AB1287 INFLAMMATION OF THE TEMPORALIS MUSCLE AND ADJACENT NERVE TISSUE IN GIANT CELL ARTERITIS: EXPANDING THE SPECTRUM OF INFLAMMATORY LESIONS
Authors: N. Ruffer, M. T. Holzer, L. Kawelke, H. H. Goebel, D. Poddubnyy, U. Schneider, C. Preuße, M. Krusche, W. Stenzel
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Cranial giant cell arteritis (C-GCA) is associated with headache, scalp tenderness and jaw claudication. Localized symptoms of the temporomandibular region are thought to result from exercise-dependent ischaemia in the context of vascular inflammation [1, 2]. However, the potential inflammation of the temporalis muscle (TM) and adjacent nerve tissue received little attention. One magnetic resonance imaging study [3] reported signs of TM inflammation in approximately 20% of patients but the histopathological features of these lesions have not been studied to the best of our knowledge. <h3>Objectives:</h3> To investigate the histomorphological features of the TM and adjacent nerve tissue in C-GCA. <h3>Methods:</h3> Temporal artery biopsy (TAB) specimens with fragments of the TM from patients with biopsy-proven C-GCA (n = 8) fulfilling the 2022 ACR/EULAR classification criteria were assessed by conventional histology and immunohistochemistry in comparison with non-disease controls (n = 3). Clinical, laboratory and imaging features based on patient charts at the time of biopsy were retrospectively recorded. <h3>Results:</h3> The majority (7/8) of temporal artery specimens showed inflammation of the TM and adjacent nerve fascicles that was characterized by prominent endomysial lymphomonocytic infiltrates, whereas controls showed no inflammatory lesions and no disruption of the local architecture. Association of C-GCA with sarcolemmal MHC class I (8/8) and MHC class II (3/8) upregulation indicates primary inflammation of the TM in most patients. αB-Crystallin positivity (7/8) highlights areas of pre-necrotic myofibers in the TM. The presence of endomysial fibrosis, signs of atrophy and variations of muscle fibre size suggests a rather longstanding and potentially subclinical process of myoinflammation and tissue damage. <h3>Conclusion:</h3> Our results expand the spectrum of inflammatory lesions known to be associated with C-GCA. Specifically, inflammatory infiltration of the TM and nerve structures could contribute to localized symptoms of the temporomandibular region and should be included in concepts of pathophysiology. <h3>REFERENCES:</h3> [1] Peral-Cagigal B, Perez-Villar A, Redondo-Gonzalez LM, et al. Temporal headache and jaw claudication may be the key for the diagnosis of giant cell arteritis. Med Oral Patol Oral Cir Bucal 2018;23(3):e290-e4. [2] Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA 2002;287(1):92-101. [3] Veldhoen S, Klink T, Geiger J, et al. MRI displays involvement of the temporalis muscle and the deep temporal artery in patients with giant cell arteritis. Eur Radiol 2014;24(11):2971-9. <h3>Acknowledgements:</h3> The outstanding technical assistance of Petra Matylewski and Sylvia Stefaniak is kindly acknowledged. <h3>Disclosure of Interests:</h3> Nikolas Ruffer: None declared, Marie-Therese Holzer: None declared, Leona Kawelke: None declared, Hans-Hilmar Goebel: None declared, Denis Poddubnyy AbbVie, Canon, DKSH, Eli Lilly, Janssen, MSD, Medscape, Novartis, Peervoice, Pfizer, and UCB, AbbVie, Biocad, Bristol-Myers Squibb, Eli Lilly, Janssen, Moonlake, Novartis, Pfizer, and UCB, AbbVie, Eli Lilly, MSD, Novartis, and Pfizer, Udo Schneider GSK (payment for presentation), Boehringer Ingelheim (payment for presentation), Vifor (payment for presentation), Corinna Preuße Alexion, Martin Krusche Novartis, Abbvie, Lilly, Galapagos, Pfizer, Medac, Novartis, Roche, Abbvie, Lilly, Galapagos, Pfizer, Medac, Werner Stenzel Argenex, Alexion, GSK.