Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
27 Мб
Скачать
356
Rodriguez-Fernandez etal. [60] developed a uorimetric sensor for measuring VSC and suggested that this method could be an alternative to commercial systems such as Halimeter. It is shown that the VSC monitor with the zinc oxide semicon­ductor sensor they developed could be used to diagnose halitosis [45]. They made a comparison with organoleptic evaluation in patients with severe halitosis. They stated that this monitor could be used in routine clinical studies and oral-dental screenings, as they found a high correlation. Hanada etal. [61] developed a portable GC system using a high-sensitivity indium oxide semiconductor gas sensor as a detector. In their study, Amano etal. [62] found a statistically signicant relation­ship when they measured the VSC level by gas chromatography and the ammonia level by ammonia monitoring in 25 patients.
İ. Dişikırık and M. A. Kanmaz
26.14.2.2 Measurement ofGalactosidase Activity
Deglycosylation of glycoproteins is considered the initial stage in forming lousy breath. β-Galactosidase is one of the essential enzymes in deglycosylation. In this method, which is based on measuring the activity of this enzyme, the color change caused by the saliva sample taken on a paper disk is scored as 0: No color change, 1: Light blue color, and 2: Dark blue color. Some studies have found a signicant relationship between β-Galactosidase test scores and organoleptic scores [63, 64].
26.14.2.3 Ammonia Monitoring
Ammonia produced by bacteria in the mouth can cause bad breath. Therefore, a portable monitor was developed to measure ammonia. Patients are asked to rinse their mouths with urea solution and measurements are made with a disposable piece placed in the mouth and connected to the gas detector. The air in the patient’s mouth is transferred to the detector with the help of a pump, and the ammonia concentra­tion produced by the bacteria can be seen on a scale.
26.14.2.4 Polymerase Chain Reaction (PCR)
This method is used for quantitative analysis of VSCs produced by oral bacteria. In this method, the amount of bacterial DNA forming VSC is determined by the amount of uorescent dye formed on the DNA probe [23, 65].

26.15 Physical Examination

After physiological halitosis and halitophobia are ruled out, physical examination begins. A meticulous oral and otolaryngological examination is performed. 90% of the cause of bad breath originates from inside the mouth, increasing oral examina­tion’s importance. It is essential in the subgingival and proximal regions. Causes such as periodontal pockets, rotten teeth, tonsils, adenoid examination, tongue structure, whether there is a cleft tongue, aphthous lesions in the mouth, ulcerations, gum diseases, tongue coating, or post-nasal discharge can be easily noticed.
In people with good oral hygiene and dental health and a healthy periodontium, although the front part of the back of the tongue usually smells good, the real cause
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
357
of the odor may be the back part of the tongue, that is, the tongue root. This area can be examined by scraping with a tongue depressor. This material usually results from postnasal discharge. Although the discharge is not initially foul-smelling when it reaches the tongue, it may cause a foul odor as it accumulates in the future. A con­clusion can be drawn by comparing the scraping taken with a tongue depressor and bad breath.
One way to understand that the smell is coming from the mouth is to compare the smell coming from the mouth with the smell coming from the nose. If the smell comes from the mouth, the place to be investigated is the mouth. The odor may intensify during sleep, under stress, when the mouth is dry due to long conversations and side effects of medications, and in such cases, gum can be chewed for a few minutes to increase saliva secretion and to see whether the odor decreases. If we think that the odor is caused by oral etiology, the patient is told to gargle for a week and pay attention to dental cleaning (brushing, ossing). If the odor disappears, it is understood that it is caused by oral etiology [45]. If the odor originates from the nasal passage, lungs, or stomach, it will not disappear with mouthwash and teeth cleaning.
Another way to understand bad breath is to stick out the tongue thoroughly, hold the tip of the tongue with gauze, and scrape the base with another gauze for 45s, Wait, and then smell. If an unpleasant odor is detected after these waiting periods, there is a halitosis problem [45].
Some people’s bad breath worsens when they start talking when it does not nor­mally exist. Therefore, in addition to exhaling through the mouth and nose, the patient should be asked to count out loudly 20 and simultaneously smell.
It is also essential to detect a ssured tongue (scrotal tongue) during physical examination. Enzymes such as lysozyme, myeloperoxidase, and immunoglobulin are higher in ssured tongues than in non-ssured tongues. When the ssured tongue becomes ulcerated and the rust is removed, saliva leaks. Excessive bacterial growth causes inammation and odor occurs [45].
26.16 Treatment ofHalitosis
A treatment plan is made to eliminate the cause and improve oral health. Although there are many factors in the etiology of bad breath, it is primarily due to oral causes. Therefore, it is aimed to reduce the amount of intraoral bacteria and convert persis­tent VSCs into non-volatile substrates. The treatment methods are listed below:
1. Using masking products
Masking products alone do not treat halitosis. These are mints, toothpaste,
mouthwashes, sprays, lozenges, and gums [4].
2. Mechanical reduction of microorganisms and their substrates
It is possible by consuming breakfast, increasing saliva secretion, chewing gum, brushing teeth, using dental oss, toothpicks, tongue cleaning, and profes­sional oral care [4].
358
İ. Dişikırık and M. A. Kanmaz
Bad breath, which is intense in the morning as a result of the proliferation of microorganisms found in food residues and releasing proteins as a result of not washing the tongue as a result of fasting throughout the night and food residues accumulating on the tongue and decreasing saliva secretion, will be eliminated by eating solid foods and bad breath will decrease [66]. In a study, a 60% decrease in the hydrogen sulde concentration and an 83% decrease in the methyl mercaptan concentration, which causes bad breath, was observed in peo­ple with bad morning breath despite no oral cleaning performed 1h after break­fast [52]. Even just eating dry bread has been shown to reduce VSC concentration without any other action [67].
3. Brushing teeth It reduces the amount of bacteria in the mouth [68, 69], but studies have
shown that tooth brushing alone is ineffective in eliminating bad breath [70, 71].
4. Tongue brushing Brushing the tongue reduces the tongue coating and, therefore, the number of
microorganisms and the amount of substrates on the tongue [37, 72, 73]. The tongue coating should be removed during tongue brushing, especially on the posterior part of the tongue. In one study, brushing the tongue dorsum with toothpaste was more effective than brushing your teeth.
The clinician must nd the source of the odor before starting treatment. It
often requires dental treatment. The most effective method in the treatment of halitosis is to reduce anaerobes that cause VSC production by correcting peri­odontal disease with oral hygiene and primary dental care. An effective mouth­wash should be added if bad breath persists despite good oral hygiene. Mouthwashes eliminate lousy breath by chemically reducing the number of microorganisms in the mouth [74]. Active agents frequently used in these prod­ucts are chlorhexidine, triclosan, essential oils, and cetylpyridinium chloride (CPC). Other effective chemical agents are allylpyrocatechol, L-triuoromethionine, and dehydroascorbic acid [4].
Chlorhexidine, the most commonly used of these, damages the bacterial cell
membrane, increasing membrane permeability and, as a result, causes cell lysis and cell death [75].
In their study, [49] reported that the 0.2% chlorhexidine regimen provided a
43% decrease in VCS values and a more than 50% decrease in organoleptic scores [49]. However, long-term use of chlorhexidine also has disadvantages, such as causing bad taste in the mouth and discoloration of teeth [75, 76].
Many essential oils used to eliminate bad breath have strong antimicrobial
properties. Olshan etal. [77] reported in their clinical study that toothpaste con­taining essential oil and 1% zinc citrate and essential oil effectively reduced bad breath for 1.5–2h. Cetylpyridinium Chloride (CPC), also used to eliminate bad breath, prevents bacterial growth [78]. Yaegaki and Sanada [70] reported in their study that mouthwash containing CPC was 80% effective in reducing VSC for
3.5 h. L-triuoromethionine, which is also recommended in the treatment of halitosis, works by inhibiting the production of methyl mercaptan, which occurs as a result of bacteria metabolizing methionine and causes bad breath.
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
Toothpaste, mouthwashes, lozenges, and other products reduce halitosis by
chemically neutralizing odor compounds, including VSC.Common active ingre­dients of these products are metal ions and oxidizing agents. Metals such as zinc, sodium, tin and magnesium are thought to interact with sulfur. Zinc, one of these products, has advantages such as being non-toxic, non-cumulative, and not caus­ing coloration compared to other metal ions. For this reason, it is one of the most preferred substances for controlling bad breath [79].
Sodium bicarbonate is frequently used in teeth cleaning in Japan and North
America. It was reported in the studies of Brunette etal. [80] that toothpastes containing sodium bicarbonate were effective in reducing VSC levels.
Oxidizing tablets are thought to reduce bad breath due to the activity of dehy-
droascorbic acid, which is formed by the peroxide-based oxidation of ascorbate.
On the other hand, probiotics are among the recommended treatment options.
Probiotics strengthen the host’s immune system by producing the antimicrobial substance necessary to destroy or inhibit pathogenic microorganisms [81].
In their study, Suzuki etal. reported that daily consumed acid-resistant probi-
otic lactobacilli would play an essential role in the regression of lousy breath and odor-related factors, along with ensuring oral care and hygiene [82].
If we consider a diagnosis of Halitophobia after all organic causes have been
excluded, the patient should be referred to the relevant branch for evaluation by a psychiatrist.
359

References

1. Armstrong BL, Sensat ML, Stoltenberg JL.Halitosis: a review of current literature. J Dent Hyg. 2010;84(2):65–74.
2. van den Broek AM, Feenstra L, de Baat C.A review of the current literature on aetiology and measurement methods of halitosis. J Dent. 2007;35(8):627–35.
3. Tonzetich J.Production and origin of oral malodor: a review of mechanisms and methods of analysis. J Periodontol. 1977;48(1):13–20.
4. van den Broek AM, Feenstra L, de Baat C.A review of the current literature on management of halitosis. Oral Dis. 2008;14(1):30–9.
5. Yaegaki K, Sanada K.Volatile sulfur compounds in mouth air from clinically healthy subjects and patients with periodontal disease. J Periodontal Res. 1992;27(4 Pt 1):233–8.
6. Lancero H, Niu J, Johnson PW.Exposure of periodontal ligament cells to methyl mercaptan reduces intracellular pH and inhibits cell migration. J Dent Res. 1996;75(12):1994–2002.
7. Amir E, Shimonov R, Rosenberg M.Halitosis in children. J Pediatr. 1999;134(3):338–43.
8. Paryavi-Gholami F, Minah GE, Turng BF.Oral malodor in children and volatile sulfur com­pound-producing bacteria in saliva: preliminary microbiological investigation. Pediatr Dent. 1999;21(6):320–4.
9. Sanz M, Roldan S, Herrera D. Fundamentals of breath malodour. J Contemp Dent Pract. 2001;2(4):1–17.
10. Rosenberg M. Clinical assessment of bad breath: current concepts. J Am Dent Assoc. 1996;127(4):475–82.
11. Dal Rio AC, Nicola EM, Teixeira AR. Halitosis—an assessment protocol proposal. Braz J Otorhinolaryngol. 2007;73(6):835–42.
12. Cortelli JR, Barbosa MD, Westphal MA.Halitosis: a review of associated factors and thera­peutic approach. Braz Oral Res. 2008;22(Suppl 1):44–54.
360
13. Miyazaki H, Sakao S, Katoh Y, Takehara T.Correlation between volatile sulphur compounds and certain oral health measurements in the general population. J Periodontol. 1995;66(8):679–84.
14. Liu XN, Shinada K, Chen XC, Zhang BX, Yaegaki K, Kawaguchi Y.Oral malodor-related parameters in the Chinese general population. J Clin Periodontol. 2006;33(1):31–6.
15. Al-Ansari JM, Boodai H, Al-Sumait N, Al-Khabbaz AK, AlShammari KF, Salako N.Factors associated with self-reported halitosis in Kuwaiti patients. J Dent. 2006;34(7):444–9.
16. Soder B, Johansson B, Soder PO.The relation between foetor ex ore, oral hygiene and peri­odontal disease. Swed Dent J. 2000;24(3):73–82.
17. Rosenberg M, Kulkarni GV, Bosy A, McCulloch CA.Reproducibility and sensitivity of oral malodor measurements with a portable sulphide monitor. J Dent Res. 1991;70(11):1436–40.
18. Iwakura M, Yasuno Y, Shimura M, Sakamoto S.Clinical characteristics of halitosis: differ­ences in two patient groups with primary and secondary complaints of halitosis. J Dent Res. 1994;73(9):1568–74.
19. Yaegaki K, Coil JM.Examination, classication, and treatment of halitosis; clinical perspec­tives. J Can Dent Assoc. 2000;66(5):257–61.
20. Loesche WJ, Kazor C. Microbiology and treatment of halitosis. Periodontol. 2002;2000(28):256–79.
21. Goldberg S, Kozlovsky A, Gordon D, Gelernter I, Sintov A, Rosenberg M.Cadaverine as a putative component of oral malodor. J Dent Res. 1994;73(6):1168–72.
22. Amano A, Yoshida Y, Oho T, Koga T.Monitoring ammonia to assess halitosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94(6):692–6.
23. Kato H, Yoshida A, Awano S, Ansai T, Takehara T.Quantitative detection of volatile sulfur compound-producing microorganisms in oral specimens using real-time PCR. Oral Dis. 2005;11(Suppl 1):67–71.
24. Washio J, Sato T, Koseki T, Takahashi N.Hydrogen sulde producing bacteria in tongue bio­lm and their relationship with oral malodor. J Med Microbiol. 2005;54(Pt 9):889–95.
25. Kazor CE, Mitchell PM, Lee AM, Stokes LN, Loesche WJ, Dewhirst FE, ve diğerleri. Diversity of bacterial populations on the tongue dorsa of patients with halitosis and healthy patients. J Clin Microbiol. 2003;41(2):558–63.
26. Waler S.On the transformation of sulfur-containing amino acids and peptides to volatile sulfur compounds (VSC) in the human mouth. Eur J Oral Sci. 1997;105:534–7.
27. Kojima K.Clinical studies on the coated tongue. Jpn J Oral Maxillofac Surg. 1985;31:1659–76.
28. Loesche WJ.The effects of antimicrobial mouthrinses on oral malodor and their status relative to US Food and Drug Administration regulations. Quintessence Int. 1999;30:311–8.
29. Morita M, Wang HL.Association between oral malodor and adult periodontitis: a review. J
İ. Dişikırık and M. A. Kanmaz
30. Hoshi K, Yamano Y, Mitsunaga A, etal. Gastrointestinal diseases and halitosis: association of gastric Helicobacter pylori infection. Int Dent J. 2002;52(Suppl3):207–11.
31. Delanghe G, Ghyselen J, Bollen C, van Steenberghe D, Vandekerckhove BN, Feenstra L.An inventory of patients_response to treatment at a multidisciplinary breath odor clinic. Quintessence Int. 1999;30:307–10.
32. Aydın M.Ağız Kokusu TeĢhisi ve Tedavisi. Dentalife. 2005;14:26–9.
33. Coli JM, Tonzetich J.Characterization of volatile sulphur compounds production at individual gingival crevicular sites in humans. J Clin Dent. 1992;3(4):97–103.
34. Persson S. Hydrogen sulde and methyl mercaptan in periodontal pockets. Oral Microbiol Immunol. 1992;7(6):378–9.
35. Bosy A, Kulkarni GV, Rosenberg M, McCulloch CA.Relationship of oral malodor to periodon­titis: evidence of independence in discrete subpopulations. J Periodontol. 1994;65(1):37–46.
36. Yaegaki K, Sanada K.Biochemical and clinical factors inuencing oral malodor in periodontal patients. J Periodontol. 1992;63(9):783–9.
37. De Boever EH, Loesche WJ.Assessing the contribution of anaerobic microora of the tongue to oral malodor. J Am Dent Assoc. 1995;126(10):1384–93.
38. Quirynen M, Mongardini C, van Steenberghe D.The effect of a 1-stage full-mouth disinfec­tion on oral malodor and microbial colonization of the tongue in periodontitis. A pilot study. J Periodontol. 1998;69(3):374–82.
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
39. Danser MM, Gomez SM, Van der Weijden GA.Tongue coating and tongue brushing: a litera­ture review. Int J Dent Hyg. 2003;1(3):151–8.
40. Madhushankari GS, Yamunadevi A, Selvamani M, Mohan Kumar KP, Basandi PS.Halitosis— an overview: part-I—classication, etiology and pathophysiology of halitosis. J Pharm Bioallied Sci. 2015;7:339–43.
41. Scully C, Porter R, Greenman J.What to do about halitosis? Br Med J. 1994;308:217–8.
42. Young K, Oxtoby A, Field EA.Halitosis: a review. Dent Update. 1993;20:57–61.
43. Yilmaz AE, Bilici M, Tonbul A, Karabel M, Dogan G, Tas T.Paediatric halitosis and helico­bacter pylori infection. J Coll Physicians Surg Pak. 2012;22:27–30.
44. Vali A, Roohafza H, Keshteli AH, Afghari P, Javad Shirani M, Afshar H, etal. Relationship between subjective halitosis and psychological factors. Int Dent J. 2015;65:120–6.
45. Güngör A, Cıncık H, Çekin E, Cunda H.Ağız kokusu, GATA Ayın Kitabı, GATA Basımevi; 2005;66.
46. Rocha EM, Carvalho CR, Saad MJ, Velloso LA.The inuence of ageing on the insülin sig­nalling system in rat lacrimal and salivary glands. Acta Ophthalmol Scand. 2003;81:639–45.
47. Oho T, Yoshida Y, Shimazaki Y, Yamashita Y, Koga T.Characteristics of patients complaining of halitosis and the usefulness of gas chromatography for diagnosing halitosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;91(5):531–4.
48. Quirynen M, Steenberghe DV.Oral malodor. In: Newman M, Taeki H, Klokkevold P, Carranza F, editors. Carranza’s clinical periodontology. 11th ed. Iowa: Elsevier; 2011.
49. Rosenberg M, Kulkarni GV, Bosy A, McCulloch CAG.Reproducibility and sensitivity of oral malodor measurements with a portable sulde monitor. J Dent Res. 1991;11:1436–40.
50. Laleman I, Dadamio J, De Geest S, Dekeyser C, Quirynen M.Instrumental assessment of halitosis for the general dental practitioner. J Breath Res. 2014;8:017103.
51. Oho T, Yoshida Y, Shimazaki Y, Yamashita Y, Koga T.Characteristics of patients complaining of halitosis and the usefulness of gas chromatography for diagnosing halitosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;91:531–4.
52. Tonzetich J, Ng SK.Reduction of malodor by oral cleansing procedures. Oral Surg Oral Med Oral Pathol. 1976;42(2):172–81.
53. Murata T, Yamaga T, Iida T, Miyazaki H, Yaegaki K.Classication and examination of halito­sis. Int Dent J. 2002;52(Suppl 3):181–6.
54. Van den Velde S, Quirynen M, van Hee P, van Steenberghe D.Halitosis associated volatiles in breath of healthy subjects. J Chromatography B. 2007;853:54–61.
55. Kozlovsky A, Goldberg S, Natour I, Rogatky-Gat A, Gelernter I, Rosenberg M.Efcacy of a 2-phase oil: water mouthrinse in controlling oral malodor, gingivitis, and plaque. J Periodontol. 1996;67(6):577–82.
56. Greenstein RB, Goldberg S, Marku-Cohen S, Sterer N, Rosenberg M.Reduction of oral mal­odor by oxidizing lozenges. J Periodontol. 1997;68(12):1176–81.
57. Furne J, Majerus G, Lenton P, Springeld J, Levitt DG, Levitt MD.Comparison of volatile sulfur compound concentrations measured with a sulde detector vs. gas chromatography. J Dent Res. 2002;81(2):140–3.
58. Kozlovsky A, Gordon D, Gelernter I, Loesche WJ, Rosenberg M.Correlation between the BANA test and oral malodor parameters. J Dent Res. 1994;73(5):1036–42.
59. Loesche WJ, Lopatin DE, Giordano J, Alcoforado G, Hujoel P.Comparison of the benzoyl­DL-arginine-naphthylamide (BANA) test, DNA probes, and immunological reagents for abil­ity to detect anaerobic periodontal infections due to Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus. J Clin Microbiol. 1992;30(2):427–33.
60. Rodriguez-Fernandez J, Costa JM, Pereiro R, Sanz-Medel A.Simple detector for oral mal­odour based on spectrouorimetric measurements of hydrogen sulphide in mouth air. Anal Chim Acta. 1999;398:23–31.
61. Hanada M, Koda H, Onaga K, Tanaka K, Okabayashi T, Itoh T, etal. Portable oral malodor analyser using highly sensitive In2O3 gas sensor combined with a simple gas chromatography system. Anal Chim Acta. 2003;475:27–35.
62. Amano A, Yoshida Y, Oho T, Koga T.Monitoring ammonia to assess halitosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94:692–6.
361
362
63. Sterer N, Greenstein RB, Rosenberg M.Beta-galactosidase activity in saliva is associated with oral malodor. J Dent Res. 2002;81(3):182–5.
64. Sterer N, Rosenberg M.Effect of deglycosylation of salivary glycoproteins on oral malodour production. Int Dent J. 2002;52(Suppl 3):229–32.
65. Suzuki N, Yoshida A, Nakano Y.Quantitative analysis of multispecies oral biolms by TaqMan real-time PCR.Clin Med Res. 2005;3(3):176–85.
66. Kleinberg I, Wolff MS, Codipilly DM.Role of saliva in oral dryness, oral feel and oral malo­dour. Int Dent J. 2002;52(Suppl 3):236–40.
67. Suarez FL, Furne JK, Springeld J, Levitt MD.Morning breath odor: inuence of treatments on sulfur gases. J Dent Res. 2000;79(10):1773–7.
68. Coil JM, Yaegaki K, Matsuo T, Miyazaki H.Treatment needs (TN) and practical remedies for halitosis. Int Dent J. 2002;52(Suppl 3):187–91.
69. Tanaka M, Anguri H, Nishida N, Ojima M, Nagata H, Shizukuishi S. Reliability of clinical parameters for predicting the outcome of oral malodor treatment. J Dent Res. 2003;82(7):518–22.
70. Yaegaki K, Sanada K. Effects of a two-phase oil-water mouthwash on halitosis. Clin Prev Dent. 1992;14(1):5–9.
71. Kleinberg I, Codipilly DM.Cysteine challenge testing: a powerful tool for examining oral malodour processes and treatments invivo. Int Dent J. 2002;52(Suppl 3):221–8.
72. Gilmore EL, Bhaskar SN.Effect of tongue brushing on bacteria and plaque formed invitro. J Periodontol. 1972;43(7):418–22.
73. Ralph WJ.Oral hygiene--why neglect the tongue? Aust Dent J. 1988;33(3):224–5.
74. Brading MG, Marsh PD.The oral environment: the challenge for antimicrobials in oral care products. Int Dent J. 2003;53(6 Suppl 1):353–62.
75. Jones CG.Chlorhexidine: is it still the gold standard? Periodontol. 1997;15:55–62.
76. Young A, Jonski G, Rolla G. Inhibition of orally produced volatile sulfur compounds by zinc, chlorhexidine or cetylpyridinium chloride—effect of concentration. Eur J Oral Sci. 2003;111(5):400–4.
77. Olshan AM, Kohut BE, Vincent JW, Borden LC, Delgado N, Qaqish J, Sharma NC, McGuire JA.Clinical effectiveness of essential oil-containing dentifrices in controlling oral malodor. Am J Dent. 2000;13.(Spec No:18C–22C.
78. Xiong H, Li Y, Slavik MF, Walker JT.Spraying chicken skin with selected chemicals to reduce attached salmonella typhimurium. J Food Prot. 1998;61(3):272–5.
79. Young A, Jonski G, Rolla G, Waler SM.Effects of metal salts on the oral production of volatile sulfur-containing compounds (VSC). J Clin Periodontol. 2001;28(8):776–81.
80. Brunette DM.Effects of baking-soda-containing dentifrices on oral malodor. Compend Contin Educ Dent Suppl. 1996;17(19):S22–32.
81. Maden EA, Altun C. Probiyotikler ve Ağız Sağlığı. Atatürk Üniv Diş Hek Fak Derg. 2012;22:334–9.
82. Suzuki N, Yoneda M, Tanabe K, etal. Lactobacillus salivarius WB21-containing tablets for the treatment of oral malodor: a double-blind, randomized, placebo-controlled crossover trial. Oral Surg Oral Med Oral Pathol Oral Radiol. 2014;117:462–70.
İ. Dişikırık and M. A. Kanmaz
Dysphonia inChildren
27
İbrahimÇukurova andİlterDenizoğlu

27.1 Introduction

Communication in the childhood has a crucial role in personal and social develop­ment. Pediatric dysphonia creates serious communication problems and restrictions in social and emotional functioning with improper voice quality, pitch and loudness, and voice breaks [1, 2]. A dysphonic child will be negatively affected (aggressive, sad, frustrated) emotionally and perceived more negatively (angry and noisy) by peers and adults [1, 3, 4]. They also report frustration and limited participation in important events due to their vocal inabilities [1].
Diagnosis, treatment, and follow-up in pediatric dysphonia must be considered with continuously changing structural and developmental biomechanical factors. Laryngeal position, vocal tract length (vertically short), histoanatomical structure, and functions of the larynx change throughout childhood. The vocal fold length is only 2.5–3.0mm in the newborn and it reaches adult dimensions (female 11–15mm and male 17–21mm around 10–14years of age) [5]. Lamina propria in the new­borns is loose and pliable and does not have a layered structure. Vocal ligament appears between 1 and 4years and the three-layered lamina propria is not clear until 15years of age [6].
İ. Çukurova (*) İzmir University of Health Sciences, Tepecik Training and Research Hospital, Section of
Otorhinolaryngology, Izmir, Turkey
İ. Denizoğlu Department of Speech Language Therapy, Tinaztepe University Faculty of Health Sciences, Izmir, Turkey
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_27
363
364
İ. Çukurova and İ. Denizoğlu

27.2 Epidemiology

It is not easy to estimate the real prevalence of pediatric dysphonia because the pediatric dysphonia remains undiagnosed mostly. However, studies show a range between 1.4% and 23.9% [711]. These values increase in school age children from 6% to 38% [1, 9, 12]. Boys are more affected than girls between 7 and 12years of age, while dysphonia is more frequent in girls after puberty [13]. Benign vocal fold lesions tend to be the most common etiology in childhood [14, 15]. Vocal fold nod­ules have been reported to have an incidence of 17–30% in the pediatric population [16, 17].
27.3 Etiology andPathogenesis
Various etiologies can be dened in pediatric dysphonia: traumatic, infectious, inammatory, iatrogenic, congenital, metabolic, and psychogenic [18, 19]. The most common reason for pediatric admission to the voice clinic is children who shout a lot and develop irritative chronic laryngitis and prenodular edema or nodules due to vocal trauma. Risk factors include childhood hearing problems, frequent upper respiratory tract problems, and family dynamics. Differential diagnosis of lesions such as vergeture that accompany and cause nodules is also important in treatment strategy.
Vocal fold nodule is a mucosal reaction to mechanical trauma. The glottic gaps (hourglass-shape, posterior gaps, etc.) create higher mucosal impact pressure on smaller parts of the vocal fold mucosa. The child tries to express him/herself by increasing the phonatory effort, and this vicious circle results with mucosal inam­matory response that continues with epithelial thickening.
The mucosal trauma creates a chronic tissue reaction, which restrains low­loudness phonation. Since low-pressure glottic closure will not be possible due to the nodular masses in between, the perception that “our boy always talks shouting” settles in the family as if it were a way of behavior. These patients develop a new type of glottic closure and breathing to compensate for this condition. Less common reasons may be congenital anomalies, laryngopharyngeal reux, chronic sinonasal infections or allergies, papillomatosis, polyps, webs, cysts, sulci, laryngeal tumors, and metabolic and hormonal disorders.
Puberphonia is a functional dysphonia that affects mainly boys during puberty. Its prevalence is reported as 2–3% [20]. Physioanatomical alterations at the pho­natory apparatus are under the effect of abrupt hormonal changes [21], the mean fundamental frequency decreases (1 octave in males and 3–5 semitones in females), and reaches the adult levels [20]. Puberphonia is a register shift between chest and falsetto registers. The child cannot adapt to the physioanatomical changes and uses the falsetto register that resembles the prepubertal pitch. The vocal output becomes a high-pitched metallic sound in addition to vocal instabil­ity, poor voice control, pitch breaks, breathiness, effortful phonation, and monot­onous speech [22].
27 Dysphonia inChildren
365

27.4 Diagnosis

Diagnosis and management of pediatric dysphonia require multidimensional think­ing and a strategic approach. Coinciding pathologies such as nasal obstruction, attention decit, and hyperactivity disorder (ADHD) should be considered. Hyperactivity, various communication disorders, aggression, academic success problems, and personality problems must be consulted with child and adolescent psychiatrists. Children are generally less aware of the problem and are referred by their families. This condition may not create a need for a denitive treatment, but providing a better voice for communication can satisfy the family and the patient. Children may not be able to provide sufcient anamnesis. Family and school envi­ronments provide important clues about pediatric dysphonia. In this context, when taking anamnesis, family members as well as responsible teachers at the school can be contacted.
27.5 Signs andSymptoms
The family or teacher often notices voice problems in children. They are referred to the clinic primarily for shouting behaviors, changes in vocal timbre, limitation of vocal communication abilities, and discomfort in the neck and face during speech.
27.5.1 Clinical Assessment
Evaluation for dysphonia in children usually involves laryngoscopy to evaluate for vocal fold lesions and vocal fold mobility [23]. Videolaryngostroboscopic evalua­tion is not as easy as in adults, but it is still a golden standard in children. It can be applied quickly by rigid or exible endoscopes, assessment through general anes­thesia may be a choice in some cases.
Acoustic evaluation can be made by voice analysis and perceptual (patient and/ or clinician-based) questionnaires. Improvements during and after treatment in self­reported quality of life scales [2426] may indicate that patients feel less limited by their voices in their social environments. Although auditory-perceptual evaluation may not give objective results [2729], the clinician’s ears are the most delicate tool for dysphonia.
Acoustic and aerodynamic voice analysis may also help for diagnostic and fol­low-up measures [3032]. Voice therapy was shown to reveal improvements in cycle-to-cycle variation in frequency and amplitude (jitter, shimmer) as well as decreased noise in the voice signal (harmonic-to-noise ratio) [33, 34]. The aerody­namic improvement can be analyzed by phonation threshold pressure [35, 36] that also indicates vocal fold biomechanical changes (increased laryngeal pliability and decreased vocal fold viscosity) following therapy [2]. Acoustic-aerodynamic analy­sis may also give clues about the changes at vocal fold mass [24] but they never substitute endoscopic visualization.