Anatomy, Shoulder and Upper Limb, Humerus - Statpearls - NCBI Bookshelf
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Body Mechanics As the Rotator Cuff Gether in a Cuff-Shape Across the Greater and Lesser Tubercles the on Head of the Humerus
EXPerT CONTENT Body Mechanics by Joseph E. Muscolino | Artwork Giovanni Rimasti | Photography Yanik Chauvin Rotator Cuff Injury www.amtamassage.org/mtj WORKING WITH CLieNTS AFFecTED BY THIS COmmON CONDITION ROTATOR CUFF GROUP as the rotator cuff group because their distal tendons blend and attach to- The four rotator cuff muscles are gether in a cuff-shape across the greater and lesser tubercles on the head of the supraspinatus, infraspinatus, the humerus. Although all four rotator cuff muscles have specific concen- teres minor, and subscapularis (Fig- tric mover actions at the glenohumeral (GH) joint, their primary functional ure 1). These muscles are described importance is to contract isometrically for GH joint stabilization. Because 17 Before practicing any new modality or technique, check with your state’s or province’s massage therapy regulatory authority to ensure that it is within the defined scope of practice for massage therapy. the rotator cuff group has both mover and stabilization roles, it is extremely functionally active and therefore often physically stressed and injured. In fact, after neck and low back conditions, the shoulder is the most com- Supraspinatus monly injured joint of the human body. ROTATOR CUFF PATHOLOGY The three most common types of rotator cuff pathology are tendinitis, tendinosus, and tearing. Excessive physi- cal stress placed on the rotator cuff tendon can cause ir- ritation and inflammation of the tendon, in other words, tendinitis. If the physical stress is chronic, the inflam- matory process often subsides and degeneration of the fascial tendinous tissue occurs; this is referred to as tendinosus. The degeneration of tendinosus results in weakness of the tendon’s structure, and with continued Teres minor physical stress, whether it is overuse microtrauma or a macrotrauma, a rotator cuff tendon tear might occur. -
Upper Jaw Chronic Osteomyelitis. Report of Four Clinical Cases Osteomielitis Crónica Maxilar
www.medigraphic.org.mx Revista Odontológica Mexicana Facultad de Odontología Vol. 16, No. 2 April-June 2012 pp 105-111 CASE REPORT Upper jaw chronic osteomyelitis. Report of four clinical cases Osteomielitis crónica maxilar. Informe de 4 casos clínicos Alberto Wintergerst Fish,* Carlos Javier Iturralde Espinosa,§ Vladimir de la Riva Parra,II Santiago Reinoso QuezadaII ABSTRACT RESUMEN Osteomyelitis is an infl ammatory bone disease commonly related La osteomielitis es una enfermedad ósea infl amatoria, comúnmente to an infectious origin caused by germs, mainly pyogenic staphy- relacionada a un origen infeccioso por gérmenes piógenos funda- lococcus, and occasionally, streptococci, pneumococci and en- mentalmente estafi lococos y en algunas ocasiones por estreptoco- terobacteriae. Several treatments and classifi cations for osteomy- cos, neumococos y enterobacterias. Se han establecido diversas elitis have been established. These are based on clinical course, clasifi caciones y tratamientos para la osteomielitis, basadas en el pathologic-anatomical or radiologic features, etiology and patho- comportamiento clínico, características anatomo-patológicas, ra- genesis. Chronic osteomyelitis is a complication of non-treated or diográfi cas, etiología y patogenia. La osteomielitis crónica es una inadequately treated acute osteomyleitis. It can also be caused by a complicación de la osteomielitis aguda no tratada, manejada inade- low grade prolonged infl ammatory reaction. This study presents four cuadamente o como una reacción infl amatoria prolongada de bajo cases of maxillary osteomyelitis treated between 2007 and 2009. grado. Se presentan 4 casos de osteomielitis crónica en el maxilar Cases were treated with antimicrobial therapy. Preoperatively, pa- tratadas entre 2007 y 2009 mediante terapia antimicrobiana preo- tients were prescribed Clindamycin, 300 mg every eight hours, Ce- peratoriamente con clindamicina 300 mg, IV cada 8 h y ceftriaxona friaxone, 1 g IV every 12 hours. -
Osteomalacia and Osteoporosis D
Postgrad. med.J. (August 1968) 44, 621-625. Postgrad Med J: first published as 10.1136/pgmj.44.514.621 on 1 August 1968. Downloaded from Osteomalacia and osteoporosis D. B. MORGAN Department of Clinical Investigation, University ofLeeds OSTEOMALACIA and osteoporosis are still some- in osteomalacia is an increase in the alkaline times confused because both diseases lead to a phosphatase activity in the blood (SAP); there deficiency of calcium which can be detected on may also be a low serum phosphorus or a low radiographs of the skeleton. serum calcium. This lack of calcium is the only feature Our experience with the biopsy of bone is that common to the two diseases which are in all a large excess of uncalcified bone tissue (osteoid), other ways easily distinguishable. which is the classic histological feature of osteo- malacia, is only found in patients with the other Osteomalacia typical features of the disease, in particular the Osteomalacia will be discussed first, because it clinical ones (Morgan et al., 1967a). Whether or is a clearly defined disease which can be cured. not more subtle histological techniques will detect Osteomalacia is the result of an imbalance be- earlier stages of the disease remains to be seen. tween the supply of and the demand for vitamin Bone pains, muscle weakness, Looser's zones, D. The the following description of disease is raised SAP and low serum phosphate are the Protected by copyright. based on our experience of twenty-two patients most reliable aids to the diagnosis of osteomalacia, with osteomalacia after gastrectomy; there is no and approximately in that order. -
Bone Limb Upper
Shoulder Pectoral girdle (shoulder girdle) Scapula Acromioclavicular joint proximal end of Humerus Clavicle Sternoclavicular joint Bone: Upper limb - 1 Scapula Coracoid proc. 3 angles Superior Inferior Lateral 3 borders Lateral angle Medial Lateral Superior 2 surfaces 3 processes Posterior view: Acromion Right Scapula Spine Coracoid Bone: Upper limb - 2 Scapula 2 surfaces: Costal (Anterior), Posterior Posterior view: Costal (Anterior) view: Right Scapula Right Scapula Bone: Upper limb - 3 Scapula Glenoid cavity: Glenohumeral joint Lateral view: Infraglenoid tubercle Right Scapula Supraglenoid tubercle posterior anterior Bone: Upper limb - 4 Scapula Supraglenoid tubercle: long head of biceps Anterior view: brachii Right Scapula Bone: Upper limb - 5 Scapula Infraglenoid tubercle: long head of triceps brachii Anterior view: Right Scapula (with biceps brachii removed) Bone: Upper limb - 6 Posterior surface of Scapula, Right Acromion; Spine; Spinoglenoid notch Suprspinatous fossa, Infraspinatous fossa Bone: Upper limb - 7 Costal (Anterior) surface of Scapula, Right Subscapular fossa: Shallow concave surface for subscapularis Bone: Upper limb - 8 Superior border Coracoid process Suprascapular notch Suprascapular nerve Posterior view: Right Scapula Bone: Upper limb - 9 Acromial Clavicle end Sternal end S-shaped Acromial end: smaller, oval facet Sternal end: larger,quadrangular facet, with manubrium, 1st rib Conoid tubercle Trapezoid line Right Clavicle Bone: Upper limb - 10 Clavicle Conoid tubercle: inferior -
Trapezius Origin: Occipital Bone, Ligamentum Nuchae & Spinous Processes of Thoracic Vertebrae Insertion: Clavicle and Scapul
Origin: occipital bone, ligamentum nuchae & spinous processes of thoracic vertebrae Insertion: clavicle and scapula (acromion Trapezius and scapular spine) Action: elevate, retract, depress, or rotate scapula upward and/or elevate clavicle; extend neck Origin: spinous process of vertebrae C7-T1 Rhomboideus Insertion: vertebral border of scapula Minor Action: adducts & performs downward rotation of scapula Origin: spinous process of superior thoracic vertebrae Rhomboideus Insertion: vertebral border of scapula from Major spine to inferior angle Action: adducts and downward rotation of scapula Origin: transverse precesses of C1-C4 vertebrae Levator Scapulae Insertion: vertebral border of scapula near superior angle Action: elevates scapula Origin: anterior and superior margins of ribs 1-8 or 1-9 Insertion: anterior surface of vertebral Serratus Anterior border of scapula Action: protracts shoulder: rotates scapula so glenoid cavity moves upward rotation Origin: anterior surfaces and superior margins of ribs 3-5 Insertion: coracoid process of scapula Pectoralis Minor Action: depresses & protracts shoulder, rotates scapula (glenoid cavity rotates downward), elevates ribs Origin: supraspinous fossa of scapula Supraspinatus Insertion: greater tuberacle of humerus Action: abduction at the shoulder Origin: infraspinous fossa of scapula Infraspinatus Insertion: greater tubercle of humerus Action: lateral rotation at shoulder Origin: clavicle and scapula (acromion and adjacent scapular spine) Insertion: deltoid tuberosity of humerus Deltoid Action: -
Osteopetrosis J
Arch Dis Child: first published as 10.1136/adc.46.247.257 on 1 June 1971. Downloaded from Archives of Disease in Childhood, 1971, 46, 257. Osteopetrosis J. S. YU,* R. K. OATES, K. HELEN WALSH, and SUSAN J. STUCKEY From the Department of Child Health, University of Sydney, and Department of Dietetics, Royal Alexandra Hospital for Children, Camperdown, N.S.W., Australia Yu, J. S., Oates, R. K., Walsh, K. H., and Stuckey, S. J. (1971). Archives of Disease in Childhood, 46, 257. Osteopetrosis. The clinical histories of nine children with osteopetrosis are reported. Two of them had the malignant infantile variety of the disease: one died within 3 months of birth and the other has survived 20 months on a regimen of a low calcium intake, cellulose phosphate, and steroids. The beneficial effect of a low calcium intake, in early infancy, is supported by the clinical course in the infant with the malignant variety and in another child with the more benign form of the disease. No calcium balance studies were performed. This study suggests that the active measures outlined may favourably influence the haematological and osteosclerotic course of the disease, pending further know- ledge of its aetiological basis, and more specific therapy. Osteopetrosis or marble bone disease is a rare positive calcium balance with a diet low in calcium metabolic bone disease characterized by dense and with steroids (Morrow et al., 1967). This bones (Albers-Schonberg, 1904; Karshner, 1926). approach to management has been recently criti- copyright. Two varieties have been clearly defined-an cized by Cohen (Children's Hospital Medical infantile progressive disease and a milder benign Center, Boston, 1965). -
Hematological Diseases and Osteoporosis
International Journal of Molecular Sciences Review Hematological Diseases and Osteoporosis , Agostino Gaudio * y , Anastasia Xourafa, Rosario Rapisarda, Luca Zanoli , Salvatore Santo Signorelli and Pietro Castellino Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy; [email protected] (A.X.); [email protected] (R.R.); [email protected] (L.Z.); [email protected] (S.S.S.); [email protected] (P.C.) * Correspondence: [email protected]; Tel.: +39-095-3781842; Fax: +39-095-378-2376 Current address: UO di Medicina Interna, Policlinico “G. Rodolico”, Via S. Sofia 78, 95123 Catania, Italy. y Received: 29 April 2020; Accepted: 14 May 2020; Published: 16 May 2020 Abstract: Secondary osteoporosis is a common clinical problem faced by bone specialists, with a higher frequency in men than in women. One of several causes of secondary osteoporosis is hematological disease. There are numerous hematological diseases that can have a deleterious impact on bone health. In the literature, there is an abundance of evidence of bone involvement in patients affected by multiple myeloma, systemic mastocytosis, thalassemia, and hemophilia; some skeletal disorders are also reported in sickle cell disease. Recently, monoclonal gammopathy of undetermined significance appears to increase fracture risk, predominantly in male subjects. The pathogenetic mechanisms responsible for these bone loss effects have not yet been completely clarified. Many soluble factors, in particular cytokines that regulate bone metabolism, appear to play an important role. An integrated approach to these hematological diseases, with the help of a bone specialist, could reduce the bone fracture rate and improve the quality of life of these patients. -
Evaluation of Humeral and Glenoid Bone Deformity in Glenohumeral Arthritis 5
Evaluation of Humeral and Glenoid Bone Deformity 1 in Glenohumeral Arthritis Brian F. Grogan and Charles M. Jobin Introduction glenoid bone wear helps the surgeon formulate a successful treatment plan and surgical goals Glenohumeral arthritis is the sequela of a vari- to address the pathoanatomy and improve the ety of pathologic shoulder processes, most durability of shoulder arthroplasty. The evalu- commonly degenerative osteoarthritis, but may ation of humeral and glenoid bone deformity also be secondary to post-traumatic conditions, in glenohumeral arthritis has profound surgical inflammatory arthritis, rotator cuff tear arthrop- implications and is fundamental to successful athy, and postsurgical conditions most com- shoulder arthroplasty. monly post-capsulorrhaphy arthritis. Patients with glenohumeral arthritis commonly demon- strate patterns of bony deformity on the glenoid Glenoid Deformity in Osteoarthritis and humerus that are caused by the etiology of the arthritis. For example, osteoarthritis com- Glenoid deformity and glenohumeral subluxation monly presents with posterior glenoid wear, are commonly seen in the setting of primary osteo- secondary glenoid retroversion, and posterior arthritis of the glenohumeral joint. The glenoid humeral head subluxation, while inflammatory wear tends to occur posteriorly and may be best arthritis routinely causes concentric glenoid viewed on axial radiographs or computed tomog- wear with central glenoid erosion. A thorough raphy (CT) axial images. Glenoid erosion, as first history and physical, as well as laboratory and characterized by Walch, is noted to be either central radiographic workup, are keys to understanding or posterior, with varying degrees of wear and pos- the etiology of arthritis and understanding the terior subluxation of the humerus [1, 2] (Fig. -
Spontaneous Healing of Osteitis Fibrosa Cystica in Primary Hyperparathyroidism
754 Gibbs, Millar, Smith Postgrad Med J: first published as 10.1136/pgmj.72.854.754 on 1 December 1996. Downloaded from Spontaneous healing of osteitis fibrosa cystica in primary hyperparathyroidism CJ Gibbs, JGB Millar, J Smith Summar biochemistry showed hypercalcaemia, hypo- A 24-year-old man with primary hyper- phosphataemia, elevated parathyroid hormone, parathyroidism and osteitis fibrosa cystica but normal alkaline phosphatase (table). developed acute hypocalcaemia. Sponta- Radiographs showed improvement in the neous healing of his bone disease was mandibular translucency and resolution of the confirmed radiographically and by correc- phalangeal tuft resorption and subperiosteal tion of the serum alkaline phosphatase. erosion (figures 1B, 2B). Thallium scan of the Hypercalcaemia associated with a raised neck showed no evidence of parathyroid serum parathyroid hormone recurred 90 activity and neck exploration failed to reveal weeks after the initial presentation. Dur- any parathyroid tissue. Venous sampling ing the fourth neck exploration a para- showed no step-up in parathyroid hormone thyroid adenoma was removed, resulting concentration in the neck or chest. Selective in resolution of his condition. Haemor- angiography suggested a parathyroid adenoma rhagic infarction of an adenoma was the behind the right clavicle but two further most likely cause of the acute hypocalcae- explorations revealed only one normal para- mic episode. thyroid gland. Computed tomography (CT) of the neck showed a low attenuation, non- Keywords: primary hyperparathyroidism, osteitis enhancing mass in the right lower pole of the fibrosa cystica, hypercalcaemia thyroid gland. Ultrasonography confirmed a hypo-echoic mass 1.5 x 0.5 cm in the right lobe of the thyroid. -
Avulsion Fracture of Brachioradialis Muscle Origin: an Exceedingly Rare Entity: a Case Report
10-039_OA1 8/13/16 5:34 PM Page 50 Malaysian Orthopaedic Journal 2016 Vol 10 No 2 Behera G, et al http://dx.doi.org/10.5704/MOJ.1607.010 Avulsion Fracture of Brachioradialis Muscle Origin: An Exceedingly Rare Entity: A Case Report Behera G, DNB, Balaji G, MS Ortho, Menon J, MRCS (Edin.), Sharma D, MCH, Komuravalli VK, DNB Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India Date of submission: March 2016 Date of acceptance: June 2016 ABSTRACT lateral supracondylar ridge just proximal to the lateral epicondyle. He had restriction of active terminal elbow Avulsion fracture of the brachioradialis origin at its proximal extension by 10 degrees with near normal active elbow attachment on the lateral supracondylar ridge of the distal flexion, pronation and supination. Active flexion and humerus is exceedingly rare, and only two cases have been extension at wrist were painful along with the painful reported in the literature so far. In this article, we present a terminal elbow extension. There was significant pain at the 38 years old patient who sustained a closed avulsion fracture lateral distal humerus when active elbow flexion against of the lateral supracondylar ridge of left humerus at the resistance was performed in the mid-pronated position of the proximal attachment of brachioradialis following a fall forearm. There was no distal neurovascular deficit. backwards on outstretched hand after being struck by a lorry from behind while riding on a two-wheeler (motorcycle). He Antero-posterior (AP) plain radiograph of the left elbow was managed with above elbow plaster for four weeks showed a fracture of the lateral distal humerus at the followed by elbow and wrist mobilization. -
Introduction to the Orthopedics
[ Color index : Important | Notes | Extra ] Editing file link Introduction to the Orthopedics Objectives: ★ To explain what Orthopedic is and what conditions will be discussed during this course ★ Explain what we mean by Red Flags ★ List the different causes of orthopedic disease. ★ Describe some of clinical examination tests ★ Introduce titles of Clinical Skills which will be taught during this course. Done by: Rana Albarrak & Lamya Alsaghan Edited By: Bedoor Julaidan Revised by: Dalal Alhuzaimi References: slides + Toronto notes + 433 team + 435 team group A Introduction Orthopedic specialty: ★ Branch of surgery concerned with conditions involving the musculoskeletal system. Orthopedic surgeons use both surgical and nonsurgical means to treat musculoskeletal trauma, spine diseases, sports injuries, degenerative diseases, infections, tumors, and congenital disorders. ★ It includes: bones, muscles, tendons, ligaments, joints, peripheral nerves (peripheral neuropathy of hand and foot), , vertebral column, spinal cord and its nerves. NOT only bones. ★ Subspecialties: General, pediatric, sport and reconstructive (commonly ACL “anterior cruciate ligament” injury), trauma, arthroplasty, spinal surgery, foot and ankle surgery, oncology, hand surgery (usually it is a mixed speciality depending on the center. Orthopedics = up to the wrist joint. Orthopedics OR plastic surgery = from carpal bones and beyond, upper limb (new) elbow & shoulder. will be discussed in details in a separate lectures Red Flags: ★ Red Flags = warning symptoms or signs = necessity for urgent or different action/intervention. ★ Should always be looked for and remembered. you have to rule out red flags with all emergency cases! Fever is NOT a red flag! Do not confuse medicine with ortho. Post-op day 1 fever is considered normal! ★ There are 5 main red flags: 1. -
Bone Homeostasis and Pathology
Bone Homeostasis and Pathology Instructor: Roman Eliseev Outline: § Bone anatomy and composi<on § Bone remodeling § Factors regulang bone homeostasis § Disorders of bone homeostasis: -Bone loss -Abnormal bone acquisi<on § Methods and Mouse Models Adult Skeleton Axial Skeleton Appendicular Skeleton 206 bones Image from www.pngall.com Adult Bone Architecture Cor<cal bone Marrow cavity Diaphysis Metaphysis Epiphysis Trabecular bone Bone Histology Subchondral bone Trabecular bone Marrow fat Bone marrow Cor<cal bone Bone Composion Bone is a mineralized organic matrix composed of: • Type I collagen and non-collagenous proteins (osteoid) • Hydroxyapate crystals (Ca5(PO4)3(OH)) Osteoblasts Bone Bone-forming cells are osteoblasts (OB) that produce collagen I and deposit HA Bone is Formed by Osteoblasts OBs originate from Bone Marrow Stromal (a.k.a. Mesenchymal Stem) Cells (BMSC) and terminally differen<ate into osteocytes (OT). Wagner et al., PPAR Res., 2010 Bone is Resorbed by Osteoclasts Image from SciencePhotoLibrary Osteoclasts (OC) are bone resorbing mul<nucleated cells that originate from hematopoie<c cells (monocyte/macrophage) Homeostasis = equilibrium (Greek: ὁμοίως + στάσις) Bone Formaon vs Resorp<on = Dynamic Equilibrium (~10% of adult human skeleton is replaced annually) Bone Bone rosorp<on formaon Intact Bone BMSC – bone marrow stromal Blood vessel (a.k.a. mesenchymal stem) cell BMSC OB – osteoblast OT – osteocyte Apoptosis OB (~70%) Lining cells BONE OT TGFb, IGF1, OCN Collagen I Remodeling: Ini<al Phase BMSC – bone marrow stromal (a.k.a. mesenchymal stem) cell Blood vessel HSC OB – osteoblast BMSC OT – osteocyte HSC – hematopoie<c stem cell RANKL, OCP – osteoclast precursor ? m-CSF OCP OB Lining cells BONE OT Remodeling: Resorp<on Pit BMSC – bone marrow stromal (a.k.a.