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Biomedical subjects

P Cayé-Thomasen

Publications and source records attributed to P Cayé-Thomasen.

At least 19 recordsLinked to original sources
PubMed2006

Hearing loss and cochlear damage in experimental pneumococcal meningitis, with special reference to the role of neutrophil granulocytes.

Hearing loss is a well-known sequelae from meningitis, affecting up to 25% of survivors. However, the principal components of the infectious and inflammatory reaction responsible for the sensorineural hearing loss remain to be identified. The present study aimed to investigate the impact of an augmented neutrophil response on the development of hearing loss and cochlear damage in a model of experimental pneumococcal meningitis in rats. Hearing loss and cochlear damage were assessed by distortion product oto-acoustic emissions (DPOAE), auditory brainstem response (ABR) and histopathology in rats treated with ceftriaxone 28 h after infection. Rats were treated with Granulocyte Colony Stimulating Factor (G-CSF) initiated prior to infection, 28 h after infection or with ceftriaxone only. Rats were followed for 7 days, and assessment of hearing was performed before infection and 24 h and day 8 after infection. Pretreatment with G-CSF increased hearing loss 24 h after infection and on day 8 compared to untreated rats (Mann-Whitney, P = 0.012 and P = 0.013 respectively). The increased sensorineural hearing loss at day 8 was associated with significantly decreased spiral ganglion cell counts (P = 0.0006), increased damage to the organ of Corti (P = 0.007), increased areas of inflammatory infiltrates (P = 0.02) and increased white blood cell (WBC) counts in cerebrospinal fluid on day 8 after infection (P = 0.0084). Initiation of G-CSF 28 h after infection did not significantly affect hearing loss or cochlear pathology compared to controls. In conclusion, the inflammatory host reaction contributes significantly to the development of hearing loss in experimental meningitis.

Animals↗
PubMed2002

Cartilage palisade tympanoplasty in sinus and tensa retraction cholesteatoma.

OBJECTIVE: The aim of this study was to investigate whether reconstruction of the eardrum with palisade cartilage technique could prevent retraction of the new eardrum after surgery for sinus and tensa retraction cholesteatoma in children and to investigate the postoperative hearing. STUDY DESIGN: In 32 children aged 5 to 15 years, operated on from June 1995 to October 2000 for cholesteatoma (21 with sinus cholesteatoma and 11 with tensa retraction cholesteatoma) the eardrum was reconstructed with the palisade cartilage technique. Postoperatively, the children were seen as outpatients and were recently reevaluated with otomicroscopy, tympanometry, and audiometry. All patients (100%) were reevaluated on an average of 37 months (range 3-63 months). MAIN OUTCOME MEASURES: Postoperative retractions, perforations, cholesteatoma recurrence, and hearing. RESULTS: At the final examination, posterosuperior retraction was observed in two patients, both operated on for sinus cholesteatoma with reconstruction of the ossicular chain. In those cases, the palisades were not placed in the posterosuperior drilling defect behind the interpositioned incus. All the patients had an intact tympanic membrane at the final follow-up visit. One small perforation was surgically closed during the observation period. No patients developed cholesteatoma during the follow-up period. The postoperative hearing was good, and the hearing did not deteriorate with increasing observation time. CONCLUSIONS: The palisade technique effectively prevented postoperative retraction of the eardrum. The postoperative hearing was good.

Acoustic Impedance Tests↗
PubMed2001

Goblet cell density in acute otitis media caused by Moraxella catarrhalis.

HYPOTHESIS AND BACKGROUND: Secretory otitis media is associated with a highly increased goblet cell density, confirming the secretory pathogenesis of this disease. Previous studies have shown that the middle ear goblet cell density, and thus the secretory capacity, are massively increased during experimental acute otitis media and at least 6 months thereafter, conceivably predisposing to the subsequent development of secretory otitis media. These studies used middle ear inoculation of either Streptococcus pneumoniae, nontypeable Haemophilus influenzae, or H. influenzae type b. The present study aimed at determining the goblet cell density during and after acute otitis media caused by Moraxella catarrhalis to clarify whether this bacterium induces an equivalently enhanced secretory capacity. METHODS: Twenty-five 25 rat middle ears were inoculated with M. catarrhalis. Five rats were killed on days 4, 8, 16, 60, and 180 after inoculation, followed by staining, dissection, and whole-mount embedding of the middle ear mucosae. The goblet cell density was determined by counting in 24 fields, covering the entire middle ear. RESULTS: In comparison with 25 normal middle ears, the goblet cell density was significantly increased in almost all counting localities, from day 4 and < or = 2 months after inoculation. The goblet cell density peaked on day 16, subsided thereafter, and in some areas reached a normal level 6 months after the acute incident. Mucosal areas containing goblet cells were consistently enlarged, thus leaving the middle ear with an increased secretory capacity during and 6 months after inoculation. CONCLUSION: The goblet cell density of the middle ear mucosa is increased during acute otitis media caused by M. catarrhalis and up to several months thereafter. This may predispose to the subsequent development of secretory otitis media. However, in comparison with acute otitis media caused by other bacteria, M. catarrhalis induced only modest changes in goblet cell density.

Acute Disease↗
PubMed2000

Effect of penicillin on experimental acute otitis media. A histopathological study of goblet cell density, bone modelling dynamics, polyp and adhesion formation.

Clinical studies have shown that the effect of antibiotic treatment on acute otitis media is modest. Experimental acute otitis media induces a number of histopathological changes in the middle ear mucosa. Among these are increased goblet cell density, polyp and adhesion formation, as well as massive osteoneogenesis. To investigate the effect of penicillin administration on these histopathological features, we employed a rat model of acute pneumococcal otitis media. Five of 25 rats were sacrificed on days 4, 8, 16, 90 and 180 post-inoculation, preceded by oral administration of penicillin V 100 mg/kg/day, initiated on day 2 and lasting 5 days. Using a light microscope, qualitative and quantitative histopathology of middle ear goblet cell density, bone-modelling dynamics, polyp and adhesion formation was registered and compared with previous studies of untreated animals. Increase in goblet cell density and new bone formation was reduced significantly by treatment, whereas polyp and adhesion formation was unaffected by penicillin administration. It is concluded that penicillin reduces middle ear secretory capacity and new bone formation during and following acute otitis media, conceivably preventing subsequent development of secretory otitis media, leaving polyp and adhesion formation unchanged.

Acute Disease↗
PubMed2000

Polyp and fibrous adhesion formation in acute otitis media caused by non-typeable or type b Haemophilus influenzae or Moraxella catarrhalis.

Among a variety of other histopathologic changes, polyps and fibrous adhesions are readily formed in the middle ear mucosa during experimental acute otitis media (AOM) caused by Streptococcus pneumoniae. Quantitative studies on experimental AOM caused by other bacteria have shown that some of these histopathologic changes, such as adaptive bone modeling and increase in goblet cell density, differ according to the type of bacteria. This investigation surveys polyp and fibrous adhesion formation in experimental AOM caused by either non-typeable or type b Haemophilus influenzae, or Moraxella catarrhalis. Seventy-five rats were inoculated with 1 of these 3 bacteria (25 rats in each of 3 groups). Five rats from each group were sacrificed on days 4, 8, 16, 60 and 180 post-inoculation. The middle ear mucosae were dissected and histopathologic changes in whole-mount and section preparations were studied using light microscopy. Polyps were found in most ears and in the greatest numbers on the early days; fewer polyps were found on the later days, regardless of the type of bacteria. However, non-typeable and type b H. influenzae induced formation of significantly more polyps than M. catarrhalis. The polyps were primarily located in the epitympanum. Fibrous adhesions were primarily located in the hypotympanum and formed in almost all ears, on all days post-inoculation, regardless of the type of bacteria. Numbers increased to a peak on day 16 and then decreased. Non-typeable and type b H. influenzae induced formation of significantly more adhesions than M. catarrhalis, and the middle ears displayed a higher number of persisting adhesions in the animals inoculated with non-typeable H. influenzae. We conclude that polyps and adhesions are formed in experimental AOM regardless of bacterial type, confirming a pathogenesis based on inflammation. Both types of H. influenzae induce formation of greater numbers of polyps/adhesions than M. catarrhalis, and the non-typeable form causes more adhesive sequelae in the mucosa than the encapsulated type b.

Acute Disease↗
PubMed2000

Adaptive bone modeling and remodeling in acute otitis media caused by non-typeable or type B Haemophilus influenzae or Moraxella catarrhalis.

Experimental studies have shown that acute otitis media caused by Streptococcus pneumoniae alters modeling dynamics in bone tissue structures surrounding the middle ear cavity. Initial resorption of bone is followed by formative activity, seen as massive osteoneogenesis. However, neither resorptive nor formative activity occurs in the otic capsule, supporting the existence of a perilymphatic zone of specialized bone. This study investigates adaptive bone modeling in acute otitis media caused by other bacteria frequently encountered in this disease. Seventy-five rats were inoculated with either non-typeable or type b Haemophilus influenzae, or Moraxella catarrhalis (25 rats in each group). Five rats from each group were sacrificed on days 4, 8, 16, 60 and 180 post-inoculation. Qualitative as well as quantitative histopathology revealed increasing apposition of new bone on both sides of the original bony wall of the middle ear bulla, i.e. at the inner and outer periosteum. Remodeling activity was seen on later days of sacrifice, as typical osteone (Haversian system) formation. Measured bone thickness in four anatomically well-defined localities progressed to a peak 2 months post-inoculation, followed by some degree of normalization. However, bone thickness was still massively increased 6 months after the acute incident. Except in the otic capsule, resorptive and formative activity was found in all bone tissue structures surrounding the middle ear cavity. These findings were irrespective of the type of inoculated bacteria. However, non-typeable or type b Haemophilus influenzae induces significantly more new bone formation than Moraxella catarrhalis. We conclude that acute otitis media caused by either of the bacteria is accompanied by massive and progressive net osteoneogenesis, already evident on day 4 and peaking 2 months post-inoculation, followed by some degree of normalization. Non-typeable and type b Haemophilus influenzae induce more new bone formation than Moraxella catarrhalis, whereas other features of bone histomorphology were equivalent. The present findings further support the existence of a perilymphatic zone of specialized bone.

Acute Disease↗
PubMed2000

Middle ear secretory capacity after acute otitis media caused by Streptococcus pneumoniae, Moraxella catarrhalis, non-typeable or type B Haemophilus influenzae. A comparative analysis based on goblet cell density.

To investigate whether the type of bacteria is correlated with an increase in goblet cell density during and after acute otitis media, we inoculated the middle ear of 25 rats with either Streptococcus pneumoniae, Moraxella catarrhalis, non-typeable or type b Haemophilus influenzae. Mucosal goblet cell density was determined by a whole-mount method on days 4, 8, 16, 60 and 180 post-inoculation. The goblet cell density was increased on all days of sacrifice, employing either bacteria, except M. catarrhalis 6 months after the acute incident. Type b H. influenzae induced the highest increase, followed by non-typeable H. influenzae, S. pneumoniae and M. catarrhalis. The mucosal area containing goblet cells was enlarged on all examination days, employing either bacteria. We conclude, that mucosal secretory capacity is highly increased during and up to 6 months after acute middle ear infection caused by either bacteria, conceivably predisposing a subsequent development of secretory otitis media. The results indicate that type b H. influenzae seems to be the bacteria most likely to induce a subsequent secretory condition.

Acute Disease↗
PubMed1999

Bone modeling dynamics in acute otitis media.

OBJECTIVE: A number of middle ear diseases are associated with pathologic bone modeling, either formative or resorptive. As such, the pathogenesis of a sclerotic mastoid has been controversial for decades. Experimental studies on acute middle ear infection have shown varying degrees of both osteoresorption and osteoneogenesis. This study presents data on the dynamics of bone modeling in a rat model of acute pneumococcal otitis media, studied longitudinally from day 1 through 6 months after inoculation. RESULTS: Qualitative, as well as quantitative histopathology revealed initial osteoresorption, followed by increasing apposition of new bone in the middle ear cavity, initiated at the outer periosteum. Measured bone thickness in four anatomically distinct locations peaked 3 months after inoculation, followed by some degree of normalization. However, bone thickness was still massively increased 6 months after the acute incident. Except in perilymphatic spaces of the otic capsule, resorptive and formative activity were found in all bone tissue structures surrounding the middle ear cavity, including the bony external auditory canal and the ossicles. CONCLUSION: These findings may support the existence of a perilymphatic barrier of specialized bone and suggest that even a single episode of acute infection may alter properties of ossicular chain conduction. The authors conclude that acute otitis media is accompanied by massive and progressing net osteoneogenesis, already evident at 3 days and peaking 3 months after inoculation, followed by some degree of normalization. This is conceivably in support of the environmental theory of mastoid pneumatization, claiming inflammatory disease as the cause of a sclerotic mastoid.

Acute Disease↗
PubMed1999

Penicillin reduces new bone formation in acute otitis media.

OBJECTIVE: Previous studies have shown that acute otitis media alters modeling dynamics in bone tissue structures surrounding the middle ear cavity. Initial resorption is followed by formative activity, which is seen as massive osteoneogenesis. However, neither resorptive nor formative activity occurs in the otic capsule, supporting the theory on existence of a perilymphatic barrier of specialized bone. STUDY DESIGN: To investigate the effect of penicillin administration on the pathological bone modeling in acute otitis media, we employed a rat model of acute pneumococcal otitis media. METHODS: Five rats were sacrificed on postinoculation days 4, 8, 16, 90, and 180, preceded by oral administration of penicillin V 100 mg/kg per day, initiated on day 2 and lasting 5 (2) days. Using a light microscope, bone histomorphology was registered and the thickness measured in four well-defined localities, followed by comparison with a previous study of untreated animals. RESULTS: Measured bone thickness was unaffected by treatment on day 4, but significantly reduced in two localities on day 8 and in all localities on following days of sacrifice. Bone cytomorphology and histomorphology were otherwise unaffected by penicillin administration. CONCLUSION: Penicillin reduces new bone formation in acute otitis media, leaving other features of histomorphology unchanged.

Acute Disease↗
PubMed1998

Changes in mucosal goblet cell density in acute otitis media caused by non-typeable Haemophilus influenzae.

The correlation between secretory otitis media and increased goblet cell density in the middle ear mucosa is well established. Previous studies have shown that a single episode of acute otitis media caused by Streptococcus pneumoniae is followed by increased goblet cell density for a period of at least 6 months, conceivably predisposing a subsequent development of secretory otitis media. In this study, 25 rat middle ears were inoculated with non-typeable Haemophilus influenzae in order to determine the effect on mucosal goblet cell density. Five rats were killed on days 4, 8, 16, 60 and 180 postinoculation, followed by dissection, staining and whole-mount embedding of the middle ear mucosae. The goblet cell density was determined in 24 well-defined localities. Compared with 25 normal middle ears, the goblet cell density was significantly increased in almost all localities, at all days on which the animals were killed. Thus, increased goblet cell density and enlargement of mucosal areas containing goblet cells persisted 6 months after the acute incident. The induced increase of goblet cell density was higher than the increase following inoculation of S. pneumoniae. We conclude that acute otitis media caused by non-typeable H. influenzae is followed by a longstanding increase in mucosal secretory capacity, likely to predispose a subsequent development of secretory otitis media.

Animals↗
PubMed1998

Effect of penicillin on formation of fibrous adhesions in acute otitis media.

Fibrous middle ear adhesions are occasionally encountered in middle ear surgery and may cause a hearing impairment. Although usually associated with chronic otitis media, adhesions are also found following a single episode of experimental acute suppurative otitis media, suggesting a pathogenesis based on the inflammatory process engaging acute infection. In a well-established rat model of pneumococcal acute otitis media, we report on the effect of penicillin V on formation of fibrous middle ear adhesions. Previous studies have shown marked impact of penicillin on mucosal goblet cell density and other histopathologic features. Number, anatomic localization, and histopathologic morphology of adhesions were assessed in a longitudinal study of 25 normal, 25 untreated, and 25 treated rats. Although penicillin administration induced a slight tendency toward fewer ears with adhesions and fewer adhesions per ear, these changes were nonsignificant. Histomorphology and the general pattern of anatomic localization of adhesions were unaffected by penicillin administration. We conclude that administration of penicillin has an inconspicuous effect on the formation of fibrous adhesions in experimental acute otitis media caused by Streptococcus pneumoniae.

Acute Disease↗
PubMed1998

Effect of penicillin on polyp formation in acute otitis media.

HYPOTHESIS/BACKGROUND: The mucoperiosteal lining of the middle ear cavity is subject to radical changes during and after acute infection. Among these is the formation of mucosal polyps. Previous studies on experimental acute otitis media have shown a marked impact of penicillin on mucosal histomorphology. This study reports on the effect of penicillin administration on polyp formation. METHODS: The mucosa of 75 rat middle ears in a model of acute otitis media was examined. Whole-mount and section preparations from 25 normal ears, 25 ears inoculated with Streptococcus pneumoniae, and 25 inoculated, penicillin-treated ears were inspected for number, size, anatomic localization, and histopathologic morphology of occurring polyps. RESULTS: The total number of polyps was unaffected by penicillin administration, although polyps occurred in fewer ears. The polyps from treated ears tended to be smaller and stalky, appeared later in the timespan covered, and often were located around the tubal orifice. Histopathologic morphology of polyp base, core, and epithelial covering was otherwise unaffected by penicillin. CONCLUSIONS: Administration of penicillin has inconspicuous effect on the formation of polyps in experimental otitis media caused by S. pneumoniae in contrast to a marked impact on mucosal goblet cell density and other histopathologic features reported in previous studies.

Acute Disease↗
PubMed1997

Increased secretory capacity of the middle ear mucosa after acute otitis media caused by Haemophilus influenzae type B.

Secretory otitis media is associated with a highly increased goblet cell density of the middle ear mucosa. Previous studies have shown that a single episode of experimental acute otitis media caused by Streptococcus pneumoniae or nontypeable Haemophilus influenzae is followed by increased goblet cell density for a period of at least 6 months. This condition may create a predisposition for subsequent development of secretory otitis media. We inoculated the middle ears of 25 rats with type B H. influenzae to determine the effect of the bacteria on mucosal secretory capacity. Five rats were euthanized 4, 8, 16, 60, and 180 days after inoculation, followed by dissection, staining, and whole-mount embedding of the middle ear mucosa. The goblet cell density was determined in 24 well-defined localities. Compared with that of 25 normal middle ears, the goblet cell density was significantly increased in almost all counting localities on all days of euthanasia. Thus increased goblet cell density and enlargement of mucosal areas containing goblet cells persisted for 6 months after the acute incident. Inoculation of type B H. influenzae induced an increase of goblet cell density that was higher than the increase after inoculation of S. pneumoniae or nontypeable H. influenzae. We conclude that experimental acute otitis media caused by type B H. influenzae is followed by a longstanding increase of mucosal secretory capacity, which is likely to induce a subsequent development of secretory otitis media.

Acute Disease↗
PubMed1996

Pathogenesis of middle ear adhesions.

Middle ear adhesions are well-known to the ear surgeon, although data on etiology, pathogenesis, and significance are lacking in current literature. This study on experimental acute otitis media presents histopathological data on these aspects. Pneumococci were inoculated in the right middle ear bulla of 25 rats; the left ear served as control. At days 4, 8, 16, 90, and 180, respectively, 5 rats were decapitated, and the bullae were removed, opened, and stained with periodic acid-Schiff (PAS)/alcian blue. The entire middle ear mucosae were dissected from the bone, embedded as whole mounts in colophonium chambers, and examined by light microscopy. Representative parts of the mucosae were sectioned and examined in the same way. All inoculated ears from day 8 and later (20 in total), contained mucosal adhesions of various sizes, shapes, and locations. None were found in control ears. The site of predilection for the development of adhesions was the hypotympanum, followed by the anterior epitympanum, the attic, the drum, the interossicular spaces, and the tubal orifice. Based on present histopathological findings, we conclude that the middle ear adhesion is a pathological phenomenon caused by infection, and we propose a six-stage hypothesis of pathogenesis: 1. Localized epithelial rupture; 2. Prolapse of subepithelial tissue; 3. Epithelialization of the prolapse; resulting in a polypous/fold-like prominence; 4. Growth and elongation of the prominence; 5. Fusion of the end/tip of the prominence with another part of the mucosa; 6. Formation of an adhesion.

Acute Disease↗
PubMed1996

Mast cell clusters in pars tensa membranae tympani in acute otitis media: a possible role in perforation healing.

Mast cells are known to reside in pars flaccida membranae tympani and other parts of the middle ear mucosa in both rats and humans. However, the normal pars tensa contains no or only a few mast cells along the manubrial vessels. We examined the pars tensa of 25 rats in an experimental model of acute otitis media and found 13 mast cell clusters in 6 membranes. A majority of clusters were located in the anterior, superior quadrant and contained from 3 to 23 cells. The mast cells resided immediately under the inner epithelial lining or in the intermediate, fibrous layer. In two membranes mast cell clusters were found in the margin of apparently healed spontaneous perforations. We conclude that mast cells in some cases infiltrate pars tensa membranae tympani in the late and receding phase of acute otitis media. As these cell clusters in some cases were found immediately around apparently healed membrane perforations, we propose that the mast cell might participate in the repair processes of tympanic membrane perforation healing. This is supported by recent studies in wound healing and functions of a number of mast cell mediators.

Animals↗
PubMed1996

Penicillin reduces secretory capacity in rat middle ear mucosa in acute otitis media.

In the United States, antibiotic treatment of acute otitis media is almost mandatory, whereas several other western countries are more reticent. Most clinical trails on antibiotic effect have important methodologic flaws, making an overall interpretation quite difficult. This study determined the effect of penicillin V administration on the secretory capacity of rat middle ear mucosa, during and after acute pneumococcal otitis media, by quantitative studies of the goblet cell density. The right middle ear bullae of 25 rats were inoculated with type 3 pneumococci. Beginning 2 days after inoculation, penicillin V 100 mg/kg/day was administered orally for 5 days. After inoculation, five randomly selected rats were killed on days 4, 8, 16, 90, and 180. The middle ear bullae were removed, split in half, stained with periodic acid-Schiff (PAS)-alcian blue, and the mucosae dissected from the bone. Whole mounts were prepared and the goblet cell density determined in 24 well-defined localities, making a total of 160 counts per ear and covering the entire bulla mucosa. Goblet cell densities were compared with those of 25 normal ears and 25 inoculated, untreated ears. Except on day 4, the penicillin V-treated ears had a significantly lower goblet cell density in almost all localities, on all days of death, when compared with untreated ears. Six months after the acute incident, the goblet cell density was almost normal. However, the enlargement of the mucosal area containing goblet cells seen in untreated ears was unaffected by penicillin V administration. We conclude that administration of penicillin V reduces the increase in secretory capacity of rat middle ear mucosa during and 6 months after acute pneumococcal otitis media.

Acute Disease↗
PubMed1995

Polyp pathogenesis--a histopathological study in experimental otitis media.

We examined the mucosa of 50 rat middle ears in an experimental model of acute otitis media, in order to obtain information on the mechanisms of polyp formation. The right middle ear of 25 rats was inoculated with type 3 pneumococci, and the left ear served as a control. The animals were killed, the middle ear bulla removed, and the mucosa was dissected from the bone, stained PAS-alcian blue and embedded as a whole-mount. The whole-mounts were examined in a light microscope for polypous mucosal prominences. Serial sections were made of all polyps, and of relevant parts of the mucosa. 15 polyps were found in 11 (44%) of 25 infected ears; none were found in normal control ears. Goblet cell density was increased in polyps and the surrounding epithelium. Epithelial microruptures were seen in areas with widespread intra-epithelial liquid vacuoles and subepithelial accumulation of liquids, luminally migrating inflammatory cells, increased vascularization and edema. Connective tissue of the lamina propria was prolapsed through most ruptures. Some prolapses showed signs of re-epithelialization, while others had a full epithelial lining that resembled a fully developed polyp. Our findings support our earlier theory on nasal polyp pathogenesis, based on the following stages: i) Localized rupture of the epithelial lining. ii) Luminal protrusion of the lamina propria through the epithelial defect. iii) Re-epithelialization of protruded tissue, and formation of a polyp.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗