Periapical Radiopacities
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Diagnosis and Treatment of Intramedullary Osteosclerosis
Abe et al. BMC Musculoskeletal Disorders (2020) 21:762 https://doi.org/10.1186/s12891-020-03758-5 CASE REPORT Open Access Diagnosis and treatment of intramedullary osteosclerosis: a report of three cases and literature review Kensaku Abe, Norio Yamamoto, Katsuhiro Hayashi, Akihiko Takeuchi* , Shinji Miwa, Kentaro Igarashi, Takashi Higuchi, Yuta Taniguchi, Hirotaka Yonezawa, Yoshihiro Araki, Sei Morinaga, Yohei Asano and Hiroyuki Tsuchiya Abstract Background: Intramedullary osteosclerosis (IMOS) is a rare condition without specific radiological findings except for the osteosclerotic lesion and is not associated with family history and infection, trauma, or systemic illness. Although the diagnosis of IMOS is confirmed after excluding other osteosclerotic lesions, IMOS is not well known because of its rarity and no specific feature. Therefore, these situations might result in delayed diagnosis. Hence, this case report aimed to investigate three cases of IMOS and discuss imaging findings and clinical outcomes. Case presentation: All three cases were examined between 2015 and 2019. The location of osteosclerotic lesions were femoral diaphyses in the 60-year-old man (Case 1) and 41-year-old woman (Case 2) and tibial diaphysis in the 44-year-old woman (Case 3). All cases complained of severe pain and showed massive diaphyseal osteosclerotic lesions in plain radiograms and computed tomography (CT) scans. Cases 2 and 3 were examined using the triphasic bone scan, and a fusiform-shaped intense area of the tracer uptake on delayed bone image was detected in both cases without (Case 2) or slightly increased vascularity (Case 3) on the blood pool image, which was reported as a specific finding of IMOS. -
Immunopathologic Studies in Relapsing Polychondritis
Immunopathologic Studies in Relapsing Polychondritis Jerome H. Herman, Marie V. Dennis J Clin Invest. 1973;52(3):549-558. https://doi.org/10.1172/JCI107215. Research Article Serial studies have been performed on three patients with relapsing polychondritis in an attempt to define a potential immunopathologic role for degradation constituents of cartilage in the causation and/or perpetuation of the inflammation observed. Crude proteoglycan preparations derived by disruptive and differential centrifugation techniques from human costal cartilage, intact chondrocytes grown as monolayers, their homogenates and products of synthesis provided antigenic material for investigation. Circulating antibody to such antigens could not be detected by immunodiffusion, hemagglutination, immunofluorescence or complement mediated chondrocyte cytotoxicity as assessed by 51Cr release. Similarly, radiolabeled incorporation studies attempting to detect de novo synthesis of such antibody by circulating peripheral blood lymphocytes as assessed by radioimmunodiffusion, immune absorption to neuraminidase treated and untreated chondrocytes and immune coprecipitation were negative. Delayed hypersensitivity to cartilage constituents was studied by peripheral lymphocyte transformation employing [3H]thymidine incorporation and the release of macrophage aggregation factor. Positive results were obtained which correlated with periods of overt disease activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive articular changes. This study suggests that cartilage antigenic components may facilitate perpetuation of cartilage inflammation by cellular immune mechanisms. Find the latest version: https://jci.me/107215/pdf Immunopathologic Studies in Relapsing Polychondritis JERoME H. HERmAN and MARIE V. DENNIS From the Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229 A B S T R A C T Serial studies have been performed on as hematologic and serologic disturbances. -
Oral Hard Tissue Lesions: a Radiographic Diagnostic Decision Tree
Scientific Foundation SPIROSKI, Skopje, Republic of Macedonia Open Access Macedonian Journal of Medical Sciences. 2020 Aug 25; 8(F):180-196. https://doi.org/10.3889/oamjms.2020.4722 eISSN: 1857-9655 Category: F - Review Articles Section: Narrative Review Article Oral Hard Tissue Lesions: A Radiographic Diagnostic Decision Tree Hamed Mortazavi1*, Yaser Safi2, Somayeh Rahmani1, Kosar Rezaiefar3 1Department of Oral Medicine, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran; 2Department of Oral and Maxillofacial Radiology, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran; 3Department of Oral Medicine, School of Dentistry, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Abstract Edited by: Filip Koneski BACKGROUND: Focusing on history taking and an analytical approach to patient’s radiographs, help to narrow the Citation: Mortazavi H , Safi Y, Rahmani S, Rezaiefar K. Oral Hard Tissue Lesions: A Radiographic Diagnostic differential diagnoses. Decision Tree. Open Access Maced J Med Sci. 2020 Aug 25; 8(F):180-196. AIM: This narrative review article aimed to introduce an updated radiographical diagnostic decision tree for oral hard https://doi.org/10.3889/oamjms.2020.4722 tissue lesions according to their radiographic features. Keywords: Radiolucent; Radiopaque; Maxilla; Mandible; Odontogenic; Nonodontogenic METHODS: General search engines and specialized databases including PubMed, PubMed Central, Scopus, *Correspondence: Hamed Mortazavi, Department of Oral Medicine, -
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. -
Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, Van Den Ende-Gupta, and Raine Syndromes
RESEARCH ARTICLE Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes Marjo K. Hytönen1,2,3, Meharji Arumilli1,2,3, Anu K. Lappalainen4, Marta Owczarek-Lipska5, Vidhya Jagannathan5, Sruthi Hundi1,2,3, Elina Salmela1,2,3, Patrick Venta6, Eva Sarkiala4, Tarja Jokinen1,4, Daniela Gorgas7, Juha Kere2,3,8, Pekka Nieminen9, Cord Drögemüller5☯, a11111 Hannes Lohi1,2,3☯* 1 Department of Veterinary Biosciences, University of Helsinki, Helsinki, Finland, 2 Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland, 3 The Folkhälsan Institute of Genetics, Helsinki, Finland, 4 Department of Equine and Small Animal Medicine, University of Helsinki, Helsinki, Finland, 5 Institute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland, 6 Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America, 7 Division of Clinical Radiology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, OPEN ACCESS University of Bern, Bern, Switzerland, 8 Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden, 9 Department of Oral and Maxillofacial Diseases, University of Helsinki, Helsinki, Citation: Hytönen MK, Arumilli M, Lappalainen AK, Finland Owczarek-Lipska M, Jagannathan V, Hundi S, et al. ☯ (2016) Molecular Characterization of Three Canine These authors contributed equally to this work. * [email protected] Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes. PLoS Genet 12(5): e1006037. doi:10.1371/journal. pgen.1006037 Abstract Editor: Leigh Anne Clark, Clemson University, UNITED STATES One to two percent of all children are born with a developmental disorder requiring pediatric hospital admissions. -
Dental ICD-10 Information
317:30-5-705. Billing Billing for dental services may be submitted on the currently-approved version of the American Dental Association (ADA) claim form. Diagnosis codes are requested to be listed in box 34 of ADA form 2012. To assist with your learning, the following codes are listed from International Classification of Disease, 10th revision, Clinical Modification (ICD-10-CM), Chapter 11: Diseases of the Digestive System (K00-K95). Most dental disorders are included in section K00- K14 - Diseases of oral cavity and salivary glands. ICD-10-CM 2016 K00 Disorders of tooth development and eruption K00.0 Anodontia K00.1 Supernumerary teeth K00.2 Abnormalities of size and form of teeth K00.3 Mottled teeth K00.4 Disturbances in tooth formation K00.5 Hereditary disturbances in tooth structure, not elsewhere classified K00.6 Disturbances in tooth eruption K00.7 Teething syndrome K00.8 Other disorders of tooth development K01 Embedded and impacted teeth K01.0 Embedded teeth K01.1 Impacted teeth K02 Dental caries K02.3 Arrested dental caries K02.5 Dental caries on pit and fissure surface o K02.51 limited to enamel o K02.52 penetrating into dentin o K02.53 penetrating into pulp K02.6 Dental caries on smooth surface o K02.61 limited to enamel o K02.62 penetrating into dentin o K02.63 penetrating into pulp K02.7 Dental root caries K03 other diseases of hard tissues of teeth K03.0 Excessive attrition of teeth K03.1 Abrasion of teeth K03.2 Erosion of teeth Last updated 7/2016 1 K03.3 Pathological resorption of teeth K03.4 Hypercementosis -
Core Decompression for Avascular Necrosis (For North Carolina Only) – Community Plan Medical Policy
UnitedHealthcare® Community Plan Medical Policy Core Decompression for Avascular Necrosis (for North Carolina Only) Policy Number: CSNCT0219.01 Effective Date: July 1, 2021 Instructions for Use Table of Contents Page Related Policies Application.......................................................................................... 1 None Coverage Rationale ........................................................................... 1 Applicable Codes .............................................................................. 1 Description of Services ..................................................................... 2 Clinical Evidence ............................................................................... 3 U.S. Food and Drug Administration ................................................ 7 References ......................................................................................... 7 Policy History/Revision Information................................................ 8 Instructions for Use ........................................................................... 8 Application This Medical Policy only applies to the state of North Carolina. Coverage Rationale Core decompression is proven and medically necessary for treating early (pre-collapse stage I and II) avascular necrosis of the femoral head. Core decompression is unproven and not medically necessary for treating late avascular necrosis of the femoral head or for avascular necrosis elsewhere, including the humeral head, the distal femur, the talus, or the -
Sclerosing Bone Dysplasias: Genetic, Clinical and Radiology Update of Hereditary and Non-Hereditary Disorders
BJR © 2016 The Authors. Published by the British Institute of Radiology Received: Revised: Accepted: http://dx.doi.org/10.1259/bjr.20150349 26 April 2015 14 December 2015 17 February 2016 Cite this article as: Boulet C, Madani H, Lenchik L, Vanhoenacker F, Amalnath DS, De Mey J, et al. Sclerosing bone dysplasias: genetic, clinical and radiology update of hereditary and non-hereditary disorders. Br J Radiol 2016; 89: 20150349. REVIEW ARTICLE Sclerosing bone dysplasias: genetic, clinical and radiology update of hereditary and non-hereditary disorders 1CEDRIC BOULET, MD, 2HARDI MADANI, FRCR, 3LEON LENCHIK, MD, 4FILIP VANHOENACKER, MD, PhD, 5DEEPAK S AMALNATH, MD, 1JOHAN DE MEY, MD, PhD and 1MICHEL DE MAESENEER, MD, PhD 1Department of Radiology, Universitair Ziekenhuis Brussel, Brussel, Belgium 2Department of Radiology, Royal Free Hospital, London, UK 3Department of Radiology, Wake Forest University, Winston Salem, NC, USA 4Department of Radiology, Universitair Ziekenhuis Anwerpen, Antwerpen, Belgium 5Department of Medicine, Indira Gandhi Medical College and Research Institute, Pondicherry, India Address correspondence to: Dr Michel De Maeseneer E-mail: [email protected] ABSTRACT There is a wide variety of hereditary and non-hereditary bone dysplasias, many with unique radiographic findings. Hereditary bony dysplasias include osteopoikilosis, osteopathia striata, osteopetrosis, progressive diaphyseal dysplasia, hereditary multiple diaphyseal sclerosis and pyknodysostosis. Non-hereditary dysplasias include melorheostosis, intramedullary osteosclerosis and overlap syndromes. Although many of these dysplasias are uncommon, radiologists should be familiar with their genetic, clinical and imaging findings to allow for differentiation from acquired causes of bony sclerosis. We present an overview of hereditary and non-hereditary bony dysplasias with focus on the pathogenesis, clinical and radiographic findings of each disorder. -
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. -
Hypophosphatasia: Enzyme Replacement Therapy Brings New Opportunities and New Challenges
PERSPECTIVE JBMR Hypophosphatasia: Enzyme Replacement Therapy Brings New Opportunities and New Challenges Michael P Whyte Department of Internal Medicine, Division of Bone and Mineral Diseases, Washington University School of Medicine, and Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children, St. Louis, MO, USA ABSTRACT Hypophosphatasia (HPP) is caused by loss-of-function mutation(s) of the gene that encodes the tissue-nonspecific isoenzyme of alkaline phosphatase (TNSALP). Autosomal inheritance (dominant or recessive) from among more than 300 predominantly missense defects of TNSALP (ALPL) explains HPP’s broad-ranging severity, the greatest of all skeletal diseases. In health, TNSALP is linked to cell surfaces and richly expressed in the skeleton and developing teeth. In HPP,TNSALP substrates accumulate extracellularly, including inorganic pyrophosphate (PPi), an inhibitor of mineralization. The PPi excess can cause tooth loss, rickets or osteomalacia, calcific arthropathies, and perhaps muscle weakness. Severely affected infants may seize from insufficient hydrolysis of pyridoxal 5‘- phosphate (PLP), the major extracellular vitamin B6. Now, significant successes are documented for newborns, infants, and children severely affected by HPP given asfotase alfa, a hydroxyapatite-targeted recombinant TNSALP. Since fall 2015, this biologic is approved by regulatory agencies multinationally typically for pediatric-onset HPP. Safe and effective treatment is now possible for this last rickets to have a medical therapy, -
Osteochondroma of the Femoral Neck: a Rare Cause of Sciatic Nerve Compression Page 1 of 7
Osteochondroma of the Femoral Neck: A Rare Cause of Sciatic Nerve Compression Page 1 of 7 HOME OF: Home Blogs News Wire iPhone App Multimedia Classified Marketplace E HIP ORTHOPEDICS August 2010;33(8):597. Osteochondroma of the Femoral Neck: A of Sciatic Nerve Compression Meetings & Courses by Kimberly Yu, BS; John P. Meehan, MD; Anto Fritz, MD; Amir A. Jamali, MD Featured Meetings Submit a Comment Print E-mail Abstract EFORT A 39-year-old man presented with weakness and a nonmobile mass in the butto Topics Hip flexion was limited to 70°. Strength was diminished for both ankle/foot planta Arthritis Sensation was decreased on the plantar and dorsal foot. A pedunculated osseo Arthroscopy on the posterior femoral neck was seen on plain radiographs and magnetic reso Biologics Electromyography showed moderate sciatic neuropathy of the peroneal and tibia underwent excision of the tumor through a posterior approach. Due to the risk of Business of Orthopedics 7.3-mm cannulated screws were passed percutaneously into the head with fluor Foot and Ankle pathological report indicated the tumor was an osteochondroma. At 22-month fo Hand/Upper Extremity resolution of the neurologic findings. Postoperatively, the patient reported improv Hip tingling in the leg but continued to have moderate buttock pain. Left hip flexion in follow-up. Imaging Infection The importance of protecting the medial femoral circumflex artery during approa Knee paramount. In this case, the tumor arose from the central aspect of the quadratu muscle protecting the medial femoral circumflex artery from harm. Although oste Oncology cause of mass effect, they should be considered in the differential diagnosis of s Osteoporosis this anatomical location. -
Computed Tomography Findings of Periostitis Ossificans
Case Report Braz J Oral Sci. January/March 2010 - Volume 9, Number 1 Computed tomography findings of periostitis ossificans Luciana Soares de Andrade Freitas Oliveira1, Thaís Feitosa L. de Oliveira2, Daniela Pita de Melo3, Alynne Vieira de Menezes4, Ieda Crusoé-Rebello5, Paulo Sérgio Flores Campos3 1Department of Health Sciences, Division of Pathology, Dental School, Federal University of Bahia, Brazil 2Department of Oral Diagnosis, Division of Periodontology, State University of Feira de Santana, Brazil 3Department of Oral Diagnosis, Division of Oral Radiology, Piracicaba Dental School, State University of Campinas, Brazil 4Department of Oral Diagnosis, Division of Oral Radiology, Piracicaba Dental School, State University of Campinas, Brazil 5Department of Oral Diagnosis, Division of Oral Radiology, Dental School, Federal University of Bahia, Brazil Abstract Periostitis ossificans (PO) is a type of chronic osteomyelitis, an inflammation of cortical and cancellous bone. In the maxillofacial region, the mandible is most frequently affected. The cause of inflammatory subperiosteal bone production in PO is spread of infection from a bacterial focus (e.g.: odontogenic disease, pulpal or periodontal infection, and extraction wounds). This pathology is most common in younger people (mean age of 13 years). Conventional radiographs are one of the most useful tools for diagnosis, but in some cases computed tomography (CT) has a key role in both diagnosis and identification of the tissues involved. This paper reports two cases of PO in which CT helped establishing the suspicious etiology: a 12-year-old boy with PO of pulpal origin and a 14-year-old boy with PO of periodontal origin. Keywords: osteomyelitis, tomography. Introduction Periostitis ossificans (PO) is a type of chronic osteomyelitis that is more popularly known as Garrè’s osteomyelitis.