DOCSLIB.ORG

Chondrocyte Death in Canine Osteochondral Explants Exposed To

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chondrocyte Death in Canine Osteochondral Explants Exposed To Louisiana State University LSU Digital Commons LSU Master's Theses Graduate School 2009 Chondrocyte death in canine osteochondral explants exposed to 0.5 percent bupivacaine Geoffrey Stuart Hennig Louisiana State University and Agricultural and Mechanical College Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_theses Part of the Veterinary Medicine Commons Recommended Citation Hennig, Geoffrey Stuart, "Chondrocyte death in canine osteochondral explants exposed to 0.5 percent bupivacaine" (2009). LSU Master's Theses. 377. https://digitalcommons.lsu.edu/gradschool_theses/377 This Thesis is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Master's Theses by an authorized graduate school editor of LSU Digital Commons. For more information, please contact [email protected]. CHONDROCYTE DEATH IN CANINE OSTEOCHONDRAL EXPLANTS EXPOSED TO 0.5 PERCENT BUPIVACAINE A Thesis Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Master of Science in The Interdepartmental Program in Veterinary Medical Sciences through the Department of Veterinary Medical Sciences by Geoffrey Stuart Hennig B.A., Indiana University, 1995 D.V.M., Ross University, 2005 May 2009 ACKNOWLEDGMENTS This research could not have been completed without the support of many individuals. First of all, I have to thank my Masters committee: Dr. Giselle Hosgood, Dr. Loretta Bubenik, and Dr. Susanne Lauer. Their guidance over the years not only with this project, but also through the residency, is appreciated more than words can express. Dr. Hosgood deserves a special thank you for her expertise in experimental design and statistical analysis. I would also like to thank Dr. Timothy Morgan for his expertise and contributions to the project design and results in the area of histopathology. Many people contributed their time, ideas and expertise to the project and their contributions collectively enhanced the quality of this research. I would like to thank Kyle Waite who played an integral role in the logistics of this project. Also, Ms. Cheryl Crowder for her work with staining and histopathology preparations. Dr. Henk, Dr. Wu, and Greg McCormick in the microscopy lab provided their time, expertise and assistance with the laser confocal microscope. I also have to thank Ms. Samuella Frazier for all of her assistance in the laboratory. This project could not have been conducted without a grant provided by the Louisiana State University Veterinary Clinical Sciences Organized Research Fund. ii TABLE OF CONTENTS ACKNOWLEDGEMENTS……………………………………………………….. ii LIST OF TABLES…………………………………………………………………. v LIST OF FIGURES………………………………………………………………... vi ABSTRACT……………………………………………………………………….. vii CHAPTER 1: BACKGROUND AND REVIEW OF THE LITERATURE………. 1 1.1 Bupivacaine…………………………………………………………… 2 1.1.1 History of Local Anesthetics………………………………... 2 1.1.2 Properties of Local Anesthetics……………………………... 3 1.1.2.1 Chemistry of Local Anesthetics…………………... 3 1.1.2.2 Grouping of Local Anesthetics……………………. 3 1.1.2.3 Mechanism of Action ……………………………... 5 1.1.2.4 Differential Nerve Blockade………………………. 5 1.1.3 Pharmacokinetics of Local Anesthetics……………………... 6 1.1.3.1 Absorption………………………………………… 6 1.1.3.2 Distribution………………………………………... 6 1.1.3.3 Elimination………………………………………… 7 1.1.3.4 Toxicity……………………………………………. 8 1.1.4 Bupivacaine as an Intra-articular Analgesic………………… 9 1.1.4.1 Intra-articular Bupivacaine in People……………... 9 1.1.4.2 Intra-articular Bupivacaine in Dogs……………….. 10 1.2 Cartilage……………………………………………………………….. 10 1.2.1 Cartilage Cells……………………………………………….. 10 1.2.2 Cartilage Matrix……………………………………………... 11 1.2.3 Types of Cartilage…………………………………………… 11 1.2.4 Articular Cartilage Metabolism……………………………... 13 1.2.5 Response to Cartilage Injury……………………………….... 13 1.3 Arthroscopy Irrigating Solutions……………………………………… 14 1.4 Chondrocytotoxicity…………………………………………………... 16 1.5 Bupivacaine-Associated Chondrolysis………………………………... 19 CHAPTER 2: MATERIALS AND METHODS…………………………………... 25 2.1 Collection of Phase 1 Tissue Samples………………………………… 25 2.2 Treatment and Evaluation of Phase 1 Tissue Samples………………... 25 2.3 Collection of Phase 2 Tissue Samples………………………………… 26 2.4 Treatment and Evaluation of Phase 2 Tissue Samples ……………….. 26 2.5 Statistical Methods…………………………………………………….. 28 CHAPTER 3: RESULTS…………………………………………………………... 34 3.1 Phase 1 Results………………………………………………………... 34 3.2 Phase 2 Results………………………………………………………... 34 3.2.1 Surface Intact ……………………………………….. ……... 34 3.2.2 Surface Removed …………………………………… ……... 35 3.2.3 Surface Intact Compared to Surface Removed .…….............. 35 3.2.4 pH …………………………………………………… ……... 35 iii CHAPTER 4: DISCUSSION……………………………………………………… 46 CHAPTER 5: SUMMARY AND CONCLUSIONS………………………………. 53 REFERENCES…………………………………………………………………….. 56 APPENDIX I: PHASE 1 RAW METHYLENE BLUE PENETRATION DATA… 69 APPENDIX II: PHASE 2 RAW CHONDROCYTE DEATH DATA……………. 72 APPENDIX III: PHASE 2 RAW pH DATA ……………………………………... 91 VITA……………………………………………………………………………….. 98 iv LIST OF TABLES Table 2.1 Phase 1 osteochondral core treatments and sample size.……………….. 30 Table 2.2 Phase 2 osteochondral core treatments and sample size.……………….. 32 Table 3.1 Mean (standard deviation) methylene blue stain penetration measured in microns from the cut sides of the cores following either 15 or 30 minute exposure……………………………………………………………………………. 36 Table 3.2 Mean (standard deviation) proportional penetration of methylene blue stain from the articular surface of surface intact and surface removed osteochondral cores following either 15 or 30 minute exposure to canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP)………………………………………..... 37 Table 3.3 Mean (standard deviation) of chondrocyte death following 5 minute, 15 minute or 30 minute exposure to canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP) for surface intact (SI) and surface removed (SR) osteochondral cores………………………… 38 Table 3.4 Mean (standard deviation) pH of canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP) for surface intact (SI) and surface removed (SR) osteochondral cores before and after 5 minute treatment…………………………………………………………………. 41 Table 3.5 Mean (standard deviation) pH of canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP) for surface intact (SI) and surface removed (SR) osteochondral cores before and after 15 minute treatment………………………………………………………………... 42 Table 3.6 Mean (standard deviation) pH of canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP) for surface intact (SI) and surface removed (SR) osteochondral cores before and after 30 minute treatment………………………………………………………………... 43 v LIST OF FIGURES Figure 1.1 Molecular structure of bupivacaine……………………………………. 24 Figure 1.2 Basic molecular structure of local anesthetics………………………… 24 Figure 2.1 Photomicrograph at 10x of H&E stained osteochondral cores with an intact surface (A) and with the surface mechanically debrided (B)..………………. 29 Figure 2.2 Humeral heads (A) were cut in a grid-like fashion using a jigsaw (B) to harvest osteochondral cores with final dimensions of 6mm x 6mm x 6mm (C)... 29 Figure 2.3 Schematic diagram of the experimental design describing the tissue sample collection and treatment distribution for Phase 1………………………...... 30 Figure 2.4 Standard light microscopic digital image at 10x of a 1mm slice of a surface intact osteochondral core treated with 0.5% bupivacaine and methylene blue at 15 minutes (A) and 30 minutes (B)………………………………………… 31 Figure 2.5 Schematic diagram of the experimental design describing the tissue sample collection and treatment distribution for Phase 2………………………….. 32 Figure 2.6 Confocal microscopic digital image at 10x of a surface intact osteochondral core treated with canine chondrocyte culture media for 5 minutes stained with calcein AM (A) and ethidium homodimer-1 (B). Images A and B are superimposed in image C showing the greater chondrocyte death that occurred in the superficial zone………………………………………………………………… 33 Figure 3.1 Mean (standard deviation) proportional penetration of methylene blue stain from the articular surface of surface intact and surface removed osteochondral cores following either 15 or 30 minute exposure to canine chondrocyte culture medium (CCCM), 0.5% bupivacaine (B), or 0.5% bupivacaine with preservative (BP)………………………………………...... 37 Figure 3.2 Mean % chondrocyte death comparisons within treatment solutions across time in the superficial zone of surface intact osteochondral cores…………. 39 Figure 3.3 Mean % chondrocyte death comparisons across time in the superficial zone of surface intact osteochondral cores………………………………………… 39 Figure 3.4 Mean % chondrocyte death comparisons within treatment solutions across time in the superficial zone of surface removed osteochondral cores ……... 40 Figure 3.5 Mean % chondrocyte death comparisons across time in the superficial zone of surface removed osteochondral cores……………………………………... 40 Figure 3.6 Mean pH within treatment solutions across time of surface intact cores………………………………………………………………………………... 44 Figure 3.7 Mean pH across time of surface intact cores…………………………... 44 Figure 3.8 Mean pH within treatment solutions across time of surface removed cores………………………………………………………………………………..
Load more

Recommended publications
  • Case Report Chondroblastoma of The
    CASE REPORT CHONDROBLASTOMA OF THE PATELLA ASSOCIATED WITH AN ANEURYSMAL BONE CYST R. TREBŠE1, A. ROTTER2,V. PIŠOT1 Chondroblastoma is a rare, benign tumor of bone, cartilage germ cells, and they redefined the tumor accounting for about 1% of all bone tumor cases. It as “benign chondroblastoma”. tends to affect the epiphyseal ends of long bones, Chondroblastoma is rare, representing about 1% most often in males during the first and second of all primary bone tumors (1, 5, 9). It is typically decades of life. It has well-characterized radio- centered in an epiphysis. Although it occurs most graphic and histologic features but despite its histo- often in the end of a long tubular bone, it can logically benign appearance a few cases of metastases appear in any secondary center of ossification. It is have been reported. Local recurrences after curet- tage and bone grafting occur in 11% to 25% of cases. most probably a tumor of cartilaginous origin and The features of a patellar chondroblastoma are the is more common in males by a ratio of about 2-to- same as for other locations. In reviewing the litera- 1 (1, 5, 9). Seventy percent of chondroblastomas ture we found an unusually high male-to-female occur during active epiphyseal plate growth, and ratio. It is interesting that the usual treatment of the about two-thirds of the patients are in the second patellar chondroblastoma has been patellectomy, decade of life (5). whereas curettage and bone grafting has predomi- Local pain of several months’ duration and nated in the other locations.
    [Show full text]
  • Fluorescent Advanced Glycation End Products in the Detection of Factual Stages of Cartilage Degeneration
    Physiol. Res. 56: 235-242, 2007 Fluorescent Advanced Glycation End Products in the Detection of Factual Stages of Cartilage Degeneration M. HANDL1,3, E. FILOVÁ2,3, M. KUBALA4, Z. LÁNSKÝ5, L. KOLÁČNÁ2,3, J. VORLÍČEK6, T. TRČ1, M. PACH7, E. AMLER2,3 1Orthopedic Clinic, Second Faculty of Medicine, Charles University in Prague, Czech Republic, 2Institute of Biophysics, Second Faculty of Medicine, Charles University in Prague, Czech Republic, 3Department of Tissue Engineering, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic, 4Department of Biophysics, Faculty of Science, Palacky University in Olomouc, Czech Republic, 5Department of Protein Structure, Institute of Physiology, Academy of Sciences of the Czech Republic, Czech Republic, 6Department of Biomathematics, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic and 7Department of Orthopaedics, Faculty of Medicine and Dentistry, Palacky University in Olomouc, Czech Republic Received January 2, 2006 Accepted February 27, 2006 On-line available March 23, 2006 Summary Patients treated for knee disorders were included in this study. They were examined clinically (Lequesne and Tegner scores) and by standard X-ray investigation. Patients underwent a surgical procedure, either arthroscopy or knee replacement. At the initial phase of surgery, a sample of cartilage was taken for laboratory examination. Progression of the disorder and the clinical examination was correlated with the actual state of the cartilage using a novel fluorescence approach. The intrinsic fluorescence of cartilages was shown as a suitable and sensitive method for detection of the actual state of cartilages because the correlation with X-ray examination and clinical status was found.
    [Show full text]
  • Osteochondritis Dissecans
    Osteochondritis Dissecans John A. Schlechter, DO Pediatric Orthopaedics and Sports Medicine Children’s Hospital Orange County Osteochondritis Dissecans • Developmental condition of the joint − Described by Paget as “quiet necrosis” − Named by Konig 1888 • Lesion of the articular cartilage & subchondral bone before closure of the growth plate Is it OCD? • OCD vs Normal Variant of Ossification • Normal Variants − Tend to be younger patients age <10 − Tend to affect both condyles − Posterior aspect of condyle − Resolves as the child ages OCD Stats • Highest rates − appear among patients aged between 10 and 15 y. Male-to-female ratio ~ 2:1 − ADHD? • Bilaterality − typically in different phases of development, are reported in 15% to 30% of cases Osteochondritis Dissecans • Etiology unknown • Proposed causative factors: − Ischemia − heredity − mechanics (trauma) Osteochondritis Dissecans • Repetitive mechanical trauma or stress, in highly active children & adolescents • Impaction of the tibial spine Osteochondritis Dissecans Symptoms, Signs & Imaging • Nonspecific knee pain • Activity-related • Wilson test • “tunnel view” • MRI - stability of the subchondral bone, arthrography AP view – does not always show OCD Notch view – reveals OCD Location • Cahill described a method of localizing lesions by dividing the knee into 15 distinct alphanumeric zones Am J Sports Med 1983;11: 329-335. Osteochondritis Dissecans Symptoms, Signs & Imaging Osteochondritis Dissecans MRI Staging Hefti et al. JPO-B 1999 • Stage I: Signal change, NO clear margin • Stage II: Clear margin, NO Dissection • Stage III: Partial Dissection of fluid • Stage IV: Complete Dissection, Fragment In Situ • Stage V: Free Fragment I - No Clear margin II- Clear margin III- Partial Dissection Hefti et al. JPO-B 1999 IV- Partial Dissection V- Loose Body Case Example – Hefti 3 MRI Coronal T2 Cartilage Breach Osteochondritis Dissecans Natural History • Patients with open physes fare better than adults.
    [Show full text]
  • Osteochondritis Dissecans (OCD) Results in the Destruction of Subchondral Bone with Secondary Damage to Overlying Articular Cartilage (1,2)
    Copy Editor: Selvi S Osteochondritis 45 Dissecans Cecilia Pascual-Garrido, Taylor M. Southworth, Mark A. Slabaugh, Neal B. Naveen, Nicole A. Friel, Ben U. Nwachukwu, and Brian J. Cole prohibited. INTRODUCTION is Osteochondritis dissecans (OCD) results in the destruction of subchondral bone with secondary damage to overlying articular cartilage (1,2). The prevalence of this condition is estimated to contentbe between 11.5 and 21 per 100,000 (3,4). OCD is classically divided into juvenile and adult forms based on the patient’s skeletal maturity (1). Juvenile OCD (JOCD) lesions occur in childrenthe and young adolescents with open growth plates. Although adult OCD lesions may arise de ofnovo, they more commonly result from an incompletely healed and previously asymptomatic JOCD lesion (5). JOCD lesions have a better prognosis and higher rates of spontaneous healing with conservative treatment than do adult OCD lesions (6). Adult OCD lesions have a greater propensity for instabil- ity and, once symptomatic, typically follow a clinical course that is progressive and unremitting (7). While lesions most frequently occur on the femoral condyles, they are also found in the elbow, wrist, ankle, and femoral head (8–12). The highest incidence rates in JOCDreproduction are among patients ages 10 and 15 years old, ranking among the most common causes of knee pain and dysfunction in young Fig. 45-1 adults (6,7,13) (Fig. 45-1). The typical presentation of OCD in the knee includes pain and swelling related to activity. Instability is not usually reported, though mechanical symptoms, such as catching and locking, ­usually occur in the presence of a loose body and are frequently the initial presenting symptoms.
    [Show full text]
  • Osteomyelitis 78
    Osteomyelitis 78 SECTION K: Bone and Joint Infections 78 Osteomyelitis Kathleen Gutierrez Osteomyelitis is inflammation of bone. Bacteria are the usual etio- months, providing a vascular connection between the metaphysis logic agents, but fungal osteomyelitis occurs occasionally. Osteo- and the epiphysis.8 As a result, in infants, infection originating in myelitis in children primarily has hematogenous origin, occurring the metaphysis can spread to the epiphysis and joint space. The less commonly as a result of trauma, surgery, or infected contigu- risk of ischemic damage to the growth plate is greater in the young ous soft tissue. Osteomyelitis due to vascular insufficiency is rare infant with osteomyelitis.9 Before puberty, the periosteum is not in children. firmly anchored to underlying bone. Infection in the metaphysis of a bone can spread to perforate the bony cortex, causing sub- ACUTE HEMATOGENOUS OSTEOMYELITIS periosteal elevation and extension into surrounding soft tissue. Bony destruction can spread to the diaphysis. By age of 2 years, Pathogenesis the cartilaginous growth plate usually prevents extension of infec- tion to the epiphysis and into the joint space. When the metaphy- Acute hematogenous osteomyelitis (AHO) is primarily a disease sis of the proximal femur or humerus is involved, however, of young children, presumably because of the rich vascular supply infection can extend into the hip or shoulder joint at any age, of their rapidly growing bones.1–3 Infecting organisms enter the because at these sites, the metaphysis is intracapsular. bone through the nutrient artery and then travel to the metaphy- Histologic features of acute osteomyelitis include localized sup- seal capillary loops, where they are deposited, replicate, and puration and abscess formation, with subsequent infarction and initiate an inflammatory response (Figure 78-1).
    [Show full text]
  • Osteochondral Injury of the Knee
    ® Volume 2, Part 3 December 2005 ORTHOPAEDIC SPORTS MEDICINE Board Review Manual Osteochondral Injury of the Knee Endorsed by the Association for Hospital www.turner-white.com Medical Education Your vision is our new bottom line. The company long respected for advancing the science of cartilage repair has more to offer than you ever anticipated. An established leader in the development of biomaterials and cell therapies, Genzyme Biosurgery is excited to now be driving the marketing and distribution of Synvisc® (hylan G-F 20). And our pioneering research into novel OA and cartilage repair solutions is destined to redefine the field of orthobiologics. So take a second look at Genzyme Biosurgery. What you see may surprise you. Genzyme Biosurgery 55 Cambridge Parkway Cambridge, MA 02142 GENZYME and SYNVISC are registered 1-800-901-7251 trademarks of Genzyme Corporation. www.genzymebiosurgery.com ® ORTHOPAEDIC SPORTS MEDICINE BOARD REVIEW MANUAL STATEMENT OF EDITORIAL PURPOSE Osteochondral Injury The Hospital Physician Orthopaedic Sports Medi- cine Board Review Manual is a peer-reviewed of the Knee study guide for orthopaedic sports medicine fellows and practicing orthopaedic surgeons. Contributors: Each manual reviews a topic essential to the current practice of orthopaedic sports medi- Jason M. Scopp, MD cine. Director, Cartilage Restoration Center, Peninsula Orthopaedic Associates, PA, Salisbury, MD PUBLISHING STAFF PRESIDENT, GROUP PUBLISHER Bert R. Mandelbaum, MD Bruce M. White Fellowship Director, Santa Monica Orthopaedic EDITORIAL DIRECTOR and Sports Medicine Group, Santa Monica, CA Debra Dreger ASSOCIATE EDITOR Editor: Tricia Faggioli Andrew J. Cosgarea, MD EDITORIAL ASSISTANT Associate Professor, Department of Orthopaedic Surgery, Farrawh Charles Johns Hopkins University School of Medicine, Baltimore, MD EXECUTIVE VICE PRESIDENT Barbara T.
    [Show full text]
  • Osteochondrosis
    Osteochondrosis (Abnormal Bone Formation in Growing Dogs) Basics OVERVIEW • Long bones (such as the humerus, radius and ulna in the foreleg and the femur and tibia in the rear leg) have three sections: the end of the bone, known as the “epiphysis”; the shaft or long portion of the bone, known as the “diaphysis”; and the area that connects the end and the shaft of the bone, known as the “metaphysis” • The metaphysis is the area where bone growth occurs in puppies; the long bones in the body grow in length at specific areas known as “growth plates”; these areas usually continue to produce bone until the bones are fully developed, at which time, no further growth is needed; the growth plates then “close” and become part of the hard bone • Bone is formed by the replacement of calcified cartilage at the growth plates; the bone-forming cells (known as “osteoblasts”) form bone on the cartilage structure; this process is known as “endochondral ossification” • “Osteochondrosis” is a disorder of bone formation in the growth plates (areas where bone grows in length in the young pet) of the bone; it is a disease process in growing cartilage, primarily characterized by a disturbance of the change from cartilage to bone (known as “endochondral ossification”) during bone development that leads to excessive retention of cartilage GENETICS • Multiple genes are involved (known as “polygenetic transmission”)—expression determined by an interaction of genetic and environmental factors • Heritability index—depends on breed, 0.25-0.45 SIGNALMENT/DESCRIPTION
    [Show full text]
  • Anterior Impingement with Exostosis and Fragmentation of the Talus
    ANTEROIR IMPINGEMENT WITH EXOSTOSIS AND FRAGMENTATION OF THE TALUS, NAVICULAR AND TIBIA IN A MALE COLLEGIATE BASKETBALL PLAYER Belter CA, Lopez RM, McDermott BP; University of Connecticut, Storrs, CT Background: During a regular season game, a 20-year-old male collegiate division I basketball player landed on an opponent’s foot after an offensive rebound. He inverted his right ankle but did not feel or hear a “pop.” He had experienced a grade one ankle sprain on the same ankle during preseason play. Upon evaluation, the athlete showed no signs of deformity. He was point tender over the anterior talofibular, calcaneofibular, and posterior talofibular ligaments. Passive range of motion (ROM) was within normal limits; however, active ROM was limited in plantarflexion and dorsiflexion. Manual muscle testing elicited soreness, but was within normal limits. All neurological tests were normal. An anterior drawer test was positive with increased laxity when compared bilaterally. The talar tilt test was negative. Differential Diagnosis: Ankle syndesmodic sprain, tarsal stress fracture, osteochondritis dissecans (OCD), lateral ankle sprain, anterior impingement with exostosis. Treatment: The team physician ordered an X-ray due to the athlete’s previous history of ankle sprains. Radiographs were negative for fractures but revealed bone spurs that were deemed asymptomatic. The athlete was given a walking boot for two days. He completed rehabilitation for a lateral ankle sprain that consisted of ice and compression, proprioception exercises, calf raises, calf stretches, and stability and agility exercises. Four days post injury, the athlete participated in a competition for approximately twenty minutes. He did not compete in subsequent competitions secondary to pain, weakness and an inability to complete prior practices.
    [Show full text]
  • Disorders of the Contractile Structures 54
    Disorders of the contractile structures 54 CHAPTER CONTENTS and is felt as a sudden, painful ‘giving way’ at the front of the Extensor mechanism 713 thigh. Alternatively, the muscular lesion may result from a direct contusion during contact sports (judo or American foot- Quadriceps strains and contusions . 713 ball), known as ‘Charley Horse’. Adherent vastus intermedius . 714 Patients who suffer an acute quadriceps strain will usually Tendinous lesions about the patella . 714 know right away. They are typically involved in sports requiring Rupture of the quadriceps tendon . 718 kicking, jumping, or initiating a sudden change in direction while running. Frequently, a sharp pain is felt, associated with Lesions of the infrapatellar tendon . 718 a loss in function of the quadriceps. Sometimes pain will not Lesions of the insertion at the tibial tuberosity . 719 fully develop during the athlete’s activity while the thigh is Patellar fracture . 719 warm; consequently, the extent of the injury is underesti- Patellofemoral disorders 719 mated. Stiffness, disability and pain then set in some time Introduction . 719 afterwards, e.g. late at night, and the following morning the patient can walk only with a limp.1 Mechanical theory . 719 Clinical examination shows a normal hip and knee, although Neural theory . 720 passive knee flexion is painful or both painful and limited, Clinical examination . 720 depending on the size of the rupture. Resisted extension of the Clinical manifestations . 722 knee is painful and slightly weak. As a rule, the lesion is in the 2 Strained iliotibial band 724 rectus femoris, usually at mid-thigh level. The affected muscle belly is hard and tender over a large area.
    [Show full text]
  • Human Osteology Method Statement N
    Human osteology method statement N. Powers (ed) Published online March 2008 Revised February 2012 2 LIST OF CONTRIBUTORS Museum of London Archaeology Centre for Human Bioarchaeology Service (MoLAS) (CHB) Brian Connell HND MSc Jelena Bekvalac BA MSc Amy Gray Jones BSc MSc Lynne Cowal BSc MSc Natasha Powers BSc MSc MIFA RFP Tania Kausmally BSc MSc Rebecca Redfern BA MSc PhD Richard Mikulski BA MSc Don Walker BA MSc AIFA Bill White Dip Arch FRSC FSA 3 CONTENTS Introduction ........................................................................................................................ 8 1 Preservation and archaeological data................................................................... 9 2 Catalogue of completeness ................................................................................... 10 2.1 Cranial elements ..................................................................................................... 10 2.2 Post-cranial elements.............................................................................................. 10 2.3 Cartilage.................................................................................................................. 11 2.4 Dentition ................................................................................................................. 11 3 Age at death estimation........................................................................................ 12 3.1 Subadult age at death.............................................................................................
    [Show full text]
  • MRI of Cartilage in the Athlete
    Shindle.fm Page 27 Monday, October 30, 2006 1:38 PM 27 COPYRIGHT © 2006 BY THE JOURNAL OF BONE AND JOINT SURGERY, INCORPORATED Magnetic Resonance Imaging of Cartilage in the Athlete: Current Techniques and Spectrum of Disease BY MICHAEL K. SHINDLE, MD, LI F. FOO, FRCR, BRYAN T. KELLY, MD, A. JAY KHANNA, MD, BENJAMIN G. DOMB, MD, ADAM FARBER, MD, TONY WANICH, MD, AND HOLLIS G. POTTER, MD Introduction other collagen types (types IV, VI, IX, X, and XI) have been n the athletic population, reproducible imaging of carti- identified1. Collagen provides the structural framework and lage damage is vital for treatment considerations. With tensile strength of articular cartilage. Chondroitin and keratin I appropriate pulse sequencing, magnetic resonance imag- sulfates are the predominant types of proteoglycan molecules ing has been shown to be an accurate noninvasive method for that are negatively charged and attract cations and water, the evaluation of articular cartilage injuries and for evaluating which provides compressive strength to the cartilage. postoperative changes following chondral repair. In addition, The normal thickness of articular cartilage ranges from magnetic resonance imaging does not utilize ionizing radia- 2 to 5 mm and is determined by the contact pressures that tion, has direct multiplanar capabilities, and allows high- occur across a joint. Higher peak pressures result in thicker resolution imaging of soft-tissue structures. The purposes of cartilage, and the patellofemoral joint has the thickest artic- the present review are to update orthopaedic surgeons on the ular cartilage in the body. Articular cartilage can be divided applications and techniques for magnetic resonance imaging into four distinct zones.
    [Show full text]
  • EVE 09-001 Mclellan Layout 1 19/11/2009 14:56 Page 1
    EVE 09-001 Mclellan_Layout 1 19/11/2009 14:56 Page 1 642 EQUINE VETERINARY EDUCATION / AE / decemBER 2009 Case Report Comparison of radiography, scintigraphy and ultrasonography in the diagnosis of patellar chondromalacia in a horse, confirmed by arthroscopy J. McLellan*, S. Plevin†, P. D. Hammock‡ and G. BonenClark§ Ferguson and Hammock Equine Hospital, 6897 NW Hwy 225A, Ocala, Florida; †Ocala Equine Hospital, Ocala, Florida; ‡Countryside Veterinary Services, Louisville, Tennessee; and §Equine Sports Practitioners, Ocala, Florida, USA. Keywords: horse; patella; chondromalacia; cartilage; stifle Summary 1982). In horses the disease may arise in response to abnormal cartilage stresses following partial upward Patellar chondromalacia is rarely reported in the horse. In fixation of the patella (Adams 1974), or through cartilage this study, several noninvasive diagnostic modalities were overload (May 1996), and the disease is a common combined to diagnose patellar chondromalacia in a complication of medial patellar ligament desmotomy horse, later confirmed by arthroscopy. Radiography failed (Gibson et al. 1989). One report in the literature also to demonstrate pathology; nuclear scintigraphy localised describes the gross development of patellar the disease process to the left femoropatellar region; and chondromalacia in a horse following traumatic disruption ultrasonography identified pathological changes within of the femoropatellar joint (Attenburrow and Goss 1994). the affected joint. It is possible that this disease is under- There is, however, a lack of information on patellar reported in the literature due to the difficulty in accurately chondromalacia as a primary disease process in the diagnosing the condition. horse. The scarcity of reports on this disease in horses may be due more to difficulty in the noninvasive diagnosis of Introduction patellar chondromalacia than to its actual prevalence.
    [Show full text]