A two-layer composite model of the vocal fold lamina propria for fundamental frequency regulation

2007 ◽  
Vol 122 (2) ◽  
pp. 1090-1101 ◽  
Author(s):  
Kai Zhang ◽  
Thomas Siegmund ◽  
Roger W. Chan
1997 ◽  
Vol 106 (7) ◽  
pp. 533-543 ◽  
Author(s):  
Steven M. Zeitels ◽  
Glenn W. Bunting ◽  
Robert E. Hillman ◽  
Traci Vaughn

Reinke's edema (RE) has been associated typically with smoking and sometimes with vocal abuse, but aspects of the pathophysiology of RE remain unclear. To gain new insights into phonatory mechanisms associated with RE pathophysiology, weused an integrated battery of objective vocal function tests to analyze 20 patients (19 women) who underwent phonomicrosurgical resection. Preoperative stroboscopic examinations demonstrated that the superficial lamina propria is distended primarily on the superior vocal fold surface. Acoustically, these individuals have an abnormally low average speaking fundamental frequency (123 Hz), and they generate abnormally high average subglottal pressures (9.7 cm H20). The presence of elevated aerodynamic driving pressures reflects difficulties in producing vocal fold vibration that are most likely the result of mass loading associated with RE, and possibly vocal hyperfunction. Furthermore, it is hypothesized that in the environment of chronic glottal mucositis secondary to smoking and reflux, the cephalad force on the vocal folds by the subglottal driving pressure contributes to the superior distention of the superficial lamina propria. Surgical reduction of the volume of the superficial lamina propria resulted in a significant elevation in fundamental frequency (154 Hz) and improvement in perturbation measures. In almost all instances, both the clinician and the patient perceived the voice as improved. However, these patients continued to generate elevated subglottal pressure (probably a sign of persistent hyperfunction) that was accompanied by visually observed supraglottal strain despite the normalsized vocal folds. This finding suggests that persistent hyperfunctional vocal behaviors may contribute to postsurgical RE recurrence if therapeutic strategies are not instituted to modify such behavior.


Author(s):  
Mark P. Ottensmeyer ◽  
Michael Yip ◽  
Conor J. Walsh ◽  
James B. Kobler ◽  
James T. Heaton ◽  
...  

Our society depends on communication, the most natural form of which is speech. Trauma, disease and the normal aging process will cause many to suffer degraded or lost vocal fold function, and it has been observed that this number is growing [1]. The vocal folds are the vibrating structures in the larynx that enable us to generate voice, from speech to opera singing. The vibrating portions of the folds consist of an external 0.1mm thick layer of epithelial cells, a soft, gel-like 0.5mm thick layer called the lamina propria (LP), a 0.3mm thick vocal ligament and an underlying thyroarytenoid muscle [2]. The fundamental frequency of speech in men is in the 100–150Hz range, and between 200 and 300Hz in women [3].


1996 ◽  
Vol 105 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Agnieszka S. Pawlak ◽  
Elizabeth Hammond ◽  
Thomas Hammond ◽  
Steven D. Gray

We evaluated the proteoglycan composition of normal vocal folds using immunocytochemical techniques. Frozen sections of 14 normal cadaveric vocal folds were obtained within 12 hours of death and sectioned immediately. Vocal fold sections were stained with antibodies against keratan sulfate, chondroitin sulfate, heparan sulfate proteoglycan (HSPG), decorin, and hyaluronate receptor. We found that the lamina propria has diffuse staining of fibrillar components with keratan sulfate and decorin. Intense staining was observed in the vocal ligament area with keratan sulfate. The HSPG was localized to the basement membrane zone. Chondroitin sulfate, HSPG, and hyaluronate receptor were detected in the cytoplasm of interstitial cells with immunocytochemical characteristics of macrophages. The keratan sulfate distribution suggests that fibromodulin may be significant in normal vocal folds. Production of HSPG and probably versican occurs in macrophages and fibroblasts in the lamina propria.


Biomaterials ◽  
2006 ◽  
Vol 27 (7) ◽  
pp. 1104-1109 ◽  
Author(s):  
Mariah S. Hahn ◽  
Benjamin A. Teply ◽  
Molly M. Stevens ◽  
Steven M. Zeitels ◽  
Robert Langer

1984 ◽  
Vol 97 (5-6) ◽  
pp. 403-406 ◽  
Author(s):  
Radovan Suboti ◽  
Santa Večerina ◽  
Zvonimir Krajina ◽  
Minoru Hirano ◽  
Shigejiro Kurita

2008 ◽  
Vol 139 (6) ◽  
pp. 816-822 ◽  
Author(s):  
Susan L. Thibeault ◽  
Wenhua Li ◽  
Stephanie Bartley

Objective Vocal fold biology research is emerging as a vital area of study in laryngology. One impediment is the lack of both commercially available vocal fold lamina propria fibroblasts and a constitutively expressed specific marker for fibroblasts. We present an in vitro technique that allows for identification of fibroblasts by ruling out the possibility of the cells belonging to other lineages that are found in vocal fold tissue. Study Design An in vitro study. Methods Two primary vocal fold fibroblast cell lines and one immortalized vocal fold fibroblast cell line were cultured. Immunohistologic staining for α-actinin, cytokeratin 19, and von Willebrand factor was completed for the three fibroblast lines in addition to skeletal, endothelial, and epithelial cell lines. Cell type was differentiated by positive staining for α-actinin, cytokeratin 19, and von Willebrand factor. Results Fibroblast cultures did not express α-actinin, cytokeratin 19, and von Willebrand factor, whereas skeletal muscle, endothelial, and epithelial cultured cells expressed each respectively. Conclusions This simple rule-out methodology for fibroblast confirmation is an important step when establishing cell culture, and it establishes sound internal validity particularly in the early stages of this emerging area of study.


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