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Aim Recently, with the second wave of COVID-19, the Indian subcontinent has witnessed a dramatic rise in mucormycosis infection in patients recovered from COVID-19. This association has been documented in various case reports/case series and institutional experiences, and the mortality associated with this fungal infection is emerging as a cause of concern. The aim of the present paper is to provide a scientific overview on the pathogenesis of mucormycosis in COVID-19 beyond the conventional understanding of the disease process, which may not otherwise explain the increased incidence of mucormycosis in SARS-CoV-2. Methodology This paper is structured as a narrative review of the published literature on the pathogenesis of COVID-19 which contributes to the development of mucormycosis. Apart from the acknowledged role of ketoacidosis, high blood sugar, and iron metabolism in the pathogenesis of mucormycosis, other factors involved in pathophysiology of COVID-19 which might alter or enhance the mucormycosis infection such as (1) the role of ferritin, (2) high serum iron, (3) free radical-induced endothelitis, (4) hepcidin activation, (5) upregulation of glucose receptor protein (GRP78) are discussed in the pathophysiology of COVID-19-associated mucormycosis. Conclusion A new proposal for the pathogenesis based on the ferritin, viral mimicry of hepcidin and GRP78–CotH3 interaction, which clearly explains the surge in mucormycosis in SARS-CoV-2 infection, has been explained.

Nerve injury Osteotomy a b s t r a c tAim: To retrospectively evaluate neurosensory disturbance (NSD) after bilateral sagittal split osteotomy (BSSO). Material and methods: A retrospective review was carried out to assess inferior alveolar nerve function in patients treated by BSSO from 2010 to 2013. All patients included in the study were assessed using objective (cotton swabs and pin prick testing) and subjective testing (questionnaire) for inferior alveolar nerve function after a minimum of 1 year of follow-up. Medical records of the patients were used to assess the incidence of NSD in the immediate post-operative period. Results: 15 patients (30 sides) had undergone BSSO during the specified time period. On subjective testing, NSD was reported in 22 operated sides (73.3%) in the immediate postoperative period, while 4 operated sides (13.3%) reported persistent NSD. On objective testing, immediate post-operative NSD was seen in 20 operated sides (66.7%). After a minimum of 1 year follow-up, recovery was seen in 18 operated sides while persistent NSD was seen in 2 operated sides (6.7%). Conclusion: NSD of the inferior alveolar nerve is a common complication after BSSO in the immediate post-operative period. However in a long term, nerve function usually recovers.