Home Print this page Email this page Small font size Default font size Increase font size
Users Online: 344
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents 
Year : 2020  |  Volume : 9  |  Issue : 8  |  Page : 3890-3897  

Oral cavity and eating disorders: An insight to holistic health

1 Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India
2 Department of Periodontology, Darshan Dental College and Hospitals, Udaipur, Rajasthan, India
3 Department of Oral Medicine and Radiology, Institute of Dental Sciences, SOA University, Bhubaneswar, Odisha, India
4 Department of Oral Medicine and Radiology, Kalinga Institute of Dental Sciences, KIIT University, Bhubaneswar, Odisha, India
5 Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh, India

Date of Submission12-Apr-2020
Date of Decision10-Jun-2020
Date of Acceptance25-Jun-2020
Date of Web Publication25-Aug-2020

Correspondence Address:
Dr. Shazina Saeed
Assistant Professor (Grade III), Amity Institute of Public Health, Amity University, Sector 125, Noida - 201 301, Uttar Pradesh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_608_20

Rights and Permissions

Oral health is vital to the general well being and is a time-tested indicator of the systemic health of an individual. Oral cavity may be the primary site affected in endocrine disorders, renal disorders, gastrointestinal, cardiovascular, hematological, autoimmune cutaneous disorders, and psychosomatic disorders. Eating disorders (primarily Anorexia nervosa and bulimia) are psychosomatic disorders having multifaceted etiology, and characterized by abnormal eating patterns. In many cases, the oral cavity may be the only site of the manifestations of eating disorders. An oral physician may often unveil the mystery of this underlying systemic pathology by a vigilant and meticulous examination of the oral cavity. This not only helps in nabbing the disease in its early course but also prevents the patients from the appalling consequences due to the disease. This article aims to highlight the etiopathogenesis and various oral features in eating disorders. The oral physician should be familiar with the bizarre oral features of eating disorders and should work in close connection with other healthcare physicians to prevent the psychosomatic and systemic consequences.

Keywords: Anorexia nervosa, bulimia, eating disorders, oral manifestations

How to cite this article:
Hasan S, Ahmed S, Panigrahi R, Chaudhary P, Vyas V, Saeed S. Oral cavity and eating disorders: An insight to holistic health. J Family Med Prim Care 2020;9:3890-7

How to cite this URL:
Hasan S, Ahmed S, Panigrahi R, Chaudhary P, Vyas V, Saeed S. Oral cavity and eating disorders: An insight to holistic health. J Family Med Prim Care [serial online] 2020 [cited 2021 Apr 15];9:3890-7. Available from: https://www.jfmpc.com/text.asp?2020/9/8/3890/293060

  Introduction Top

Published literature has established an association between mental and general physical health, although the connection between oral and mental well being remains an unexplored subject.[1] Eating disorders (EDs) are psychosomatic ailments, associated with abnormal eating patterns, disrupted physical and psychosocial abilities, indigent life quality, suicidal tendencies, and potentially fatal systemic complications causing higher death rates.[2],[3],[4] EDs exhibits certain manifestations in the oral cavity, either directly or through nutritional deficiency. Tooth erosion; dental caries, qualitative and quantitative salivary changes (xerostomia, altered buffering capacity, and salivary pH), gingival and periodontal diseases, and oral mucosal lesions (palatal erythema and ulcers) constitutes the primary oral features of EDs.[5] Previously conducted studies have suggested that features of EDs are noticeable primarily within the oral cavity during the first 6 months of abnormal behavior.[6] Hence, early and accurate diagnosis of the condition is imperative, considering the associated psycho-somatic and oral health consequences.[7] EDs are now regarded as a social epidemic; AN and BN are considered as the commonest disorder among adolescents in western nations.[8]

  Classification Top

Based on the diagnostic and statistical manual of mental disorders (DSM-5), EDs can be categorized into Anorexia Nervosa (AN), Bulimia Nervosa (BN), Binge Eating Disorder (BED), and Other Specified Feeding or Eating Disorders (OSFED).[5]

AN is identified primarily by weight loss and food limitation.[7] AN is an intricate disorder and leads to diminished self-esteem, and susceptibility to habit-forming behaviors (narcotics, alcohol, tobacco, sugar, sodas, endurance sports, etc.).[9] According to DSM-5, there are three diagnostic criteria for AN.[10] [Box 1] AN is further sub-classified into restrictive type; where abstinence/reduced feeding, and strenuous workouts result in weight loss or purgative type; where the weight loss is accomplished by induced vomiting, and the excessive intake of diuretics, laxatives, and/or appetizer's suppressors.[2]

BN is identified by first overeating followed by adopting incongruous compensative practices, viz. self-inflicting vomit, excessive intake of laxatives, and strenuous workouts.[7] Gag reflex is usually induced by fingers or sometimes using pencils/combs, leading to the development of callus on the dorsal aspects of the fingers (Russell's sign).[10] [Box 2] defines the three diagnostic criteria for BN [Box 2].[11]

EDs have a gender predilection, as it is seen primarily in adolescent females, with a mean age of occurrence being 16 and 25 years for AN and BN, respectively. AN primarily affects the upper- and middle-class individuals, in contrast to BN, which affects individuals of all social-economic strata.[12] However, BED has a higher prevalence among elderly males.[5]

EDs are frequently accompanied by a wide array of comorbid conditions like cardiovascular diseases, endocrine system dysfunction, gastrointestinal, pulmonary, and musculoskeletal ailments. The impact of comorbid conditions is influenced by the patient's age, a period of irrational feeding, speed, and severity of weight loss.[13]

[Table 1] depicts the various comorbidities associated with EDs.
Table 1: Medical alterations in eating disorders

Click here to view

  Etio-Pathogenesis Top

The precise etiopathogenesis of EDs is obscure, although a wide array of factors (biological and socio-psychological factors) has an essential role play. However, the primary factor in the genesis and development of EDs remains indeterminate self-esteem and displeasure with bodily looks.[14] Some people may also have a genetic predisposition. To summarize, EDs are mostly the result of a snugly woven network of psychological factors, personality traits, and environmental factors, like a peer and parental pressure, child maltreatment, social isolation, and cultural differences.[15]

[Table 2] summarizes the various etiological factors associated with EDs.
Table 2: Etiological factors associated with eating disorders

Click here to view

  Eating Disorders and Oro-Dental Features Top

The earliest features of EDs are noticeable primarily in or around the oral cavity; hence, the oral health physicians may be the first to come across undiagnosed patients with EDs.[13]

The oral signs and symptoms of EDs are usually seen either due to nutrition deficits or due to the long-standing history of self-induced vomiting. However, improper personal hygiene, incongruous eating patterns, and particular medications may worsen the condition.[16]

The effects of EDs on oral health were reported by Hellstrom and Hurst et al. Three main types of oral pathologies are seen: (a) Dental erosion or pathological tooth loss. (b) Dental caries caused due to microbial action. Dental plaque microbes produce organic acids; thus ensuing the demineralization of enamel and dentin. (c) Chronic self-induced vomiting or protracted fasting may result in decreased salivary production. Certain antidepressant medications may further exaggerate these effects.[1]

[Figure 1] depicts the oral features in EDs.
Figure 1: Possible oral features in eating disorders

Click here to view

Dental erosion

Published literature has established dental erosion as the most salient and commonest oral feature of EDs.[17] Dental erosion is described as gradual, irreversible destruction of the calcified tooth framework, caused by non-bacterial chemical action. Initially, it appears as soft smooth-shining glossy tooth surfaces; gradually progressing to flat or superficial, flat indentations, coronal to the cementoenamel junction. Advanced lesions appear as cup-shaped defects on the occlusal/incisal aspects of the tooth, with markedly altered tooth morphology.[2] Holst and Lange (1939) coined the term 'perimylolysis' and refers to palatal erosions on the maxillary teeth.[12] The mandibular lingual tooth surfaces are usually spared as they are shielded by the tongue and saliva from sublingual and submandibular glands [18]

[Figure 2] Perimylolysis presenting as palatal erosion on the maxillary teeth.
Figure 2: Erosion on the palatal aspect of maxillary teeth

Click here to view

The origin of acid produced dictates the site predilection, with intrinsic (gastric) and extrinsic (dietary) acid causing palatal and labial erosion, respectively. It is also essential to delineate the erosion pattern due to BN and gastroesophageal reflux, with the former affecting the mandibular anterior lingual tooth surfaces and the latter affecting the occlusal and lingual aspects of the posterior teeth.[16]

Patients with tooth erosion are more prone to dentinal sensitivity. The interplay between the intensity of the tooth erosion and sensitivity has further reinforced the vomit-associated reflux effect as the primary cause.[2] Nevertheless, eds cannot be considered as the sole etiology for hypersensitivity and may occur secondary to palatal/cervical erosion, or dental caries as periomylolysis.[15] Dentin hypersensitivity is described as a sharp, fleeting, and localized dentinal pain due to a thermal/chemical trigger. Hypersensitivity usually occurs at the cervical region owing to the thinnest enamel layer; thus unveiling the dentin and dentinal tubules.[18]

Dental caries

Dental caries is one of the important features in EDs. Dental caries usually has a multifactorial etiology; hence, its occurrence cannot be exclusively attributed to EDs.[15]

Personal oral hygiene, genetic tendency, malnutrition, dietary cariogenicity, fluoride exposure during odontogenesis, and specific drug intake usually accounts for the differences in the caries prevalence in EDs. The carious lesions seen in patients with EDs exhibit the following characteristics: (a) preponderance to cervical caries and (b) leathery dentinal lesion with large areas of undermined enamel.[19]

The chronic self-inflicted vomits, excessive intake of the laxatives, diuretics, and/or appetite suppressors, and strenuous workouts usually provoke unremitting dehydration. This, in turn, imparts a negative influence on the volume of salivary production and secretion. The intake of antidepressants as a therapeutic regimen for eating disorders may further induce a xerostomic effect, thus, worsening the scenario. The interrelation between the increased salivary viscosity and a decreased buffering capacity may culminate in an acidic salivary pH, thus, serving as a contributing factor for demineralization and decay of the tooth structure.[2]

Salivary glands

Sialadenosis is regarded as a chronic presentation in patients with EDs, more commonly seen in patients with Bulimia.[16]

Sialadenosis is frequently described as a relapsing, bilateral, asymptomatic, non-inflammatory, non- neoplastic salivary gland enlargement, and does not affect the gland functioning.[20]

Lavender (1969) first suggested the association between chronic vomiting and bilateral parotid enlargement and demonstrated that bilateral parotid enlacement may sometimes the first noticeable feature of bulimia.[21] Five studies have demonstrated the enlargement of parotid glands among the bulimic subjects.[7],[15],[22],[23],[24]

Peripheral autonomic neuropathy appears to be the main reason for sialadenosis; thus resulting an increased acinar protein production and/or an interrupted granular release. Zymogen granules accumulation in the acinar cells causes parotid hypertrophy and impaired salivary secretion.[25] A study by Donath et al. demonstrated that the salivary synthesis and secretion is controlled by myoepithelial cells and postganglionic sympathetic neurons. The degenerative alteration in these regulatory cells is believed to be the cause of sialadenosis.[26],[27]

The disorder is mostly seen in patients with BN who expel by vomiting.[28] Generally, the salivary swellings are soft and asymptomatic,[29],[30] although rarely painful swellings are also seen.[29] Painful swellings are associated with different etiology.[31]

[Figure 3] Sialadenosis in bulimia nervosa.
Figure 3: Bilateral Parotid swelling in bulimia

Click here to view

Necrotizing sialometaplasia is regarded as an acute presentation of EDs, primarily in bulimia.[32] The first documentation of necrotizing sialometaplasia (NS) was made by Abraham et al. NS is defined as an inflammatory, self-limiting, necrotizing pathology and primarily affects the minor salivary glands of the hard palate.[33]

NS is regarded to arise due to ischemic necrosis of the salivary gland lobules, although, the exact etiopathogenesis is not fully elucidated. Habits (smoking and alcohol), trauma (ill-fitting denture, recent surgery, and tooth extractions), pulmonary and systemic ailments, bulimia, and anorexia may serve as potential predisposing factors.[34],[35],[36] Schoning et al. reported two cases of NS in BN subjects.[37]

[Figure 4] Necrotizing sialometaplasia in bulimia nervosa.
Figure 4: Necrotizing sialometaplasia presenting as ulcer on the posterolateral aspect of palate

Click here to view

The patients with ED may exhibit quantitative/qualitative alterations in saliva, that is, altered salivary flow rates or altered salivary composition or both.[23],[28],[30],[38],[39],[40],[41],[42],[43] Metabolic acidosis/alkalosis seen in the patients with ED could be recognized as an indirect effect of the altered biochemical salivary composition.[8]

Xerostomia refers to the subjective perception of dryness of mouth and is defined as a deficiency in the amount of salivary production and the buffering capacity. Hyposalivation is usually seen in anorexic patients during protracted starvation compared to the binge eating patterns in bulimia.[18]

Published literature has demonstrated the effect of EDs on the salivary flow rates.[23],[39],[41],[44] Predisposition to increased caries activity, opportunistic mucosal lesions (candidal infections), and taste alterations have been established with decreased salivary flow rates.

The patients with BN have been comprehensively evaluated for the qualitative salivary content.[41],[42],[43],[44] According to a study by Riad et al.,[41] significantly greater levels of amylase were reported in both unstimulated and stimulated salivary samples of the patients with BN. However, a study by Tylenda et al.[42] reported an insignificant difference in the salivary composition of bulimic and control patients. The study also suggested that the oral changes in EDs result primarily due to cariogenic dietary patterns and binging/purging habits and not due to physiologic salivary alterations.

It is essential to maintain the critical salivary pH as acidic pH causes enamel demineralization and promotes the survival of acidogenic and cariogenic microbes (e.g., S. mutans, and Candida).[17]

Research has reported elevated amylase levels in 25%-60% of bulimic patients.[29],[45] Serum amylase levels has attracted significant attention due to their diagnostic and regulatory role.[29],[30],[40],[44],[45],[46],[47]

Eating disorders and oral function

Owing to prolonged gastric purging, bulimic patients undergo the desensitization process and become habituated to suppress the most strenuous self-inflicted pharyngeal stimulus.[44]

Gustometric studies have revealed taste alterations and hypogeusia in AN and BN subjects,[48] thus promoting self-starvation in such patients. There exists a wide array of factors affecting the taste perception in the patients with ED. For example, diminished fungi form tongue papillae in anorexia nervosa and palatal abnormalities due to chronic self-induced vomiting in bulimic patients.[49] However, these findings were refuted by other studies.[50],[51] Patients with ED may also present with dysphagia (diffculty in swallowing). Johansson et al. reported the occurrence of a throat lump (Globus sensation) in these individuals.[7]

Obsessive-compulsive disorders in the form of compelling repetitive tooth brushing, a focus on hygiene, chewing gum intake, and parafunctional habit of nail-biting (onychophagy) causing tooth attrition are also associated with EDs.[9]

Gingivitis and periodontitis

The patients with ED lack meticulous oral hygiene; hence, they are more vulnerable to gingivitis and periodontitis. Vitamin C deficiency may result in marginal gingivitis.[10] Gingival recession occurs mainly in adult patients, either due to traumatic brushing or by constant acid attacks.[9] However, cases where gingivitis and periodontitis occur in young adolescents, a differential diagnosis of eating disorders should always be given consideration.[16] Periodontal health may further be affected by micronutrient deficit (e.g., zinc, iron, selenium, calcium, copper, and magnesium).[2]

Oral mucosal lesions

Numerous oral mucosal entities arise due to dietary imbalances (vitamin and hematinic); thus hindering the revival and regeneration of the oral mucosa.[17] Erythematous palate and trauma-induced ulcerations of the soft palate and pharynx are usually seen in bulimics due to chronic acidic contact and the repeated digital trauma.

Angular cheilitis/Cheilosis is primarily a feature of BN, where the angles of the mouth typically appear pale and macerated.[16] Angular cheilitis is primarily due to chronic candidal infection, although, may also occur as a result of a coexisting staphylococcus infection.[52]

Burning sensation or stomatodynia is also seen in EDs. The patients report with the perception of burning/stinging of the tongue or oral cavity, despite the non significant clinico-pathological findings. Burning sensations may occur secondary to the underlying psychological (anxiety, depression, and stress) and neurological disorders. Oral mucosa atrophy, owing to nutritional deficiencies and chronic vomiting may also serve as a contributory factor to the burning sensations in such patients.[2]

Oral microflora

Owing to chronic self-induced vomiting resulting in acid regurgitation, anorexic and bulimic patient's saliva have an increased concentration of acidogenic and cariogenic microbes.[53] Furthermore, a viscous salivary flow rate with its low pH may facilitate the growth of aciduric oral microbes.[54] Studies have demonstrated that increased salivary loads of S. sobrinus are congruous in bulimics; thus, suggesting the significance of S. sobrinus salivary culture as a diagnostic aid in patients with bulimia.[53]

[Table 3] summarizes the common oral features of EDs.
Table 3: Summary of oral features in eating disorders

Click here to view

The primary healthcare professional plays a role in the delineation of in the identification of the varied patterns of disordered eating. The primary physician must be familiar with the various risk factors and oral presentation of EDs and should be able to provide initial intervention in such patients. The primary physician should be efficient in making decisions and be able to differentiate the patients warranting urgent hospitalization; thus, directly influencing the patient care and outcomes. Also, the primary healthcare professional is often a member of a multidisciplinary team effort including a physician, nutritionist, dentist and psychiatrist.[55]

Numerous individual remedial measures (e.g., attitude modification, psychotherapy, pharmacological therapy, and family therapy) are proposed for EDs. Hence, a multidisciplinary therapeutic protocol beneficial to the varied morbid states may be implemented. However, the precise therapeutic regimen still needs to be accomplished.[56]

  Conclusion Top

EDs are typified by abnormal eating patterns and altered body weight and usually linked with numerous psycho-somatic sequelae, leading to impecunious quality of life and higher death rates.[57] These subjects have an increased propensity to develop poor oral health. A snugly woven network of deleterious cariogenic diet, self-inflicted vomit, impaired altered salivary composition and poor oral hygiene usually predispose for some oral disorders such as tooth erosion, dental caries and dry mouth.[58] The primary healthcare physician cannot only serve as a portal to specialized medical care but also has a pivotal function in motivating both the individual and the peer group for a speedy recovery.[59] The specific course of therapy for EDs still needs to be accomplished, owing to the plethora of etiologic factors.[60] However, the associated complications like electrolyte imbalance with dehydration, hypotension, bradycardia, arrhythmias, and suicide tendencies may warrant urgent hospitalization.[61]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Kisely S, Baghaie H, Ratilal Lalloo R, Johnson NW. Association between poor oral health and eating disorders: Systematic review and meta-analysis. Br J Psychiatry 2015;207:299-305.  Back to cited text no. 1
Lourenço M, Azevedo A, Brandão I, Gomes PS. Orofacial manifestations in outpatients with anorexia nervosa and bulimia nervosa focusing on the vomiting behavior. Clin Oral Invest 2018;22:1915–22.  Back to cited text no. 2
Nascimento VS, Santos AV, Arruda SB, Silva GA, Cintra JD, Pinto TC, et al. Association between eating disorders, suicide and depressive symptoms in undergraduate students of health-related courses. Einstein (São Paulo) 2020;18:1-7.  Back to cited text no. 3
Bhargavaa S, Motwani MB, Patni V. Oral implications of eating disorders: A review. Arch OrofacSci 2013;8:1-8.  Back to cited text no. 4
Garrido-Martínez P, Domínguez-Gordillo A, Cerero-Lapiedra R, Burgueño-García M, Martínez-Ramírez MJ, Gómez-Candela C, et al. Oral and dental health status in patients with eating disorders in Madrid, Spain. Med Oral Patol Oral Cir Bucal 2019;24:595-602.  Back to cited text no. 5
Askounes SE, William KA. Eating disorders within the dental practice: A literature review. Global J Med Res J DentOtolaryngol 2016;16:1-4.  Back to cited text no. 6
Johansson AK, Norring C, Unell L, Johansson A. Eating disorders and oral health: A matched case–control study. Eur J Oral Sci 2012;120:61-8.  Back to cited text no. 7
Mascitti M, Coccia E, Vignini A, Aquilanti L, Santarelli A, Salvolini E, et al. Anorexia, oral health and antioxidant salivary system: A clinical study on adult female subjects. Dent J 2019;7:1-12.  Back to cited text no. 8
Colon P, Cougot N, Famery C. Adverse effects of eating disorders on the oral health of teenagers. J Dentofacial Anom Orthod 2018;21:1-7.  Back to cited text no. 9
Coutinho I, Manuela K, Ara MA. Eating disorders: Condition of interest to a restoring dentist: A narrative review. Int J Oral Health Dent 2019;5:168-73.  Back to cited text no. 10
Rosten A, Newton T. The impact of bulimia nervosa on oral health: A review of the literature. Br Dent J 2017;223:533-9.  Back to cited text no. 11
Milosevic A. Eating disorders and the dentist. Br Dent J 1999;186:109-13.  Back to cited text no. 12
Rikani AA, Choudhry Z, Choudhry AM, Ikram H, Asghar MW, Kajal D. A critique of the literature on etiology of eating disorders. Ann Neurosci 2013;20:158-61.  Back to cited text no. 13
American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC, USA: American Psychiatric Association; 2013.  Back to cited text no. 14
Jugale PV, Pramila M, Murthy AK, Rangat S. Oral Manifestations of Suspected Eating Disorders among Women of 20-25 Years in Bangalore City, India. J Health Popul Nutr 2014;32:46-50.  Back to cited text no. 15
Bern EM, Woods RE, Rodriguez L. Gastrointestinal manifestations of eating disorders. J Pediatr GastroenterolNutr 2016;63:77-85.  Back to cited text no. 16
Frydrych AM, Davies GR, McDermott BM. Eating disorders and oral health: A review of the literature. Aust Dent J 2005;50::6-15.  Back to cited text no. 17
Alves KC, Paula PN, Fernandes AJ, Simamoto PC, Cabral LC. Oral manifestations of eating disorders: Literature review. Demetra Food, Nutr Health 2018;13:783-92.  Back to cited text no. 18
DeBate RD, Tedesco LA, Kerschbaum WE. Knowledge of oral and physical manifestations of anorexia and bulimia nervosa among dentists and dental hygienists. J Dental Educ 2004;69:346-54.  Back to cited text no. 19
Arya S, Pilania A, Kumar J, Talnia S. Diagnosis of bilateral parotid enlargement (Sialosis) by sonography: A case report and literature review. J Indian Acad Oral Med Radiol 2019;31:79-83.  Back to cited text no. 20
  [Full text]  
Garcia Garcia B, Dean Ferrer A, Diaz Jimenez N, Alamillos Granados FJ. Bilateral parotid sialadenosis associated with long-standing bulimia: A case report and literature review. J Maxillofac Oral Surg 2018;17:117-21.  Back to cited text no. 21
Dynesen AW, Bardow A, Petersson B, Nielsen LR, Nauntofte B. Salivary changes and dental erosion in bulimia nervosa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;106:696-707.  Back to cited text no. 22
Touyz SW, Liew VP, Tseng P, Frisken K, Williams H, Beumont PJ. Oral and dental complications in dieting disorders. Int JEat Disord 1993;14:341-7.  Back to cited text no. 23
Oliva CL, Jornet PL, Alonso FC, Salinas JE. Study of oral changes in patients with eating disorders. Int JDent Hyg 2008;6:119-22.  Back to cited text no. 24
Mandel L. Salivary gland disorders. Med Clin North Am 2014;98:1407-49.  Back to cited text no. 25
Donath K, Seifert G. Ultrastructural studies of the parotid glands in sialadenosis. Virchows Arch A Pathol Anat Histol 1975;365:119-35.  Back to cited text no. 26
Coleman H, Altini M, Nayler S, Richards A. Sialadenosis: A presenting sign in bulimia. Head Neck 1998;20:758-62.  Back to cited text no. 27
Brown S, Bonifazi DZ. An overview of anorexia and bulimia nervosa, and the impact of eating disorders on the oral cavity. Compendium 1993;140:1594-608.  Back to cited text no. 28
Anderson L, Shaw J, McCargar L. Physiological effects of bulimia nervosa on the gastrointestinal tract. Can J Gastroenterol 1997;11:451-9.  Back to cited text no. 29
Zachariasen R. Oral manifestations of bulimia nervosa. Women Health 1995;22:67-76.  Back to cited text no. 30
Sato Y, Fukudo S. Gastrointestinal symptoms and disorders in patients with eating disorders. Clin J Gastroenterol 2015;8:255-63.  Back to cited text no. 31
Solomon LW, Merzianu M, Sullivan M, Rigual NR. Necrotizing sialometaplasia associated with bulimia: case report and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:39-42.  Back to cited text no. 32
Hasan S, Elongovan S, Siddiqui A. Necrotising sialometaplasia of palate-report of a case with review of literature. J Orofacial Health Sci 2013;4:30-3.  Back to cited text no. 33
Brannon RB, Fowler CB, Hartman KS. Necrotizing sialometaplasia. A clinicopathologic study of sixty-nine cases and review of the literature. Oral Surg Oral Med Oral Pathol 1991;72:317-25.  Back to cited text no. 34
Imbery TA, Edwards PA. Necrotizing sialometaplasia: Literature review and case reports. J Am Dent Assoc 1996;127:1087-92.  Back to cited text no. 35
Kaplan I, Alterman M, Kleinman S, Reiser V, Shuster A, Dagan Y, et al. The clinical, histologic, and treatment spectrum in necrotizing sialometaplasia. Oral Surg Oral Med Oral Pathol Oral Radiol 2012;114:577-85.  Back to cited text no. 36
Schöning H, Emshoff R, Kreczy A. Necrotizing sialometaplasia in two patients with bulimia and chronic vomiting. Int J Oral Maxillofac Surg 1998;27:463-5.  Back to cited text no. 37
Ruff J, Koch M, Perkins S. Bulimia: Dentomedical complications. Gen Dent 1992;40:22-5.  Back to cited text no. 38
Öhrn R, Enzell K, Angmar-Mansson B. Oral status of 81 subjects with eating disorders. Eur J Oral Sci 1999;107:157-63.  Back to cited text no. 39
Philipp E, Willershausen-Zonnchen B, Hamm G, Pirke K. Oral and dental characteristics in Bulimic and anorectic patients. Int J Eat Disord 1991;4:423-31.  Back to cited text no. 40
Riad M, Barton JR, Wilson JA, Freeman CP, Maran AG. Parotid salivary secretory pattern in bulimia nervosa. Acta Otolaryngol 1991;111:392-5.  Back to cited text no. 41
Tylenda CA, Roberts MW, Elin RJ, Li SH, Altemus M. Bulimia nervosa. Its effect on salivary chemistry. J Am Dent Assoc 1991;122:37-41.  Back to cited text no. 42
Milosevic A, Dawson LJ. Salivary factors in vomiting bulimics with and without pathological tooth wear. Caries Res 1996;30:361-6.  Back to cited text no. 43
Roberts MW, Tylenda CA, Sonies BC, Elin RJ. Dysphagia in bulimia nervosa. Dysphagia 1989;4:106-11.  Back to cited text no. 44
Levine JM, Walton BE, Franko DL, Jimerson DC. Serum amylase in bulimia nervosa: Clinical status and pathology. Int J Eat Disord 1992;12:431-9.  Back to cited text no. 45
Walsh BT, Wong LM, Pesce MA, Hedigan CM, Bodourian SH. Hyperamylasaemia in bulimia nervosa. J Clin Psychiatry 1990;51:373-7.  Back to cited text no. 46
Kronvall P, Fahy TA, Isaksson A, Theander S, Russsel GF. The clinical relevance of salivary amylase monitoring in bulimia nervosa. Biol Psychiatry 1992;32:156-63.  Back to cited text no. 47
Aschenbrenner K, Scholze N, Joraschky P, Hummel T. Gustatory and olfactory sensitivity in patients with anorexia and bulimia in the course of treatment. J Psychiatr Res 2008;43:129-37.  Back to cited text no. 48
Rodin J, Bartoshuk L, Peterson C, Schank D. Bulimia and taste: possible interactions. J Abnorm Psychol 1990;99:32-9.  Back to cited text no. 49
Goldzak-Kunik G, Friedman R, Spitz M, Sandler L, Leshem M. Intact sensory function in anorexia nervosa. Am J Clin Nutr 2012;95:272-82.  Back to cited text no. 50
Dazzi F, Nitto SD, Zambetti G, Loriedo C, Ciofalo A. Alterations of the olfactory-gustatory functions in patients with eating disorders. Eur Eat Disord Rev 2013;21:382-5.  Back to cited text no. 51
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. 2nd ed. Philadelphia: WB Saunders Company; 2002. p. 192.  Back to cited text no. 52
Bretz WA, Krahn DD, Drewnowski A, Loesche WJ. Salivary levels of putative cariogenic organisms in patients with eating disorders. Oral Microbiol Immunol 1989;4:230-32.  Back to cited text no. 53
Hofer E, Jensen SB, Pedersen AML, Bardow A, Nauntofte B. Oral microflora in patients with salivary gland hypofunction. Oral Biosci Med 2004;1:93-108.  Back to cited text no. 54
Davidson AR, Braham S, Dasey L, Reidlinger DP. Physicians' perspectives on the treatment of patients with eating disorders in the acute setting. J Eat Disord 2019;7:1-9.  Back to cited text no. 55
Yagi T, Ueda H, Amitani H, Asakawa A, Miyawaki S, Inui A. The role of ghrelin, salivary secretions, and dental care in eating disorders. Nutrients 2012;4:967-89.  Back to cited text no. 56
Galmiche M, Déchelotte P, Lambert G, Tavolacci MP. Prevalence of eating disorders over the 2000–2018 period: A systematic literature review. Am J Clin Nutr 2019;109:1402-13.  Back to cited text no. 57
Johansson AK, Norring C, Unell L, Johansson A. Diet and behavioral habits related to oral health in eating disorder patients: A matched case-control study. J Eat Disorders 2020;8:7.  Back to cited text no. 58
Johns G, Taylor B, John A, Tan J. Current eating disorder healthcare services-the perspectives and experiences of individuals with eating disorders, their families and health professionals: Systematic review and thematic synthesis. BJPsych Open 2019;5:e59.  Back to cited text no. 59
Chao AM, Roy A, Franks AT, Joseph PV. A systematic review of taste differences among people with eating disorders. Biol Res Nurs 2020;22:82-91.  Back to cited text no. 60
Mitchell JE, Peterson CB. Anorexia nervosa. N Engl J Med 2020;382:1343-51.  Back to cited text no. 61


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2], [Table 3]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
   Eating Disorders...
   Article Figures
   Article Tables

 Article Access Statistics
    PDF Downloaded200    
    Comments [Add]    

Recommend this journal