Histology of the vocal folds

Histology is the study of the minute structure, composition, and function of tissues.[1]

Histoanatomy of the glottis

The glottis is defined as the true vocal folds and the space between them. It is composed of an intermembranous portion or anterior glottis, and an intercartilaginous portion or posterior glottis. The border between the anterior and posterior glottises is defined by an imaginary line drawn across the vocal fold at the tip of the vocal process of the arytenoid cartilage. The anterior glottis is the primary structure of vocal fold vibration for phonation and the posterior glottis is the widest opening between the vocal folds for respiration. Thus, voice disorders often involve lesions of the anterior glottis. There are gradual changes in stiffness between the pliable vocal fold and hard, hyaline cartilage of the arytenoid. The vocal processes of the arytenoid cartilages form a firm framework for the glottis but are made of elastic cartilage at the tip. Therefore, the vocal process of the arytenoid bends at the elastic cartilage portion during adduction and abduction of the vocal folds.

Attachments of the vocal fold

The vibratory portion of the vocal fold in the anterior glottis is connected to the thyroid cartilage anteriorly by the macula flava and anterior commissure tendon, or Broyles' ligament. Posteriorly, this vibratory portion is connected to the vocal process of the arytenoid cartilage by the posterior macula flava. The macula flava in newborn vocal folds is important for the growth and development of the vocal ligament and layered structure of the vocal folds. In the adult, the macula flavae are probably required for metabolism of the extracellular matrices of the vocal fold mucosa, replacing damaged fibers in order to maintain the integrity and elasticity of the vocal fold tissues. Age-related changes in the macula flava influence the fibrous components of the vocal folds and are partially responsible for the differences in the acoustics of the adult and aged voice.

Layered structure of the adult vocal fold

The histological structure of the vocal fold can be separated into 5[2] or 6[3] tissues, depending on the source, which can then be grouped into three sections as the cover, the transition, and the body.

The cover is composed of the epithelium (mucosa), basal lamina (or basement membrane zone), and the superficial layer of the lamina propria.

The transition is composed of the intermediate and deep layers of the lamina propria. The body is composed of the thyroarytenoid muscle. This layered structure of tissues is very important for vibration of the true vocal folds.

The cover

Epithelium

The free edge of the vibratory portion of the vocal fold, the anterior glottis, is covered with stratified squamous epithelium. This epithelium is five to twenty-five cells thick with the most superficial layer consisting of one to three cells that are lost to abrasion of the vocal folds during the closed phase of vibration. The posterior glottis is covered with pseudostratified ciliated epithelium. On the surfaces of the epithelial cells are microridges and microvilli. Lubrication of the vocal folds through adequate hydration is essential for normal phonation to avoid excessive abrasion, and the microridges and microvilli help to spread and retain a mucous coat on the epithelium. Surgery of the vocal folds can disturb this layer with scar tissue, which can result in the inability of the epithelium to retain an adequate mucous coat, which will in turn impact lubrication of the vocal folds. The epithelium has been described as a thin shell, the purpose of which is to maintain the shape of the vocal fold.[2]

Basal lamina or basement membrane zone (BMZ)

This is transitional tissue composed of two zones, the lamina lucida and lamina densa. The lamina lucida appears as a low density clear zone medial to the epithelial basal cells. The lamina densa has a greater density of filaments and is adjacent to the lamina propria. The basal lamina or BMZ mainly provides physical support to the epithelim through anchoring fibers and is essential for repair of the epithelium.

Superficial layer of the lamina propria

This layer consists of loose fibrous components and extracellular matrices that can be compared to soft gelatin. This layer is also known as Reinke’s space but it is not a space at all. Like the pleural cavity, it is a potential space. If there really is a space, there is a problem.[4] The superficial layer of the lamina propria is a structure that vibrates a great deal during phonation, and the viscoelasticity needed to support this vibratory function depends mostly on extracellular matrices. The primary extracellular matrices of the vocal fold cover are reticular, collagenous and elastic fibers, as well as glycoprotein and glycosaminoglycan. These fibers serve as scaffolds for structural maintenance, providing tensile strength and resilience so that the vocal folds may vibrate freely but still retain their shape.

The transition

Intermediate and deep layers of the lamina propria

The intermediate layer of the lamina propria is primarily made up of elastic fibers while the deep layer of the lamina propria is primarily made up of collagenous fibers. These fibers run roughly parallel to the vocal fold edge and these two layers of the lamina propria comprise the vocal ligament. The transition layer is primarily structural, giving the vocal fold support as well as providing adhesion between the mucosa, or cover, and the body, the thyroarytenoid muscle.

The body

The thyroarytenoid muscle

This muscle is variously described as being divided into the thyroarytenoid and vocalis muscles[5] or the thyrovocalis and the thyromuscularis,[6] depending on the source.

Vocal fold lesions

The majority of vocal fold lesions primarily arise in the cover of the folds. Since the basal lamina secures the epithelium to the superficial layer of the lamina propria with anchoring fibers, this is a common site for injury. If a person has a phonotrauma or habitual vocal hyperfunction, also known as pressed phonation, the proteins in the basal lamina can shear, causing vocal fold injury, usually seen as nodules or polyps, which increase the mass and thickness of the cover. The squamous cell epithelium of the anterior glottis are also a frequent site of laryngeal cancer caused by smoking.

Reinke’s edema

A voice pathology called Reinke’s edema, swelling due to abnormal accumulation of fluid, occurs in the superficial lamina propria or Reinke’s space. This causes the vocal fold mucosa to appear floppy with excessive movement of the cover that has been described as looking like a loose sock.[7] The greater mass of the vocal folds due to increased fluid lowers the fundamental frequency (F°) during phonation.

Histological changes from birth to old age

The histologic structure of the vocal fold differs from the pediatric to the adult and old-age populations.

Pediatrics

The infant lamina propria is composed of only one layer, as compared to three in the adult, and there is no vocal ligament. The vocal ligament begins to be present in children at about four years of age. Two layers appear in the lamina propria between the ages of six and twelve, and the mature lamina propria, with the superficial, intermediate and deep layers, is only present by the conclusion of adolescence. As vocal fold vibration is a foundation for vocal formants, this presence or absence of tissue layers influences a difference in the number of formants between the adult and pediatric populations. In females, the voice is three tones lower than the child’s and has five to twelve formants, as opposed to the pediatric voice with three to six. The length of the vocal fold at birth is approximately six to eight millimeters and grows to its adult length of eight to sixteen millimeters by adolescence. The infant vocal fold is half membranous or anterior glottis, and half cartilaginous or posterior glottis. The adult fold is approximately three-fifths membranous and two-fifths cartilaginous.

Puberty

Puberty usually lasts from 2–5 years, and typically occurs between the ages of 12 to 17. During puberty, voice change is controlled by sex hormones. In females during puberty, the vocal muscle thickens slightly, but remains very supple and narrow. The squamous mucosa also differentiates into three distinct layers (the lamina propria) on the free edge of the vocal folds. The sub- and supraglottic glandular mucosa becomes hormone-dependent to estrogens and progesterone. For women, the actions of estrogens and progesterone produce changes in the extravascular spaces by increasing capillary permeability which allows the passage of intracapillary fluids to the interstitial space as well as modification of glandular secretions. Estrogens have a hypertrophic and proliferative effect on mucosa by reducing the desquamating effect on the superficial layers. The thyroid hormones also affect dynamic function of the vocal folds; (Hashimoto's thyroiditis affects the fluid balance in the vocal folds). Progesterone has an anti-proliferative effect on mucosa and accelerates desquamation. It causes a menstrual-like cycle in the vocal fold epithelium and a drying out of the mucosa with a reduction in secretions of the glandular epithelium. Progesterone has a diuretic effect and decreases capillary permeability, thus trapping the extracellular fluid out of the capillaries and causing tissue congestion. Testosterone, an androgen secreted by the testes, will cause changes in the cartilages and musculature of the larynx for males during puberty. In women, androgens are secreted principally by the adrenal cortex and the ovaries and can have irreversible masculinizing effects if present in high enough concentration. In men, they are essential to male sexuality. In muscles, they cause a hypertrophy of striated muscles with a reduction in the fat cells in skeletal muscles, and a reduction in the whole body fatty mass. Androgens are the most important hormones responsible for the passage of the boy-child voice to man voice, and the change is irreversible. The thyroid prominence appears, the vocal folds lengthen and become rounded, and the epithelium thickens with the formation of three distinct layers in the lamina propria.[8]

Adulthood

There is a steady increase in the elastin content of the lamina propria as we age (elastin is a yellow scleroprotein, the essential constituent of the elastic connective tissue) resulting in a decrease in the ability of the lamina propria to expand caused by cross-branching of the elastin fibers. Among other things, this leads to the mature voice being better suited to the rigors of opera.

Old age

There is a thinning in the superficial layer of the lamina propria in old age. In aging, the vocal fold undergoes considerable sex-specific changes. In the female larynx, the vocal fold cover thickens with aging. The superficial layer of the lamina propria loses density as it becomes more edematous. The intermediate layer of the lamina propria tends to atrophy only in men. The deep layer of the lamina propria of the male vocal fold thickens because of increased collagen deposits. The vocalis muscle atrophies in both men and women. However, the majority of elderly patients with voice disorders have disease processes associated with aging rather than physiologic aging alone.[9][10][11]

See also

References

  1. ↑ Dorland's Medical Dictionary (Abridged 25th ed.). (1980). Philadelphia, PA: The Saunders Press.
  2. 1 2 Hirano, M., & Bless, D.M. (1993). Videostroboscopic Examination of the Larynx. San Diego CA: Singular Publishing.
  3. ↑ Sato, K. (2003). Functional Fine Structures of the Human Vocal Fold Mucosa. In Rubin, J.S., Sataloff, R.T., & Korovin, G.S. (Eds.), Diagnosis and Treatment of Voice Disorders (pp. 41-48). Clifton Park, NY: Delmar Learning.
  4. ↑ A. Blanton (Personal Communication, March 11, 2009).
  5. ↑ Saunders, W.H. (1964). The Larynx. Summit, NJ: Ciba_Geigy Co.
  6. ↑ Sanders, I. (2003). The Microanatomy of the Vocal Fold Musculature. In Rubin, J.S., Sataloff, R.T., & Korovin, G.S. (Eds.), Diagnosis and Treatment of Voice Disorders (pp. 49-68). Clifton Park, NY: Delmar Learning.
  7. ↑ T. Watterson (Personal communication, February 5, 2008).
  8. ↑ Abitbol, A. & Abitbol, P. (2003). The Larynx: A Hormonal Target. In Rubin, J.S., Sataloff, R.T., & Korovin, G.S. (Eds.), Diagnosis and Treatment of Voice Disorders (pp. 355-380). Clifton Park, NY: Delmar Learning.
  9. ↑ Zemlin, W.R. (1988). Speech and Hearing Science (3rd ed.). Englewood Cliffs, NJ: Prentice-Hall, Inc.
  10. ↑ Andrews, M.L. (2006). Manual of Voice Treatment (3rd ed.). Clifton Park, NY: Delmar Learning.
  11. ↑ SPHP 127, Class of 2009, CSU Sacramento.
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