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      Tumoral Calcinosis of the Cervical Spine Associated with a Pathologic Odontoid Fracture

      case-report

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          Abstract

          Tumoral calcinosis involves focal calcium deposits in the soft tissues surrounding a joint and most commonly occurs in the hips and elbows, rarely in the cervical spine. Furthermore, it has not been known to be associated with pathologic fractures. To the best of our knowledge, our case report highlights the first case of a pathologic type II odontoid fracture associated with adjacent tumoral calcinosis, resulting in pain, dysphagia, and severe spinal stenosis. The patient underwent a posterior occipitocervical fusion and C1 laminectomy, along with planned tracheostomy and gastrostomy to avoid expected difficulty with postoperative extubation and dysphagia. Additionally, we present a review of existing literature on tumoral calcinosis in the upper cervical spine.

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          Review of tumoral calcinosis: A rare clinico-pathological entity.

          Ibrahim Fathi, Mahmoud Sakr (2014)
          Tumoral calcinosis (TC) has long been a controversial clinico-pathological entity. Its pathogenesis and genetic background have been gradually unravelled since its first description in 1943. According to the presence or absence of an underlying calcifying disease process, TC has been divided into primary and secondary varieties. Two subtypes of the primary variety exist; a hyper-phosphatemic type with familial basis represented by mutations in GalNAc transferase 3 gene (GALNT3), KLOTHO or Fibroblast growth factor 23 (FGF23) genes, and a normo-phosphatemic type with growing evidence of underlying familial base represented by mutation in SAMD9 gene. The secondary variety is mainly associated with chronic renal failure and the resulting secondary or tertiary hyperparathyroidism. Diagnosis of TC relies on typical radiographic features (on plain radiographs and computed tomography) and the biochemical profile. Magnetic resonance imaging can be done in difficult cases, and scintigraphy reflects the disease activity. Treatment is mainly surgical for the primary variety; however, a stage-oriented conservative approach using phosphate binders, phosphate restricted diets and acetazolamide should be considered before the surgical approach is pursued due to the high rate of recurrences and complications after surgical intervention. Medical treatment is the mainstay for treatment of the secondary variety, with failure warranting subtotal or total parathyroidectomy. Surgical intervention in these patients should be kept as a last resort.
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            Proposal for a pathogenesis-based classification of tumoral calcinosis.

            Darren Fitzpatrick, D P Smack, Raymond S. Norton (1996)
            Deposition of calcium in skin is currently categorized into a group of disorders referred to as calcinosis cutis. Divisions between types and subtypes within this confusing classification are predominantly based on morphologic differences in the calcification and serve to obscure pathogenesis. This is especially evident in a subtype of calcinosis cutis, known as tumoral calcinosis. Calcifications in cases of tumoral calcinosis share the following characteristics, but without evidence of a common pathogenesis: large size, juxtaarticular location, progressive enlargement over time, a tendency to recur after surgical removal, and an ability to encase adjacent normal structures. The goal of this study was to formulate a pathogenesis-based classification for cases of tumoral calcinosis. In a literature review 121 cases of tumoral calcinosis were identified. These cases, along with a case evaluated in our clinic, were reviewed retrospectively, and their features compared. Analysis suggests three pathogenetically distinct subtypes of tumoral calcinosis: (1) Primary normophosphatemic tumoral calcinosis: patients have normal serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; (2) primary hyperphosphatemic tumoral calcinosis: patents have elevated serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; and (3) secondary tumoral calcinosis: patients have a concurrent disease capable of causing soft tissue calcification. Justification for this classification is based on the presence or absence of disorders known to promote soft tissue calcification and statistically significant differences in family history, mean calcification number, mean serum phosphate level, and calcification recurrence after excision. A classification for tumoral calcinosis is devised that outlines potential pathogenetic mechanisms and predicts response to therapy and prognosis. Analysis of other forms of calcinosis cutis may reveal definable pathogenetic differences that suggest a coherent classification for all cutaneous calcinoses.
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              Tumoral calcinosis: pearls, polemics, and alternative possibilities.

              Kathryn M Olsen, Felix S. Chew (2015)
              Massive periarticular calcinosis of the soft tissues is a unique but not rare radiographic finding. On the contrary, tumoral calcinosis is a rare familial disease. Unfortunately, the term tumoral calcinosis has been liberally and imprecisely used to describe any massive collection of periarticular calcification, although this term actually refers to a hereditary condition associated with massive periarticular calcification. The inconsistent use of this term has created confusion throughout the literature. More important, if the radiologist is unfamiliar with tumoral calcinosis or disease processes that mimic this condition, then diagnosis could be impeded, treatment could be delayed, and undue alarm could be raised, possibly leading to unwarranted surgical procedures. The soft-tissue lesions of tumoral calcinosis are typically lobulated, well-demarcated calcifications that are most often distributed along the extensor surfaces of large joints. There are many conditions with similar appearances, including the calcinosis of chronic renal failure, calcinosis universalis, calcinosis circumscripta, calcific tendonitis, synovial osteochondromatosis, synovial sarcoma, osteosarcoma, myositis ossificans, tophaceous gout, and calcific myonecrosis. The radiologist plays a critical role in avoiding unnecessary invasive procedures and in guiding the selection of appropriate tests that can result in a conclusive diagnosis of tumoral calcinosis. Copyright RSNA, 2006.
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                Author and article information

                Contributors
                Andy Y. Wang:
                ORCID: https://orcid.org/0000-0001-8689-9624
                Journal
                Journal ID (nlm-ta): Case Rep Neurol Med
                Journal ID (iso-abbrev): Case Rep Neurol Med
                Journal ID (publisher-id): CRINM
                Title: Case Reports in Neurological Medicine
                Publisher: Hindawi
                ISSN (Print): 2090-6668
                ISSN (Electronic): 2090-6676
                Publication date Collection: 2022
                Publication date (Electronic): 7 January 2022
                Volume: 2022
                Electronic Location Identifier: 2798490
                Affiliations
                1Department of Neurosurgery, Tufts Medical Center, Boston, MA, USA
                2Department of Surgery, Tufts Medical Center, Boston, MA, USA
                Author notes

                Academic Editor: Peter Berlit

                Author information
                https://orcid.org/0000-0001-8689-9624
                https://orcid.org/0000-0002-9095-1947
                Article
                DOI: 10.1155/2022/2798490
                PMC ID: 8759912
                PubMed ID: 35036015
                SO-VID: 008fb9a3-2a44-4577-acc5-5c6bde202f41
                Copyright © Copyright © 2022 Andy Y. Wang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 August 2021
                Date revision received : 6 December 2021
                Date accepted : 31 December 2021
                Categories
                Subject: Case Report

                Data availability:

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