Masticatory Myositis Research Articles

Masticatory Myositis of a Dog – Case Study

Atrophic myositis is the result of prominent atrophy of masticatory muscles. The masseter, temporal, and pterygoid muscles are selectively affected. A dog was presented to the Emergency Clinic of our Veterinary Faculty with the following clinical signs: progressive dyspnea and weight loss, apathy, cough, adinamia. The 11 years old, female, crosss-breed dog was reported to be unable to completely open his mouth (trismus), with the head having a fine fox-like contour, with unusual prominences of zygomatic arches. Following necropsy, the gross exam revealed advanced bilateral atrophy and fibrosis of temporal, pterigoid and masseter muscle, accompanied by a primary mammary carcinoma with pulmonary metastases. Histological lesions from the masticatory muscles were very patchy. In some areas there was an admixed inflammatory infiltrate predominately composed of lymphocytes and plasma cells. Muscle fiber atrophy was associated with focal areas of chronic proliferative fibrosis. In conclusion, masticatory muscle myositis needs to be included in the differential diagnosis of disorders in dogs with trismus and abnormal jaw function.

The dolognawmeter: A novel instrument and assay to quantify nociception in rodent models of orofacial pain

Rodent pain models play an important role in understanding the mechanisms of nociception and have accelerated the search for new treatment approaches for pain. Creating an objective metric for orofacial nociception in these models presents significant technical obstacles. No animal assay accurately measures pain-induced orofacial dysfunction that is directly comparable to human orofacial dysfunction. We developed and validated a high throughput, objective, operant, nociceptive animal assay, and an instrument to perform the assay termed the dolognawmeter, for evaluation of conditions known to elicit orofacial pain in humans. Using the device our assay quantifies gnawing function in the mouse. We quantified a behavioral index of nociception and demonstrated blockade of nociception in three models of orofacial pain: (1) TMJ inflammation, (2) masticatory myositis, and (3) head and neck cancer. This assay will be useful in the study of nociceptive mediators involved in the development and progression of orofacial pain conditions and it will also provide a unique tool for development and assessment of new therapeutic approaches.

Central nervous system infection withStaphylococcus intermediussecondary to retrobulbar abscessation in a dog

In this report, we describe a case of retrobulbar abscessation in a dog that was initially diagnosed as masticatory myositis and treated with immunosuppressive doses of corticosteroids. Secondary bacterial infection of the central nervous system (CNS) occurred and was definitively diagnosed by the analysis and culture of the cerebrospinal fluid. This is the first time that retrobulbar infection has been definitively shown to result in secondary bacterial infection of the CNS in the dog and highlights the importance of ruling out infectious causes of retrobulbar disease before assuming and treating for an immune-mediated etiology.

Life Threatening Complication Associated with Anesthesia in a Dog with Masticatory Muscle Myositis

To report a serious complication in a dog with masticatory muscle myositis (MMM) that occurred during general anesthesia for diagnostic testing. Case report. A 2-year-old male Pug. MMM was diagnosed in a Pug with a 2-week history of trismus by electrodiagnostics, histopathology, and 2M antibody test. During anesthesia tongue protrusion occurred and because of trismus, an inability to reposition the tongue resulted in venous congestion and severe swelling. Forceful physical attempts and subsequent removal of the rostral digastricus and masseter muscle attachments from the mandible did not increase jaw mobility. Mandibular symphysiotomy was necessary to resolve lingual venous congestion and to reposition the tongue into the oral cavity. Tongue swelling rapidly subsided after symphysiotomy allowing the tongue to be repositioned into the oral cavity. After treatment of MMM with corticosteroids, jaw range of motion improved and at 6 months was approximately 70% normal. Trismus could not be overcome by detachment of the masseter and digastricus muscle insertions from the mandible, and symphysiotomy was required to reposition the tongue in the oral cavity. In dogs with MMM, tongue position should be monitored during anesthesia to avoid inadvertent protrusion and swelling from venous congestion. Use of anesthetic monitoring equipment on the tongue, such as a pulse oximeter probe, should be avoided in these patients.

G.P.5.12 Decorin and lumican are differentially expressed in canine masticatory muscle myositis

G.P.5.12 Decorin and lumican are differentially expressed in canine masticatory muscle myositis

IMAGING DIAGNOSIS—MASTICATORY MUSCLE MYOSITIS IN A YOUNG DOG

Veterinary Radiology & UltrasoundVolume 49, Issue 3 p. 270-272 IMAGING DIAGNOSIS—MASTICATORY MUSCLE MYOSITIS IN A YOUNG DOG TODD M. BISHOP, TODD M. BISHOP Red Bank Veterinary Hospital, Department of Neurology and Neurosurgery, Tinton Falls, NJ,Search for more papers by this authorERIC N. GLASS, ERIC N. GLASS Red Bank Veterinary Hospital, Department of Neurology and Neurosurgery, Tinton Falls, NJ,Search for more papers by this authorALEXANDER DE LAHUNTA, ALEXANDER DE LAHUNTA Concord, NH, andSearch for more papers by this authorG. DIANE SHELTON, G. DIANE SHELTON Comparative Neuromuscular Laboratory, Department of Pathology, University of California-San Diego, LA Jolla, CASearch for more papers by this author TODD M. BISHOP, TODD M. BISHOP Red Bank Veterinary Hospital, Department of Neurology and Neurosurgery, Tinton Falls, NJ,Search for more papers by this authorERIC N. GLASS, ERIC N. GLASS Red Bank Veterinary Hospital, Department of Neurology and Neurosurgery, Tinton Falls, NJ,Search for more papers by this authorALEXANDER DE LAHUNTA, ALEXANDER DE LAHUNTA Concord, NH, andSearch for more papers by this authorG. DIANE SHELTON, G. DIANE SHELTON Comparative Neuromuscular Laboratory, Department of Pathology, University of California-San Diego, LA Jolla, CASearch for more papers by this author First published: 02 May 2008 https://doi.org/10.1111/j.1740-8261.2008.00364.xCitations: 16 Address correspondence and reprint requests to Todd M. Bishop, at the above address. E-mail tmbishopdvm@yahoo.com Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume49, Issue3May/June 2008Pages 270-272 RelatedInformation

Locked Jaw Syndrome in Dogs and Cats: 37 Cases (1998–2005)

A consecutive series of cases of dogs and cats with locked jaw syndrome (inability to open or close the mouth) are reported in this study. Dogs were significantly overrepresented (84.0%) and adult dogs were more frequently affected (81.0%). Temporomandibular joint ankylosis due to fracture was the most common cause (54.0%) of locked jaw syndrome. Additional potential causes of locked jaw syndrome are masticatory muscle myositis, neoplasia, trigeminal nerve paralysis and central neurological lesions, temporomandibular joint luxation and dysplasia, osteoarthritis, retrobulbar abscess, tetanus, and severe ear disease. Treatment of locked jaw is directed towards the primary cause. It is important to treat the tonic spasm in order to minimize periarticular fibrosis. Surgical intervention is recommended for temporomandibular joint ankylosis. Masticatory muscle myositis treatment is initiated by gradually opening the mouth, with medical treatment based on immunosuppressive therapy. Fracture and masticatory muscle myositis are associated with a relatively good prognosis in regard to short-term outcome as compared to animals with central neurologic lesions or osteosarcoma which have a poor prognosis.

下顎の歯性感染症から継発した脳膿瘍の１例

We report a rare case of brain abscess secondary to mandibular odontogenic infection. A 50-year-oldman developed an abscess of the infratemporal fossa, masticatory myositis, and temporal myositis caused bylower first molar marginal periodontitis. Incision and drainage were performed by an intraoral approach, andantibiotics were administered intravenously. On the 8th disease day, vomiting occurred, but responded to anantiemetic drug. On the 9th disease day, extraction of lower first molar and adrasion was performed, resulting inthe alleviation of local symptoms. However, a persistent headache occurred, CT and MRI scans revealed a brainabscess and subdural abscess in the temporal lobe, immediately above the skull internal base. The patient wasgiven a diagnosis of brain abscess caused by odontogenic infection. The abscess almost disappeared after conservativetherapy administered at the department of brain surgery, and no sequelae were noted. The abscess apparentlyexpanded directly and continuously from the skull base through the foramen ovale and foramen spinosum.This case emphasizes the need to diagnose brain abscess and subdural abscess as complications of odontogenicinfection.

Autoantibodies in Canine Masticatory Muscle Myositis Recognize a Novel Myosin Binding Protein-C Family Member

Inflammatory myopathies are a group of autoimmune diseases that affect muscles. In humans, the most common inflammatory myopathies are polymyositis, dermatomyositis, and inclusion body myositis. Autoantibodies may be found in humans with inflammatory myopathies, and these play an important role in diagnosis and disease classification. However, these Abs are typically not muscle specific. Spontaneously occurring canine inflammatory myopathies may be good parallel disorders and provide insights into human myositis. In dogs with inflammatory myopathy, muscle-specific autoantibodies have been found, especially in masticatory muscle myositis. We have identified the major Ag recognized by the autoantibodies in canine masticatory muscle myositis. This Ag is a novel member of the myosin binding protein-C family, which we call masticatory myosin binding protein-C (mMyBP-C). mMyBP-C is localized not only within the masticatory muscle fibers, but also at or near their cell surface, perhaps making it accessible as an immunogen. The gene for mMyBP-C also exists in humans, and mMyBP-C could potentially play a role in certain human inflammatory myopathies. Understanding the role of mMyBP-C in this canine inflammatory myopathy may advance our knowledge of mechanisms of autoimmune inflammatory muscle diseases, not only in dogs, but also in humans.

Computed tomographic appearance of masticatory myositis in dogs: 7 cases (1999–2006)

To document computed tomography (CT) features in dogs with masticatory myositis. Retrospective case series. 7 dogs with an immunologic diagnosis of masticatory myositis and an absence of clinical abnormalities of any skeletal muscles other than the masticatory muscles. History; clinical, hematologic, biochemical, immunologic, cytologic, and histologic findings; and pre- and postcontrast CT imaging features of masticatory muscles and head and neck lymph nodes were extracted from medical records. On CT images, changes in size (atrophy or swelling) were common for all masticatory muscles except the digastricus muscles, which were involved only in 1 dog. Pre-contrast attenuation changes, most often hypoattenuation with varied distribution patterns, were seen in masticatory muscles of 4 dogs. Contrast enhancement with a predominantly inhomogeneous distribution pattern was seen in the temporalis, masseter, and pterygoid muscles of all dogs. Head and neck lymph nodes were enlarged in all but 1 dog and had contrast enhancement with predominantly central or homogeneous distribution patterns. Muscle biopsy was performed in 6 dogs, with biopsy specimens obtained from areas that had the most obvious contrast enhancement on CT images. For all 6 dogs, biopsy specimens had histologic features indicative of masticatory myositis. Results suggested that CT may be a useful adjunct in the diagnosis of masticatory myositis in dogs, including selection of sites for diagnostic muscle biopsy.

Expression of major histocompatibility complex class I and class II antigens in canine masticatory muscle myositis

Studies in human immune-mediated inflammatory myopathies have documented expression of major histocompatibility complex class I (MHC class I) and class II (MHC class II) antigens on muscle fiber membranes in the presence or absence of cellular infiltration. Here we evaluate the presence and distribution of these antigens in canine masticatory muscle myositis, an immune-mediated inflammatory myopathy. Twelve samples of temporalis and masseter muscles from dogs with a clinical diagnosis of canine masticatory muscle myositis were examined by immunohistochemistry and double-immunofluorescence confocal microscopy. MHC class I and class II antigens were expressed in muscle fibers independent of inflammatory cell infiltration. Furthermore MHC class I and class II antigens were expressed on the sarcolemma and co-localized with dystrophin. Our results suggest that MHC class I and class II expression in canine masticatory muscle myositis may play a role in the initiation and maintenance of the pathological condition, rather than just a consequence of a preceding local inflammation.

Atypical masticatory muscle myositis in three cavalier King Charles spaniel littermates

This case report describes a novel manifestation of the immune-mediated disease, masticatory muscle myositis. Clinical signs, including difficulty in opening the mouth (trismus), were seen in three of four 12-week-old cavalier King Charles spaniel littermates. Diagnosis was established by 2M immunohistochemistry, supported by characteristic histopathological changes in affected temporal muscle. Treatment using corticosteroids at immune-modifying doses resulted in resolution of clinical signs in all the affected animals. Masticatory muscle myositis should be considered as a differential diagnosis in groups of young dogs with clinical signs of myositis localised to the head.

Evidence for MHC‐1–restricted CD8+ T‐cell–mediated immunopathology in canine masticatory muscle myositis and polymyositis

Evidence for MHC‐1–restricted CD8⁺ T‐cell–mediated immunopathology in canine masticatory muscle myositis and polymyositis

Evidence for MHC I–restricted CD8+ T‐cell–mediated immunopathology in canine masticatory muscle myositis and polymyositis

Masticatory muscle myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated muscles of 53 dogs with MMM, 32 dogs with polymyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4(+) and CD8(+)T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8(+)T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on muscle fibers. CD8(+)T cells invading intact and neighboring necrotic muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8(+) T-cell infiltrations and muscle-fiber lesions. Since MHC class I antigen and CD8(+) T cells were detected in the presence of CD4(+) T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8(+) T-cell-mediated immunopathological disease that initiates muscle-fiber destruction and leads to production of myosin autoantibodies.

Canine inflammatory myopathy: analysis of cellular infiltrates.

Inflammatory myopathies (IMs) occur relatively frequently in dogs, and, with the exception of masticatory muscle myositis (MMM), have not been characterized. This study analyzed the distribution and types of cellular infiltrates in 21 cases of generalized IM, 3 cases of focal IM (MMM), and 1 case with features of both generalized and focal IM, using a panel of monoclonal antibodies to cell surface markers. In generalized IM, mononuclear cells showed an endomysial and perimysial distribution with invasion of non-necrotic fibers similar to human IM. T lymphocytes with T-cell receptor (TCR)alphabeta predominated. Distinct differences were seen in MMM including prominent B-cell infiltration, dendritic cells and macrophages in greater numbers than T cells, and numerous T cells with TCRgammadelta. Thus, generalized IM and MMM appear to be distinct diseases with different mechanisms. Canine generalized IM may be an important animal model for human IM.

Canine Inflammatory Myopathies: A Clinicopathologic Review of 200 Cases

A retrospective study was performed on 200 randomly selected cases of inflammatory myopathy in dogs from diagnostic muscle biopsies received at the Comparative Neuromuscular Laboratory, University of California, San Diego. The most common clinical signs in dogs diagnosed with an inflammatory myopathy were generalized weakness, stilted gait, dysphagia, masticatory or generalized muscle atrophy, inability to open the jaw, megaesophagus, and dysphonia. Myalgia was rarely described. Age of onset ranged from 0.25 to 14 years. Genders were equally represented. Breed distribution approximated the 2002 American Kennel Club registration statistics (r = .85) with the notable exception of Boxers and Newfoundlands. From the results of muscle biopsies, clinical signs, and presence or absence of antibodies against type 2M fibers, dogs were classified as a generalized inflammatory myopathy (gIM)--including immune-mediated polymyositis; infectious and preneoplastic myositis; and, rarely, dermatomyositislike or overlap syndromes or unclassified myositis-or a focal inflammatory myopathy (flM)--including masticatory muscle and extraocular myositis. Average creatine kinase (CK) and aspartate aminotransferase (AST) concentrations in gIMs were significantly higher than those with fIMs (P < .05). Neoplasia developed in 12 of 200 dogs within 12 months of diagnosis of polymyositis, with lymphoma diagnosed in 6 of 32 Boxers. Inflammatory myopathy was associated with antibody titers against infectious diseases in 38 dogs. Neospora caninum and Hepatozoon americanum cysts were found in tissues of 2 dogs not serologically tested. Antibodies against an unidentified sarcolemmal antigen were found in 9 of 19 Newfoundlands with polymyositis. The spectrum of canine inflammatory myopathies can be broad, with infectious etiologies relatively common, and can include preneoplastic and uncharacterized syndromes.

Titin and ryanodine receptor autoantibodies in dogs with thymoma and late-onset myasthenia gravis

Similar to human autoimmune myasthenia gravis (MG), canine MG occurs spontaneously and is associated with autoantibodies against the nicotinic acetylcholine receptor (AChR). In addition to AChR, human MG patients with thymoma or late-onset MG have antibodies against titin and ryanodine receptor (RyR). The objective of this study was to establish if dogs with confirmed MG (AChR antibody titer >0.6 nmol/l) also developed titin and RyR antibodies and identify possible associations with thymoma, late age of onset, or severity of clinical signs. Sera from dogs ( n=430) with previously diagnosed autoimmune MG ( N=415), other immune-mediated neuromuscular disorders including polymyositis (PM) and masticatory muscle myositis ( N=5), and control dogs ( N=10) were evaluated for the presence of titin antibodies in ELISA using MGT-30 as antigen, a peptide representing the main immunogenic region (MIR) for human titin antibodies. Titin antibody positive sera were further examined for RyR antibodies in Western blots using a RyR fusion protein (pc2–RyR) as antigen, which covers the MIR for human MG sera. Titin antibodies were found in sera of 80/430 dogs. Thymoma was present in 11/80 and age of onset was after 4 years in 66/80 titin positive dogs. Two of the titin positive dogs had PM. RyR antibodies were found in 13/80 sera (8/13 thymoma, 12/13 age of onset after 4 years, and 1/13 PM). Neither titin nor RyR antibodies were found in sera of healthy control dogs. Acute fulminating MG was described in five dogs with both titin and RyR antibodies. From these studies we conclude that titin and RyR antibodies in canine and human MG have a similar association with thymoma, late-onset MG, and possibly with more severe forms of MG.

Masticatory and skeletal muscle myositis in canine leishmaniasis (Leishmania infantum)

Twenty-four dogs with a parasitologically and serologically established diagnosis of leishmaniasis were studied to investigate the atrophy of the masticatory muscles which commonly occurs in this disease, and to compare...

Extraocular muscle myositis and restrictive strabismus in 10 dogs.

Ten cases of uni- or bilateral restrictive ventromedial strabismus in young dogs of different breeds are reported. Clinically, abnormalities were restricted to the extraocular muscles with sparing of the masticatory muscles and limb muscles. This was supported in some cases by imaging studies, electrophysiology, and immunocytochemical assay for antibodies against type 2M fibers. Histologically, there was variable lymphocytic plasmacytic mononuclear cell infiltration and fibrosis. This disorder is similar in many aspects to chronic masticatory myositis with focal myositis and subsequent fibrosis. Surgical correction may restore eye position and vision.

Involvement of the medial pterygoid muscle in masticatory muscle myositis

Involvement of the medial pterygoid muscle in masticatory muscle myositis