Abstract

AbstractAim & ObjectivesTo carry out detailed light microscopic analysis of excised specimen of elongated styloid processes (ESPs) from patients suffering from Eagle's syndrome (ES). To thus gain a clear and precise insight into the aetiology, origin, development and progression of styloid enlargement, and to accurately hypothesize the underlying histopathological mechanisms bringing about their thickening and elongation.Study Design & SettingThis 3‐year study was conducted in 10 patients of ES, who were treated by transoral styloidectomy. The excised ESPs were subjected to a systematic and comprehensive histological analysis of sections from their base, mid and apical thirds.Material & MethodsImaging and diagnostic workup, operative procedure, postsurgical protocols and regimen, tissue processing and analysis of excised specimen were the same in all patients.ResultsImmature woven bone trabeculae and dystrophic calcifications were found within fibrocollagenous mesenchymal condensations of the stylohyoid ligament (SL) at the apical region of the ESPs, and in the tendinous insertions of the styloid group of muscles into the ESPs, indicative of their osseous metaplasia as a form of reactive response.ConclusionRepetitive stress, traction or traumatic stimuli brought to bear upon the apices and lateral surfaces of styloid processes via tendinous insertions of the SL and styloid group of muscles, as a result of neck and hyoid movements, are likely to serve as triggering factors, stimulating an osseous metaplasia of connective cells within these mesenchymal structures as well as in the periosteal fibrous tissue, into osteoblasts and osteocytes. This reactive response is followed by osteogenesis and laying down of woven bone at these sites, resulting in increase in length and circumference of the SPs and their attendant, associated clinical sequelae.

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