Leslie Michaels Born in London, England, Dr Michaels completed his medical education at Westminster Hospital Medical School in London in 1949. He underwent training in both clinical and anatomical pathology in Bristol, Manchester and London UK. He subsequently practised clinical and anatomical pathology in North America from 1959, spending most of the time in Northern Ontario, Canada. He returned to London in 1970 as pathologist to the Royal National Throat, Nose and Ear Hospital and Professor of ENT Pathology and Dean of the Institute of Laryngology and Otology. His main research interest has been in the pathology of the ear and he has contributed publication in this field until now. In recent years he has contributed particularly in the field of Meniere’s disease and otosclerosis.
Sava Soucek Born in Czechoslovakia, Dr Soucek completed her medical education there in Charles University, Prague in 1959. Subsequently she underwent training in otorhinolaryngology and practised this form of surgery in Prague till 1980. She then moved to London, England, where she modified her specialty to the medical discipline of audiovestibular medicine. She subsequently practised that specialty at St. Mary\'s Hospital, London. She has published widely in ENT pathology including a thesis on the pathology of hearing loss in the elderly, for which she was awarded a PhD degree of the University of London. Her research work has recently been concerned with aspects of Meniere\'s disease and otosclerosis. rnrn
We studied stained step sections embedded in celloidin of 54 temporal bones from 27 patients with otosclerosis at the Royal National Throat, Nose and Ear Hospital, London and the House Ear Institute, Los Angeles, California, in order to investigate the histopathologic changes in that disease of the otic capsule (OC). The outer layer of the normal OC is composed of regularly arranged osteons (Volkmann\'s canals and osteocytes) formed from the primitive connective tissue covering the OC externally. Otosclerosis is composed of multiple new plaques in the outer layer of the OC, each showing some resemblance to the structure of the normal outer layer of OC bone. The plaques, however, have each a basophilic area composed of irregular osteons comprising atypical osteoblasts with numerous, irregular Volkmann\'s canals. This has the appearance of an invasive front leading the growth of the otosclerotic plaque. This invasive front is always on the side of the plaque opposite to the periosteal surface of the involved temporal bone. Each plaque also shows increasingly more differentiated and paler-staining bony tissue retrogressively towards the periosteal covering of the OC from which the plaque appears to arise. The invasive front shows infiltration of the tissues that it contacts, by irregularly shaped, thin elongated processes of basophilic osteoblasts. Such invaded tissues are often the inner layer of the OC and beyond this the cochlea and vestibule. Since otosclerotic plaques are most commonly derived from the outer layer of OC near the periosteal connective tissue adjacent to the tensor tympani muscle, the structures most often invaded by otosclerosis are the stapediovestibular joint and the stapes footplate. The presence of multiple, similarly-structured plaques of otosclerosis, each with its undifferentiated invasive front edge and, posterior to that, progressive differentiation of the otosclerotic bony lesion towards the primitive connective tissue base are strongly suggestive of an invasive bony neoplasm of the OC. Otosclerosis has been in its long history rarely considered to be such a lesion. On the basis of the histopathology we put forward here, we consider neoplasia to be the most like pathologic basis for this condition.
Avlonitou Eirini has completed her PhD from the Physiology Department of Athens Medical School in the field of Sleep Apnea Syndrome. She has published more than 17 papers in reputed journals and participated in more than 50 congresses in Europe and USA.
Sleep related breathing disorders are observed at all ages. In Greece, at a study of 3.680 patients (1-18 years) from Thessaly, the prevalence of OSAS was 4.3%. The main risk factors for OSAS in children are adenotonsillar hypertrophy and obesity. The only reliable diagnostic method for the diagnosis of the syndrome is the full night polysomnography. Pulse oximetry is also a useful diagnostic tool but negative results must be confirmed with a full sleep study. The appropriate treatment is based on the AHI. Children with mild OSAS (AHI≤5) and adenotonsillar hypertrophy can be treated with nasal corticosteroids for six weeks and leukotriene receptor antagonists and reexamined after 6 months. Most of them show a significant improvement after this kind of treatment. Adenotonsillectomy has not been proved to improve the AHI in this category of children. Children with moderate to severe OSAS (AHI>5) and adenotonsillar hypertrophy are treated with adenotonsillectomy and most of them show a significant improvement in the AHI postoperatively. Obese children with adenotonsillar hypertrophy are treated as children with normal weight but concomitant weight control is a complementary treatment. In obese children without adenotonsillar hypertrophy weight control and possible use of CPAP (if AHI>5) are indicated. Children with residual OSAS can be managed with nasal corticosteroids and montelukast (very helpful especially in atopic children), body weight control (in obese children), use of CPAP (if AHI>5-10 events/hour).