rdc.2008.04.008] [PMID: 18687274][5]Warner SC, Valdes AM. The genetics of osteoarthritis: A review. J Fun Morp Kines 2016; 1(1): 140-53. [http://dx.doi.org/10.3390/jfmk1010140][6]Goldring MB, Goldring SR. Osteoarthritis. J Cell Physiol 2007; 213(3): 626-34. [http://dx.doi.org/10.1002/jcp.21258] [PMID: 17786965][7]Reynard LN. Analysis of genetics and DNA methylation in osteoarthritis: What have we learnt about the disease?. In Seminars in Cell and Developmental Biology 2016. Apr 26. Academic Press.[8]Roach HI, Aigner T. DNA methylation in osteoarthritic chondrocytes: a new molecular target. Osteoarthritis Cartilage 2007; 15(2): 128-37. [http://dx.doi.org/10.1016/j.joca.2006.07.002] [PMID: 16908204][9]Mills SE. Histology for pathologists. Lippincott Williams & Wilkins 2007. pp. 112-21.[10]The Noninflammatory ArthritidesBullough PG. Orthopaedic Pathology. (5th ed.), Philadelphia: Mosby 2010.[11]The Dysfunctional JointBullough PG. Orthopaedic Pathology. (5th ed.), Philadelphia: Mosby 2010.[12]Bullough PG. Sternberg SS, Antonioli DA, Mills SE, Carter D, Oberman HA. Joint diseases. In: Sternberg SS, Antonioli DA, Mills SE, Carter D, Oberman HA, eds. Diagnostic Surgical Pathology. (3rd ed.) Philadelphia, Pa: Lippincott Williams & Wilkins 1999. pp. 230-2.Exercise in the Prevention and Treatment of Osteoarthritis
Ashley L. Artese*,Brandon F. GrubbsAbstract
Exercise can reduce the risk for osteoarthritis by aiding in the prevention of obesity, joint instability, and muscle weakness. It can also serve as an effective treatment by helping patients manage weight, improve muscular strength, decrease joint stiffness, improve range of motion, increase functionality, and reduce the risk for falls. Before starting an exercise program, patients should obtain a physician’s consent and complete a thorough fitness assessment with an exercise specialist. The exercise program should be progressive, beginning with low-to-moderate intensity exercises followed by gradual increases in intensity. Low impact aerobic training and isometric or isotonic strength training are recommended modes of exercise for effective management of osteoarthritis symptoms. Yoga and tai chi provide low impact exercises and are considered effective therapy options for osteoarthritis symptom management. In addition, water-based exercise programs may improve adherence to an exercise program and be equally effective as land-based exercise for improving gait, functionality and pain. Since exercise adherence is the primary predictor of long-term outcomes in osteoarthritic patients, strategies to improve exercise adherence should be implemented.
Introduction
Obesity, physical injury, joint instability, and muscle weakness are modifiable extrinsic risk factors associated with the development and progression of osteoarthritis. Obesity is a risk factor for several cardiovascular and metabolic diseases that plague more than one-third of U.S. adults and approximately 17% of American youth [1]. Gradual weight gain that leads to obesity can result from a combination of genetics, sedentary activity, and poor nutrition. Despite physical activity, aging adults reach their peak strength between the second and third decades in life. After 50 years of age, muscular strength declines at a rate of 12-15% per decade with even greater losses after 65 years [2]. Muscular power, the ability to generate force and velocity, is suggested to decline with greater magnitude and exceed losses in strength with age [3].
A lack of physical activity can accelerate declines in muscular performance and contribute to excessive weight gain. Higher body weight is associated with increased joint pain in older adults, and it has been estimated that the risk for developing osteoarthritis increases by 36% for every 5 kg increase in body weight [4]. Excess weight places additional load on the joint, which can lead to increased inflammation and structural changes in the joint and articular cartilage [5]. In addition to excess weight, a loss in both muscle mass and muscular strength, two important factors for joint movement, stability, and protection, are associated with joint degeneration and increased risk for osteoarthritis. These losses may be due to factors such as age-related sarcopenia, muscle-wasting diseases, and physical inactivity. Furthermore, obesity may contribute to these changes as intramuscular adipose tissue has been linked to losses in muscular strength and functional ability in older adults [6]. Both obesity and muscular weakness can affect movement and gait kinematics, which can cause the load-bearing portion of the joint to be shifted to areas that are not normally accustomed to the excess loading, resulting in cartilage degeneration and the progression of osteoarthritis [7]. The knees and the hips are the two most common joints affected by osteoarthritis as they are the joints which bear the greatest weight.
Comparatively, those who are physically active and participate in high impact sports are also at risk for osteoarthritis, as physical trauma can increase the disease’s incidence [8]. Not only does damage to the joint affect the cartilage, but injury may lead to muscle weakness from disuse and weight gain from inactivity. Incorporating a safe and comprehensive exercise program into an individual’s daily routine can help induce weight loss, prevent obesity, maintain muscular strength, and reduce injury, thus attenuating the development and symptoms of osteoarthritis.
Exercise Recommendations
The American College of Sports Medicine (ACSM), the largest sports medicine and exercise science organization in the world, has several position stands formulated from evidence of heavily scrutinized scientific literature. These position stands provide guidelines for appropriate physical activity intervention strategies for weight loss, weight regain, and health benefits. To avoid significant weight gain, ACSM recommends that adults engage in a minimum of 150 minutes per week of moderate intensity physical activity [9]. Overweight and obese adults can use the same recommendation to induce moderate weight loss; however, there is most likely a dose response relationship for exercise and weight reduction [9]. To achieve greater weight loss and prevent weight regain, ACSM recommends approximately 200 to 250 minutes of moderate intensity physical activity, which is equivalent to expending approximately 2,000 kcal, per week [9].
ACSM has also provided guidelines for physical activity for healthy older adults. These recommendations were developed based on evidence of the benefits of aerobic exercise and resistance training on health and functional capacity. For endurance, older adults should engage in moderate-intensity aerobic exercise accumulating at least 30 minutes of exercise time per day in bouts of at least 10 minutes to total 150-300 minutes per week. If working at a vigorous intensity, older adults should accumulate 20-30 minutes per day or more to total 75-150 minutes per week [10]. To determine the level of physical exertion, a 0 to 10 point scale is used where a score of 10 equals maximal physical exertion. Moderate intensity is a 5 to 6 and vigorous intensity is 7 to 8. Aerobic exercise modalities that do not exacerbate symptoms of orthopedic stress such as walking, cycling, and aquatics are recommended [10].
In addition to endurance training, ACSM recommends that older adults engage in at least 2 days per week of resistance training. This can be accomplished with the use of free weights or dumbbells, machines, ankle weights, or strengthening activities such as stair climbing. Exercisers should work between moderate (5-6) and vigorous (7-8) intensities [10]. Older adults participating in a strength program should do so with caution as there is risk for musculoskeletal injury. Using a progressive weight training program design that increases the exercise intensity gradually throughout the program can minimize this risk and optimize gains in strength. Resistance training may be optimal for obese older adults or those experiencing mobility impairment since minimal ambulation is required. While resistance training is not recommended as an effective strategy for weight loss, it does provide favorable changes in body composition that result in reductions in abdominal adipose tissue and increases in lean mass.
Treatment of Osteoarthritis
Osteoarthritic changes are most common in older adults. While no cure exists for osteoarthritis, the most effective strategy is to utilize interventions that target the disease’s symptoms. Exercise has been shown to help osteoarthritic patients manage weight, improve muscular strength, decrease joint stiffness, improve range of motion, increase functionality, and reduce the risk for falls and fractures [11], which can ultimately lead to increased quality of life. Those who do not exercise are prone to accelerated degeneration at the joint along with more pain and inflammation [12]. Exercise can delay the need for arthroplasty and sometimes avoid it all together.
Pain is the most common symptom of osteoarthritis and this can be accompanied by joint stiffness, inflammatory swelling, instability, and muscle weakness. Together these symptoms can lead to physical limitations which develop into impairments of independent living for older adults. Activities of daily living such as walking, house-cleaning, gardening, and stair-climbing become challenging and may then require the assistance of an aid. Exercise can improve functionality by increasing muscular strength, range of motion, proprioception (sensing of body stimuli and awareness of body part position, equilibrium, and motion), and cardiovascular fitness. Although exercise can reduce the symptoms associated with osteoarthritis, exercise cannot influence the structural impact of the disease.
While exercise is beneficial, adherence to a regular exercise regimen in this population is often difficult because of joint pain, symptom exacerbation, fatigue, decreased stability and balance, and additional comorbidities experienced by these patients [11]. Therefore, initial exercise intensity, frequency, volume, mode, and the individual’s disease status must be taken into account when implementing an exercise training program in order to manage pain and discomfort and to prevent further symptom exacerbation. Since adherence is the primary predictor of long-term outcomes from exercise in these patients [13], strategies to improve exercise adherence should be implemented. These strategies include emphasis on group or individual instructional settings instead of a home-based exercise program, patient education on the benefits of exercise and the pathogenesis of the disease, and self-efficacy enhancement through progressive programs that emphasize small short-term goals along with encouragement provided by the instructor [14].
