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Table of Contents   
REVIEW ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 8  |  Page : 61-67
Orofacial bacterial infectious diseases: An update


Department of Oral Pathology, Dental Research Center, Research Centre for Molecular Medicine, Dental Faculty, Hamadan University of Medical Sciences, Hamadan, Iran

Date of Submission06-Aug-2017
Date of Acceptance22-Sep-2017
Date of Web Publication30-Oct-2017

Correspondence Address:
Soussan Irani
Department of Oral Pathology, Dental Research Center, Research Centre for Molecular Medicine, Dental Faculty, Shahid Fahmideh Street, Hamadan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jispcd.JISPCD_290_17

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   Abstract 

Objectives: Most of the oral infections with odontogenic origin are very common and can be treated by tooth extraction, endodontic therapy, or surgical treatment. Other infectious lesions are the manifestations of systemic diseases such as tuberculosis and syphilis. Skin and underlying subcutaneous tissue, fascia, or muscle is also involved with infectious diseases which range from superficial epidermal infections to very serious necrotizing fasciitis.
Materials and Methods: An extensive literature in PubMed, Google Scholar, and Scopus search was performed from 1980 to 2017. All related articles were analyzed.
Results: Most oral infections have odontogenic origin. Skin and the underlying subcutaneous tissue, fascia, or muscles are also involved with infectious diseases which range from superficial epidermal infections to very serious necrotizing fasciitis.
Conclusions: These facts prove that the interaction between the oral cavity, face skin, and the other organs can risk the people's life. The establishment of a correct diagnosis and recognition of clinical findings are the crucial steps to support and improve professional orofacial health status.


Keywords: Bacterial, infectious diseases, orofacial, skin


How to cite this article:
Irani S. Orofacial bacterial infectious diseases: An update. J Int Soc Prevent Communit Dent 2017;7, Suppl S2:61-7

How to cite this URL:
Irani S. Orofacial bacterial infectious diseases: An update. J Int Soc Prevent Communit Dent [serial online] 2017 [cited 2017 Nov 18];7, Suppl S2:61-7. Available from: http://www.jispcd.org/text.asp?2017/7/8/61/217422



   Introduction Top


Orofacial infections have threatened humans since the rise of human existence. Most oral infections which have the odontogenic origin are very common and can be treated by tooth extraction, endodontic therapy, or surgical treatment.[1] However, prescribing an antibiotic may be necessary.[2] Other infectious lesions are the manifestations of systemic diseases such as tuberculosis and syphilis.[3] A variety of bacteria which have synergistic or antagonistic interactions shape the oral biofilm.[4],[5],[6],[7],[8] Teeth provide hard, nonshedding surfaces for the deposition of oral microorganisms which remain within dental plaque. The accumulation and metabolism of the bacteria on hard oral surfaces is the primary cause of dental caries, gingivitis, periodontitis, peri-implant infections, and stomatitis.[9] Oral epithelium is a barrier which separates the oral cavity from its environment. The main functions of oral mucosa are resistance to microorganisms, trauma, and exogenous substances.[10]

Skin and the underlying subcutaneous tissue, fascia, or muscle is also involved with the infectious diseases which range from superficial epidermal infections to very serious necrotizing fasciitis. The incidence is about 24.6/1000 person-years in developed societies. As the diseases are variable in etiology, clinical presentation, and the diagnosis and therapy, it is critical to identify and differentiate them.[11] The aim of this study was to review the bacterial profiles associated with the orofacial infections.


   Materials and Methods Top


In this review article, a relevant English Literature search in PubMed, ScienceDirect, and Google Scholar from 2000 to mid-2017 was performed. All relevant articles were selected and reviewed. The diseases were classified into oral infections and facial infections.


   Results Top


Oral infectious diseases

Odontogenic infectious diseases

Dental caries and pulpitis

Dental caries is considered to be the most prevalent human disease, affecting 80%–90% of the world population[12] and mostly the children aged 5–17 years. A published article found a higher prevalence of dental caries in males compared to females (73% vs. 27%).[13] Both primary dentition and permanent dentition can be affected[14] with more prevalence in molar teeth.[13],[15] Based on the degree of pulp inflammation, patient's clinical symptoms differ. The sensibility tests such as thermal test can assess the response of nerve fibers in dental pulp, but due to resistance of the nerve fibers to inflammation, they may still remain active even after the degeneration of pulp tissue.[16] Over the time, the patient suffers from pain caused by irreversible pulpitis.[17] Pulpitis, the inflammation of the dental pulp, is a common sequel to caries. Bacteria are involved in inducing dental tissue damage and inflammation in the pulp tissue. The pulp is affected by bacterial virulence factors and antigens diffused by the dentinal fluid or bacterial cells. Clinically, pulpitis is classified as reversible or irreversible. In the reversible form, removing the causative agent leads to the return to normal condition, whereas in the irreversible pulpitis, root canal treatment is required. In the cases of deep dentinal caries, the bacterial composition differs from enamel caries. Streptococcus mutans was isolated in the 1920s from carious lesions and considered as the etiological agent of dental caries. The other species playing a key role in the microbial community and dentin caries include Veillonella, Rothia, and Leptotrichia in enamel caries and Streptococcus sanguinis, Atopobium, Schlegelella, Pseudoramibacter, and Lactobacillus.[18] Besides lactobacillus which is a very prevalent bacterium in dental caries, asaccharolytic and/or proteolytic anaerobic bacteria have been frequently detected in pulpitis. Most microorganisms in dental caries initiate endodontic infections. Atopobium, Pseudoramibacter alactolyticus, Streptococcus species, and S. mutans are the most frequent bacteria found in teeth with irreversible pulpitis.[19]

Gingivitis and periodontitis

Gingivitis is the reversible inflammation of only the gingiva. The prevalence of gingivitis has been reported to be as high as 90%–100% among children 7–14 years of age.[20] Clinically, inflammation begins in childhood and increases with age.[21] Redness, hypertrophy, and bleeding are the most common symptoms of gingivitis.[22] Gingivitis is initiated by the enzymatic effects and toxins released by the pathogenic microorganisms of the supragingival dental calculus and plaque. Spirochaetes, numerous Gram-positive cocci and Gram-negative bacilli as well as a variety of aerobic and capnophilic microorganisms present in the supragingival calculus.[23] The host-bacteria interaction results in the destruction of gingiva and periodontal tissues.

Necrotizing ulcerative gingivitis is a different pattern of gingivitis. It may occur in any age, but it is more frequent in young and middle-aged adults.[21] In this case, the interdental papillae are edematous, inflamed, and hemorrhagic. The blunted “punched-out” appearance of the affected papillae and craterlike necrosis of papillae covered with a gray pseudomembrane are the clinical features. Both necrotizing ulcerative periodontitis and necrotizing ulcerative mucositis (necrotizing stomatitis) are developed by the extension of the infection to the adjacent tissues. A fusiform bacterium, Bacillus fusiformis (currently Fusobacterium nucleatum), and a spirochete, Borrelia vincentii, are the causative microorganisms.[21]

Periodontitis is a chronic inflammation of supporting structures of teeth related to the oral biofilm which causes the destruction of connective tissue attachment to the tooth, alveolar bone resorption, and tooth loss.[24] The patient's age ranges between 18 and 81.[25] The most frequent areas are the first and second molars.[26] Porphyromonas gingivalis is the main etiology of periodontitis. It has the ability to colonize on the oral soft-tissue surfaces and interacts with other oral bacteria inducing immune response and finally invades host cells. P. gingivalis invasion protects the bacteria from immune system and antibiotic treatment.[27] The other more prevalent pathogens in the periodontal diseases are Prevotella intermedia, Bacteroides forsythus, Aggregatibacter actinomycetemcomitans, F. nucleatum, and Capnocytophaga.[28]

Pericoronitis

Pericoronitis is an inflammatory process arising within the tissues surrounding the crown of a partially erupted tooth, mostly third molar.[21],[29] The main causes of inflammation are food debris and bacteria beneath the gingival flap overlying the crown. Abscess develops most frequently in association with the mandibular third molars.[21] The third molar impaction usually occurs between the ages of 17 and 21 years. Previous studies suggest that impaction of mandibular third molar has a higher incidence in females compared to males.[30] Periodontitis, pain (in 5%–53% of cases), cellulitis, and osteomyelitis (in 5% of cases) are the most common clinical features.[30] Hemolytic streptococci, obligate anaerobes, the genus Prevotella, Veillonella are the most common microorganisms which have been detected in pericoronitis patients.[29] In addition, in a published study, Parvimonas micra was found in 66.7% of pericoronitis samples.[31]

Endodontic infections

Endodontic disease is initiated by the infection with multiple microorganisms, and later, the infiltration of inflammatory cells leads to pulpitis and periapical periodontitis. The results of a previous investigation have shown that the endodontic treatment is the most prevalent in female and the patient's age ranges between 46 and 60 years old. Besides, this study indicated that maxillary premolars and molars are the most prevalent teeth for the endodontic treatments.[32] The most common clinical features are pain, sensitivity of the tooth to pressure, and the swelling of surrounding tissues.[33]

Black-pigmented organisms such as Prevotella followed by Porphyromonas, especially, P. gingivalis are the most isolated microorganisms through culture of samples obtained from necrotic pulps.[34] While Fusobacterium, Parvimonas, and Peptostreptococcus were indicated as the most prevalent microorganisms in acute endodontic infections, phyla Firmicutes, Bacteroidetes, and Actinobacteria were the most prevalent microorganisms in chronic endodontic infections.[35]

Nonodontogenic infectious diseases

Peri-implantitis

An inflammation and destruction of hard and soft tissues surrounding dental implants is called peri-implantitis. In cases where infection is limited to the peri-implant mucosa, it is named peri-implant mucositis.[36] It is suggested that a disturbance of the balance between the microbiological challenge and the host response may result in peri-implantitis. Loss of supporting bone is the main characteristic of peri-implantitis. The lesion is a multifactorial process as all microorganisms; immunological, environmental, iatrogenic, mechanical, anatomical, genetic factors are involved in developing of the lesion.[37] The history of periodontitis is the most common risk factor.[38] As the attachment between the titanium surface of an implant and supra-alveolar connective tissue is weak, it is easily destroyed leading to bacterial contamination spreading to the bone.[39],[40] The lesion is more frequent in males older than 65 years.[41],[42] The submucosal presence of P. gingivalis, P. intermedia, T. forsythia, and F. nucleatum has been demonstrated around implants with peri-implantitis.[37],[43]

Syphilis

Syphilis is an acute and chronic sexually transmitted disease which is caused by an anaerobic tightly coiled helical bacterial species, Treponema pallidum. The disease is most common in males older than 15 years.[44] Oral lesions include chancre mostly in the lower lip (primary syphilis) and mucous patches mainly on the tongue and associated with secondary syphilis.[21] The other lesion is a white plaque with verrucous aspect, so-called “leukoplakia-like” lesion.[45] One-third of patients with secondary syphilis and the characteristic skin rash present oral manifestations.[46],[47],[48]

Tuberculosis

Tuberculosis is a chronic granulomatous affecting various systems of the body. It is caused mainly by Mycobacterium tuberculosis, Mycobacterium bovis, and other atypical mycobacterial species.[49] The disease can be found in all age groups and both genders.[50] The lungs are the most common primary sites of disease. The oral cavity lesions are rare and appear secondary to pulmonary tuberculosis.[51] Oral lesions seem to occur as chronic ulcers, nodular or granular areas, and rare, firm leukoplakia regions.[52] Oral lesions are painless in most cases.[51]

Leprosy

Leprosy is a chronic infectious contagious disease produced by Mycobacterium leprae. It is more common in males older than 15 years old.[53] Clinical presentations of leprosy are related to the immune response against M. leprae. Orofacial lesions (oral and nasal lesions) are the most frequent source of the spread of pathogen. Well-circumscribed hypopigmented lesions in tuberculoid leprosy and ill-defined hypopigmented macules or papules on the skin particularly on the face of patients with lepromatous leprosy are the common skin lesions.[21] Severe destruction of the anterior face including the maxilla occurs in the patients.[54] Initially, the nasal mucosa is affected, usually preceding skin lesions. The oral cavity may be contaminated in advanced stages of disease when the microorganism invades the oral cavity due to bacterial dissemination in the circulating blood.[55] Oral lesions are rare occurring in a lepromatous form. These lesions initially appear yellowish to red, sessile, firm, and papule or as nodules that develop ulceration and necrosis. According to the WHO, the most affected sites of oral cavity in leprosy patients are: the hard palate, soft palate, labial maxillary gingiva, and buccal mucosa.[56]

Scarlet fever

Scarlet fever is a systemic infection caused by group A, β-H. streptococci. The disease is the most prevalent in children between 3 and 12 years old.[21] First, the disease begins as a streptococcal tonsillitis with pharyngitis. During the first 2 days, a white coat covers the dorsum of tongue (white strawberry tongue). After desquamating of white coat, erythematous dorsal surface of tongue appears (red strawberry tongue). Within the first 2 days, the disease is associated with elaboration of an erythrogenic toxin which attacks the blood vessels and develops the cutaneous rash.[57]

Gonorrhea

Gonorrhea is caused by the bacterium  Neisseria More Details gonorrhoeae. Gnorrhea is a young person's disease and the male:female ratio is 1.5:1.[58] Oral lesions are common on the soft palate and oropharynx which clinically present as aphthous ulcers.[59]

Facial bacterial infectious diseases

Cellulitis

Cellulitis is a bacterial skin infection which can spread to other parts of body in severe cases.[60] The most common causative organisms in adults are streptococci (particularly Streptococcus pyogenes) and Staphylococcus aureus in children.[61] Orbital cellulitis is caused by primary infection of the skin, sinuses, or teeth. The most common cause is the primary sinus bacterial infection (64%). Some cases (16%) arisen from cutaneous lesions, such as eczema, furuncles, or facial cellulitis. Odontogenic infection is the least frequent cause of orbital cellulitis, however, is very important due to poor prognosis.[62] Redness of the skin, warmth, and fever are the clinical symptoms. The other clinical manifestations include abscess formation, blindness, cavernous sinus thrombosis, pulmonary embolism, and death.[60]

Impetigo

Impetigo is a superficial infection of the skin caused by Staphylococcus aureus/or in combination with Streptococcus pyogenes (group A, β-hemolytic). The scalp and face are the most commonly involved sites in the maxillofacial area. The facial lesions usually appear around the nose and mouth. It is believed that the pathogenic bacteria which are harbored in the nose, spread onto the previously damaged skin.[21] The disease is most common in children aged 2–5 years. The lesions are divided into bullous and nonbullous types. The bullous type is almost caused by S. aureus. The lesion starts as a small blister which gradually becomes a flaccid blister, measuring up to 2 cm in diameter. However, the nonbullous type mainly occurs in adult. In majority of cases S. aureus alone or in combination of group A, β-hemolytic Streptococci is the main causative pathogen. Initially, the disease starts with a vesicle, located on erythematous base. The rupture of the vesicle results in ulcer formation. Finally, the ulcer turns to a yellowish crust.[63]

Erysipelas

Erysipelas involves the upper dermis and superficial lymphatics.[64] It is mostly found in immunosuppressed males older than 50 years.[65] The affected areas appear as painful, red well-circumscribed, and swollen regions.[21] The most common causative pathogens are β-H. streptococci (usually group A, such as S. pyogenes). Other microorganisms, such as Staphylococcus aureus, may be involved in the development of the lesions. On the face, the lesions appear on the cheeks, eyelids, and bridge of the nose and look like the lesions in lupus erythematosus. High fever and lymphadenopathy are other clinical features.[21]

[Table 1] and [Table 2] summarize the clinical features and the most prevalent pathogens of orofacial bacterial infections.
Table 1: Clinical characteristics of orofacial bacterial infectious diseases

Click here to view
Table 2: The most prevalent bacterial pathogens in orofacial infections

Click here to view



   Discussion and Conclusions Top


This study provided details regarding orofacial bacterial infectious diseases. Several local or systemic diseases lead to orofacial lesions. These facts prove that the interaction between the oral cavity, face skin, and the other organs can risk the people's life. The establishment of a correct diagnosis and recognition of clinical findings are the crucial steps to support and improve professional orofacial health status. More work has to be performed to identify causative pathogens.

Acknowledgment

The author would like to acknowledge the funding from Hamadan University of Medical Sciences.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Huang TT, Tseng FY, Yeh TH, Hsu CJ, Chen YS. Factors affecting the bacteriology of deep neck infection: A retrospective study of 128 patients. Acta Otolaryngol 2006;126:396-401.  Back to cited text no. 1
[PUBMED]    
2.
Sandor GK, Low DE, Judd PL, Davidson RJ. Antimicrobial treatment options in the management of odontogenic infections. J Can Dent Assoc 1998;64:508-14.  Back to cited text no. 2
    
3.
Chunduri NS, Madasu K, Goteki VR, Karpe T, Reddy H. Evaluation of bacterial spectrum of orofacial infections and their antibiotic susceptibility. Ann Maxillofac Surg 2012;2:46-50.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Ramage G, Lappin DF, Millhouse E, Malcolm J, Jose A, Yang J, et al. The epithelial cell response to health and disease associated oral biofilm models. J Periodontal Res 2017;52:325-33.  Back to cited text no. 4
    
5.
Irani S, Monsef Esfahani A, Bidari Zerehpoush F. Detection of Helicobacter pylori in oral lesions. J Dent Res Dent Clin Dent Prospects 2013;7:230-7.  Back to cited text no. 5
    
6.
Irani S, Monsef Esfehani A, Sabeti Sh, Bidari Zerehpoush F. Detection of Helicobacter pylori in Oral lichen planus and oral lichenoid reaction. Avicenna J Dent Res 2014;6:e23213.  Back to cited text no. 6
    
7.
Monsef Esfahani A, Irani S, Sabeti Sh, Bidari Zerehpoush F. The possible role of Helicobacter pylori in the development of Sjogren's Syndrome and chronic sialadenitis. Avicenna J Dent Res 2015;7:e23212.  Back to cited text no. 7
    
8.
Irani S. Pre-cancerous lesions in the oral and maxillofacial region: A Literature review with special focus on etiopathogenesis. Iran J Pathol 2016;11:303-22.  Back to cited text no. 8
    
9.
Dani S, Prabhu A, Chaitra KR, Desai NC, Patil SR, Rajeev R, et al. Assessment of Streptococcus mutans in healthy versus gingivitis and chronic periodontitis: A clinico-microbiological study. Contemp Clin Dent 2016;7:529-34.  Back to cited text no. 9
[PUBMED]  [Full text]  
10.
Groeger SE, Meyle J. Epithelial barrier and oral bacterial infection. Periodontol 2000 2015;69:46-67.  Back to cited text no. 10
    
11.
Stahlman S, Williams VF, Oh GT, Millar EV, Bennett JW. Skin and soft tissue infections, active component, U.S. Armed forces, 2013-2016. MSMR 2017;24:2-11.  Back to cited text no. 11
    
12.
Irani S. Oral health and related factors: An update. J Int Oral Health 2016;8:140-4.  Back to cited text no. 12
    
13.
Shyam R, Manjunath BC, Kumar A, Narang R, Goyal A, Piplani A, et al. Assessment of dental caries spectrum among 11 to 14-year-old school going children in India. J Clin Diagn Res 2017;11:ZC78-81.  Back to cited text no. 13
    
14.
Bagramian RA, Garcia-Godoy F, Volpe AR. The global increase in dental caries. A pending public health crisis. Am J Dent 2009;22:3-8.  Back to cited text no. 14
    
15.
Baginska J, Rodakowska E, Milewski R, Kierklo A. Dental caries in primary and permanent molars in 7-8-year-old schoolchildren evaluated with Caries Assessment Spectrum and Treatment (CAST) index. BMC Oral Health 2014;14:74.  Back to cited text no. 15
    
16.
Naseri M, Khayat A, Zamaheni S, Shojaeian S. Correlation between histological status of the pulp and its response to sensibility tests. Iran Endod J 2017;12:20-4.  Back to cited text no. 16
    
17.
Ramalho KM, de Souza LM, Tortamano IP, Adde CA, Rocha RG, de Paula Eduardo C, et al. Arandomized placebo-blind study of the effect of low power laser on pain caused by irreversible pulpitis. Lasers Med Sci 2016;31:1899-905.  Back to cited text no. 17
    
18.
Simón-Soro A, Mira A. Solving the etiology of dental caries. Trends Microbiol 2015;23:76-82.  Back to cited text no. 18
    
19.
Rôças IN, Lima KC, Assunção IV, Gomes PN, Bracks IV, Siqueira JF Jr., et al. Advanced caries microbiota in teeth with irreversible pulpitis. J Endod 2015;41:1450-5.  Back to cited text no. 19
    
20.
Oppermann RV. An overview of the epidemiology of periodontal diseases in Latin America. Braz Oral Res 2007;21:8-15.  Back to cited text no. 20
    
21.
Neville BD, Allen C, Chi A. Oral and Maxillofacial Pathology. 4th ed. China: Elsevier; 2016.  Back to cited text no. 21
    
22.
Li Y, Lee S, Hujoel P, Su M, Zhang W, Kim J, et al. Prevalence and severity of gingivitis in American adults. Am J Dent 2010;23:9-13.  Back to cited text no. 22
    
23.
Gupta S, Jain PK, Kumra M, Rehani S, Mathias Y, Gupta R, et al. Bacterial viability within dental calculus: An untrodden, inquisitive clinico-patho- microbiological research. J Clin Diagn Res 2016;10:ZC71-5.  Back to cited text no. 23
    
24.
Chen H, Peng S, Dai L, Zou Q, Yi B, Yang X, et al. Oral microbial community assembly under the influence of periodontitis. PLoS One 2017;12:e0182259.  Back to cited text no. 24
    
25.
Demmer RT, Papapanou PN. Epidemiologic patterns of chronic and aggressive periodontitis. Periodontol 2000 2010;53:28-44.  Back to cited text no. 25
    
26.
Corraini P, Baelum V, Pannuti CM, Pustiglioni AN, Romito GA, Pustiglioni FE, et al. Periodontal attachment loss in an untreated isolated population of Brazil. J Periodontol 2008;79:610-20.  Back to cited text no. 26
    
27.
Ho MH, Huang L, Goodwin JS, Dong X, Chen CH, Xie H, et al. Two small molecules block oral epithelial cell invasion by Porphyromons gingivalis. PLoS One 2016;11:e0149618.  Back to cited text no. 27
    
28.
Sakamoto M, Umeda M, Benno Y. Molecular analysis of human oral microbiota. J Periodontal Res 2005;40:277-85.  Back to cited text no. 28
    
29.
Sixou JL, Magaud C, Jolivet-Gougeon A, Cormier M, Bonnaure-Mallet M. Microbiology of mandibular third molar pericoronitis: Incidence of beta-lactamase-producing bacteria. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95:655-9.  Back to cited text no. 29
    
30.
Santosh P. Impacted mandibular third molars: Review of literature and a proposal of a combined clinical and radiological classification. Ann Med Health Sci Res 2015;5:229-34.  Back to cited text no. 30
[PUBMED]  [Full text]  
31.
Jakovljevic A, Andric M, Knezevic A, Milicic B, Beljic-Ivanovic K, Perunovic N, et al. Herpesviral-bacterial co-infection in mandibular third molar pericoronitis. Clin Oral Investig 2017;21:1639-46.  Back to cited text no. 31
    
32.
Hollanda AC, de Alencar AH, Estrela CR, Bueno MR, Estrela C. Prevalence of endodontically treated teeth in a Brazilian adult population. Braz Dent J 2008;19:313-7.  Back to cited text no. 32
    
33.
George N, Flamiatos E, Kawasaki K, Kim N, Carriere C, Phan B, et al. Oral microbiota species in acute apical endodontic abscesses. J Oral Microbiol 2016;8:30989.  Back to cited text no. 33
    
34.
Rajaram A, Kotrashetti VS, Somannavar PD, Ingalagi P, Bhat K. Culture-based identification of pigmented Porphyromonas and Porphyromonas species in primary endodontic infections. J Dent Res Dent Clin Dent Prospects 2016;10:136-41.  Back to cited text no. 34
    
35.
Siqueira JF Jr., Rôças IN. Microbiology and treatment of acute apical abscesses. Clin Microbiol Rev 2013;26:255-73.  Back to cited text no. 35
    
36.
Smeets R, Henningsen A, Jung O, Heiland M, Hammächer C, Stein JM, et al. Definition, etiology, prevention and treatment of peri-implantitis – A review. Head Face Med 2014;10:34.  Back to cited text no. 36
    
37.
Poli PP, Cicciu M, Beretta M, Maiorana C. Peri-implant mucositis and peri-implantitis: A Current understanding of their diagnosis, clinical implications, and a report of treatment using a combined therapy approach. J Oral Implantol 2017;43:45-50.  Back to cited text no. 37
    
38.
Konstantinidis IK, Kotsakis GA, Gerdes S, Walter MH. Cross-sectional study on the prevalence and risk indicators of peri-implant diseases. Eur J Oral Implantol 2015;8:75-88.  Back to cited text no. 38
    
39.
Salvi GE, Lang NP. Diagnostic parameters for monitoring peri-implant conditions. Int J Oral Maxillofac Implants 2004;19 Suppl:116-27.  Back to cited text no. 39
    
40.
Chai WL, Brook IM, Palmquist A, van Noort R, Moharamzadeh K. The biological seal of the implant-soft tissue interface evaluated in a tissue-engineered oral mucosal model. J R Soc Interface 2012;9:3528-38.  Back to cited text no. 40
    
41.
Schwarz F, Becker K, Sahm N, Horstkemper T, Rousi K, Becker J, et al. The prevalence of peri-implant diseases for two-piece implants with an internal tube-in-tube connection: A cross-sectional analysis of 512 implants. Clin Oral Implants Res 2017;28:24-8.  Back to cited text no. 41
    
42.
Poli PP, Beretta M, Grossi GB, Maiorana C. Risk indicators related to peri-implant disease: An observational retrospective cohort study. J Periodontal Implant Sci 2016;46:266-76.  Back to cited text no. 42
    
43.
de Waal YC, Eijsbouts HV, Winkel EG, van Winkelhoff AJ. Microbial characteristics of peri-implantitis: A Case-control study. J Periodontol 2017;88:209-17.  Back to cited text no. 43
    
44.
Jakopanec I, Grjibovski AM, Nilsen Ø, Aavitsland P. Syphilis epidemiology in Norway, 1992-2008: Resurgence among men who have sex with men. BMC Infect Dis 2010;10:105.  Back to cited text no. 44
    
45.
de Paulo LF, Servato JP, Oliveira MT, Durighetto AF Jr., Zanetta-Barbosa D. Oral manifestations of secondary syphilis. Int J Infect Dis 2015;35:40-2.  Back to cited text no. 45
    
46.
Siqueira CS, Saturno JL, de Sousa SC, da Silveira FR. Diagnostic approaches in unsuspected oral lesions of syphilis. Int J Oral Maxillofac Surg 2014;43:1436-40.  Back to cited text no. 46
    
47.
Czerninski R, Pikovski A, Meir K, Casap N, Moses AE, Maly A, et al. Oral syphilis lesions – A diagnostic approach and histologic characteristics of secondary stage. Quintessence Int 2011;42:883-9.  Back to cited text no. 47
    
48.
Herrero-González JE, Parera Amer ME, Ferran Farrés M, Toll Abelló A, Barranco C, Pujol RM, et al. Syphilitic mucous patches: The resurgence of an old classic. Int J Dermatol 2008;47:1281-3.  Back to cited text no. 48
    
49.
Kumar S, Sen R, Rawal A, Dahiya RS, Dalal N, Kaushik S, et al. Primary lingual tuberculosis in immunocompetent patient: A case report. Head Neck Pathol 2010;4:178-80.  Back to cited text no. 49
    
50.
Wu B, Yu Y, Xie W, Liu Y, Zhang Y, Hu D, et al. Epidemiology of tuberculosis in chongqing, china: A secular trend from 1992 to 2015. Sci Rep 2017;7:7832.  Back to cited text no. 50
    
51.
Okano Y, Yoshida S, Shinohara T, Takahashi N, Naito N, Kagawa K, et al. Primary gingival tuberculosis diagnosed based on genetic identification. Intern Med 2015;54:2765-8.  Back to cited text no. 51
    
52.
de Souza BC, de Lemos VM, Munerato MC. Oral manifestation of tuberculosis: A case-report. Braz J Infect Dis 2016;20:210-3.  Back to cited text no. 52
    
53.
Nazario AP, Ferreira J, Schuler-Faccini L, Fiegenbaum M, Artigalás O, Vianna FSL, et al. Leprosy in Southern Brazil: A twenty-year epidemiological profile. Rev Soc Bras Med Trop 2017;50:251-5.  Back to cited text no. 53
    
54.
Ghosh S, Gadda RB, Vengal M, Pai KM, Balachandran C, Rao R, et al. Oro-facial aspects of leprosy: Report of two cases with literature review. Med Oral Patol Oral Cir Bucal 2010;15:e459-62.  Back to cited text no. 54
    
55.
de Abreu MA, Michalany NS, Weckx LL, Neto Pimentel DR, Hirata CH, de Avelar Alchorne MM, et al. The oral mucosa in leprosy: A clinical and histopathological study. Braz J Otorhinolaryngol 2006;72:312-6.  Back to cited text no. 55
    
56.
Taheri JB, Mortazavi H, Moshfeghi M, Bakhshi M, Bakhtiari S, Azari-Marhabi S, et al. Oro-facial manifestations of 100 leprosy patients. Med Oral Patol Oral Cir Bucal 2012;17:e728-32.  Back to cited text no. 56
    
57.
García-Vera C, de Dios Javierre B, Castán Larraz B, Arana Navarro T, Cenarro Guerrero T, Ruiz Pastora R, et al. Scarlet fever: A not so typical exanthematous pharyngotonsillitis (based on 171 cases). Enferm Infecc Microbiol Clin 2016;34:422-6.  Back to cited text no. 57
    
58.
Berntsen S, Karlsen APH, Pedersen ML, Mulvad G. Gonorrhoea in greenland, incidence and previous preventive measures: A review to improve future strategies. Int J Circumpolar Health 2017;76:1350092.  Back to cited text no. 58
    
59.
Chan PA, Robinette A, Montgomery M, Almonte A, Cu-Uvin S, Lonks JR, et al. Extragenital infections caused by Chlamydia trachomatis and Neisseria gonorrhoeae: A review of the literature. Infect Dis Obstet Gynecol 2016;2016:5758387.  Back to cited text no. 59
    
60.
Linder KA, Malani PN. Cellulitis. JAMA 2017;317:2142.  Back to cited text no. 60
    
61.
Morris AD. Cellulitis and erysipelas. BMJ Clin Evid 2008;2008. pii: 1708.  Back to cited text no. 61
    
62.
Park CH, Jee DH, La TY. A case of odontogenic orbital cellulitis causing blindness by severe tension orbit. J Korean Med Sci 2013;28:340-3.  Back to cited text no. 62
    
63.
Hartman-Adams H, Banvard C, Juckett G. Impetigo: Diagnosis and treatment. Am Fam Physician 2014;90:229-35.  Back to cited text no. 63
    
64.
Sukumaran V, Senanayake S. Bacterial skin and soft tissue infections. Aust Prescr 2016;39:159-63.  Back to cited text no. 64
    
65.
Inghammar M, Rasmussen M, Linder A. Recurrent erysipelas – Risk factors and clinical presentation. BMC Infect Dis 2014;14:270.  Back to cited text no. 65
    



 
 
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