See discussions, stats, and author profiles for this publication at: https://www.researchgate.
net/publication/331824781
Gingivitis: An Overall View for Undergraduate
Article · November 2018
CITATIONS                                                                                                 READS
3                                                                                                         24,873
1 author:
            Mohammed A. Alawadh
            Qassim University
            3 PUBLICATIONS 3 CITATIONS
              SEE PROFILE
 All content following this page was uploaded by Mohammed A. Alawadh on 20 September 2022.
 The user has requested enhancement of the downloaded file.
                                      https://orcid.org/0000-0002-4928-6500
  Gingivitis: An overall review
      for undergraduates
Mohammed A. Alawadh.
General Dentist, Qassim University, Qassim, Saudi Arabia                                           24 Nov. 2018
KEYWORDS: Gingival diseases. Classi cation. Gingival hemorrhage. Gingivitis. Periodontitis. Diabetes
Mellitus. Hypersensitivity. Infections. Medications.
                   ABSTRACT                                               INTRODUCTION
    Gingivitis is a non-destructive disease that causes     The gingiva is a part of the soft tissue lining of the
inflammation of the gingiva.                                mouth. It surrounds the teeth and provide a seal
                                                            around them. Unlike the soft tissue linings of the
The most common form of gingivitis, and the most            lips and cheeks, most of the gingiva is tightly
common form of periodontal disease overall, is in           bound to the underlying bone which helps resist
response to bacterial plaque that is attached to tooth      the friction of food passing over them. Thus when
surfaces, termed plaque-induced gingivitis.                 healthy, it presents an effective barrier to the
                                                            barrage of periodontal insults to deeper tissue.
Gingivitis is reversible with good oral hygiene;            Healthy gums are usually coral pink in light-
however, without treatment, gingivitis can progress to      skinned people but may be naturally darker with
Periodontitis, in which the inflammation of the gums        melanin pigmentation.
results in tissue destruction and bone resorption
around the teeth. Periodontitis can ultimately lead to      The gingiva is divided anatomically into marginal,
tooth loss.(1)                                              attached, and interdental areas.
                                                                                                                  1
                                 fi
     Periodontal disease is a major public health           exacerbate the in ammatory reaction to
     problem, particularly in low-income settings like      commensal bacteria (11). The two main features of
     sub-Saharan Africa (2). Aside from irreversible        periodontal disease are gingival in ammation
     tooth loss, chronic periodontitis may also increase    (gingivitis) and the formation of periodontal
     the risk of adverse systemic conditions (3), such as   pockets (periodontitis).
     cardiovascular disease (4) and preterm birth;
     however for preterm birth, different studies have
     reported con icting results (5).                       While it is clear that gingivitis always precedes
                                                            periodontitis (12), gingivitis does not always
     The association between periodontitis and              progress to periodontitis (13), suggesting that these
     systemic disease may be due to both increased          conditions may not simply represent different
     systemic in ammation and to translocation of           stages of a continuous spectrum of disease. While
     bacteria into the bloodstream (6).                     there is some evidence that a steady continuous
                                                            progression may be expected (14), most models
     Despite its importance, the microbial ecology of       involve acute bursts of exacerbation and longer
     periodontal disease in different oral habitats         periods of remission (15, 16).
     remains incompletely understood. Studies of the
     oral microbiome in periodontal disease typically       CLINICAL FEATURES
                                                            Most cases of gingivitis occur from a lack of
                                                            proper oral hygiene, which leads to the
                                                            accumulation of dental plaque and calculus;
                                                            however, many other factors can affect the
                                                            gingiva’s susceptibility to the oral ora. The
                                                            frequency of gingivitis is high in all age groups,
                                                            but its true prevalence is dif cult to determine
                                                            because of the lack of a standardized method of
                                                            measurement. Clinically detectable in ammatory
                                                            changes of the gingiva begin in childhood and
                                                            increase with age. With similar amounts of dental
                                                            plaque, the severity of gingivitis is greater in
                                                            adults than in prepubertal children. Around the
                                                            time of puberty, there is a period of increased
       Di erence between Periodontitis (Upper image)        susceptibility to gingivitis (puberty gingivitis),
               and Gingivitis (Lower image).                with the peak prevalence of involvement occurring
                                                            between the ages of 9 and 14 years. Between the
     focus on small populations in developed countries      ages of 11 and 17 years, the frequency declines;
     with advanced dental health care systems, which        then a slow increase is seen until the prevalence
     may not be representative of the natural history of    approaches 100% in the sixth decade of life.
     periodontal disease in the absence of treatment (7).
                                                            In most age groups, females demonstrate a lower
     In periodontal disease, the immune system              frequency of gingivitis than males (although
     responds with in ammation to oral bio lms (8).         females have periods of increased susceptibility).
     After an initial focus on identifying particular       This may be due more to better oral hygiene in
     periodontal pathogens (9), it is now widely            females than to a physiologic difference between
     accepted that oral bacterial communities undergo a     the sexes. In addition to the years of puberty (17).
     shift or dysbiosis (10) and that the presence of
     particular disease-associated species may
                                                                                                               2
ff
          fl
           fl
                fl
                     fl
                             fi
                                      fl
                                      fl
                                           fl
                                                fi
                                                            destruction of the periodontal attachment
      FACTORS ASSOCIATED WITH                               apparatus (18).
      GINGIVITIS                                            The plaque accumulates in the small gaps between
                                                            teeth, in the gingival grooves and in areas known
      1. Hormonal changes                                   as plaque traps: locations that serve to accumulate
      2. Stress                                             and maintain plaque. Examples of plaque traps
      3. Poor nutrition
                                                            include bulky and overhanging restorative
                                                            margins, claps of removable partial dentures and
      4. Certain medications:                               calculus that forms on teeth.
               ● Phenytoin
                                                            Although these accumulations may be tiny, the
               ● Calcium channel blockers
                                                            bacteria in them produce chemicals, such as
               ● Cyclosporine
                                                            degradative enzymes, and toxins, such as
      5. Diabetes mellitus                                  lipopolysaccharide (LPS, otherwise known as
                                                            endotoxin) or lipoteichoic acid (LTA), that
      6. Immune dysfunction                                 promote an in ammatory response in the gum
      7. Local trauma                                       tissue.
      8. Dental caries
                                                            This in ammation can cause an enlargement of the
      9. Tooth crowding with overlapping                    gingiva and subsequent formation. Early plaque in
                                                            health consists of a relatively simple bacterial
                                                            community dominated by Gram-positive cocci and
                                                            rods.
                             TYPES OF GINGIVITIS            As plaque matures and gingivitis develops, the
                                                            communities become increasingly complex with
      • Plaque-induced gingivitis                           higher proportions of Gram-negative rods,
                                                            fusiforms, laments, spirilla and spirochetes. Later
      • Necrotizing ulcerative gingivitis (NUG)             experimental gingivitis studies, using culture,
                                                            provided more information regarding the speci c
      • Medication-in uenced gingivitis                     bacterial species present in plaque.(19)
      • Allergic gingivitis
      • Speci c infection-related gingivitis
      • Systemic diseases gingivitis
      • Plaque-induced gingivitis
      The cause of plaque-induced gingivitis is bacterial
      plaque, which acts to initiate the body's host                    Plaque-induced gingivitis
      response. This, in turn, can lead to destruction of
      the gingival tissues, which may progress to
                                                                                                             3
fi
     fl
          fi
                   fl
                        fl
                                                   fi
• Necrotizing ulcerative gingivitis (NUG)                  • Medication-in uenced gingivitis
Has a distinctive pattern of gingival pathologic           Refers to abnormal growth of the gingival tissues
changes that have been recognized for hundreds of          secondary to the use of systemic medication. The
years. Until recently, the name of this process has        term is a misnomer because neither the epithelium
been preceded by the term acute (i.e., ANUG);              nor the cells within the connective tissue exhibit
however, several investigators have discontinued           either hyperplasia or hypertrophy.
the use of this word because there is no chronic
form of the disease.
                                                           The increased gingival size is due to an increased
The infection frequently occurs in the presence of         amount of extracellular matrix, predominantly
psychologic stress. decreased neutrophilic                 collagen. Therefore, several authors designate the
chemotaxis and phagocytic response seen in                 alteration as medication-associated gingival
patients with NUG. Stress-related epinephrine may          enlargement.
result in localized ischemia, which pre- disposes
the gingiva to NUG.                                        These designations are further supported by
In addition to stress, other factors have been             investigators who have suggested the gingival
related to an increased frequency of NUG:                  changes arise from interference with normal
                                                           intracellular collagen degradation.
        ● Immunosuppression
        ● Smoking                                          It is known that gingival collagen constantly
        ● Local trauma                                     undergoes physiologic remodeling, and the process
                                                           must be tightly controlled to maintain a constant
        ● Poor nutritional status                          volume of the gingival tissues.
Although the association with bacteria is strong,
controversial research has suggested that viruses          Investigators have suggested that cyclosporine,
such as cytomegalovirus, Epstein- Barr virus, and          phenytoin, and nifedipine are all associated with
herpes simplex may contribute to the onset and             calcium deregulation, which disrupts the normal
progression of the process (20, 21).                       collagen phagocytosis and remodeling process. If
                                                           this is true, then the increased collagen does not
                                                           occur from hyperplasia but from impaired collagen
                                                           degradation and remodeling. (22, 23, 24)
       Necrotizing ulcerative gingivitis (NUG).
 Gingiva is hemorrhagic with necrosis of the interdental
                       papillae.
                                                               Cyclosporine-related gingival hyperplasia.
                                                                  Gingiva is brotic and erythematous.
                                                                                                            4
  fi
            fl
               • Speci c infection-related gingivitis                         • Allergic gingivitis
                   ๏ Bacterial infections:                                    A distinctive pattern of gingival in ammation,
               Bacterial infections can affect patients with and              plasma cell gingivitis, was brought to the attention
               w i t h o u t i m m u n o d e c i e n c y. N e i s s e r i a   of health care practitioners during the late 1960s
               gonorrhoeae, Treponema pallidum, streptococci,                 and early 1970s. A rash of cases occurred during
               Mycobacterium chelonae, are the most common                    that time, and most appear to have been related to
               bacterial infections that give rise to gingival                a hypersensitivity to a component of chewing gum.
               lesions.                                                       Since that time, the number of cases has dwindled,
                                                                              but similar gingival alterations are reported
               They can manifest as ery red, edematous, and                   occasionally. (28)
               painful ulcerations, asymptomatic chancres,
               mucous patches or atypical non-ulcerated, highly
               in amed gingiva.(25)                                           Although the association with chewing gum has
                                                                              decreased, allergy still is responsible for many
                   ๏ Viral infections:                                        reported cases. A brand of herbal toothpaste, a
               The most common viral infections are herpes                    speci c type of mint candy, and peppers used for
               simplex virus type1(HSV-1) and 2 (HSV-2) and                   cooking have all been implicated in more recent
               varicella-zoster virus.                                        reports.
               HSV is the most common viral infection of the
               oral/facial area. It has two subtypes: type 1, which
               affects the oral cavity; and type 2, which affects             The list of allergens appears to be variable, and a
               the genitals. Primary herpetic gingivo-stomatitis is           thorough evaluation often is required to rule out an
               most commonly observed in children from 7                      allergic cause. (29)
               months to 4 years of age but can also be found in
               adolescents or young adults. Children are often
               infected with HSV by their own parents if these
               have recurrent herpes lesions.
               The primary infection may be asymptomatic but
               can manifest as severe gingivostomatitis, in which
               the gingiva are painful, in amed and ulcerated.
               Fever and lymphadenopathy are classic features
               and affected individuals experience dif culty in
               chewing. (26)
                  ๏ Fungal infections:
               Gingival in ammation can also be caused by
               fungal infections such as candidosis, linear
               gingival erythema, and histoplasmosis. (27)
                                                                                                                                5
fl
     fi
          fi
                     fl
                                  fi
                                       fi
                                            fl
                                                    fl
                                                         fi
               • Systemic diseases gingivitis
               Other systemic diseases with gingival                   Diabetes mellitus
               manifestations include gastrointestinal diseases        Diabetes mellitus is characterized by disorders in
               (e.g., Crohn´s disease), leukemia, and diabetes         insulin production, the metabolism of
               mellitus.                                               carbohydrates, fats, and proteins and in the
                                                                       functioning and structure of blood vessels.
               Crohn´s disease
               An in ammatory disease of the intestines that can       Patients with type I diabetes are at greater risk of
               involve any part of the gastrointestinal tract,         developing gingivitis. Both children and adults
               causing a wide variety of symptoms. It primarily        with poor metabolic control show a greater
               causes abdominal pain, diarrhea (which may be           tendency towards more severe gingivitis.
               bloody if the in ammation is severe), vomiting, or
               weight loss.
                                                                       The prevalence of gingivitis in children and
                                                                       adolescents with diabetes is nearly twice that
               The oral lesions in Crohn´s disease are similar to      observed in children and adolescents without this
               those of the gastrointestinal tract, including large    disease. The association between diabetes and
               ulcerations. The oral lesions are sometimes the         gingivitis in children and adolescents is so widely
                 rst signs of the disease. Typical oral                accepted that diabetes mellitus– associated
               manifestations are folds in the labial or buccal        gingivitis appears as a speci c entity in the most
               sides of the sulcus.(30)                                recent classi cation of periodontal diseases. Adults
                                                                       with type II diabetes may show higher rates of
               Leukemia                                                gingival in ammation versus adults without
                                                                       diabetes.
               A malignant hematological disorder characterized
               by an abnormal increase in white blood cells.
                                                                       Almost 64% of diabetics are estimated to have
               Oral manifestations have been reported in patients      gingival in ammation, in comparison to 50% of
               with acute monocytic leukemia, chronic myeloid          non-diabetics.(32)
               leukemia, acute lymphocytic leukemia, and
               chronic lymphocytic leukemia. Gingival
               in ltration is the initial presenting complication in
               5% of acute monocytic leukemia cases.(31)
                                                                                                                         6
fi
     fi
          fl
                   fl
                        fi
                             fl
                                  fl
                                       fi
                                                              decrease the dental plaque responsible for the
     MANAGEMENT                                               in ammatory alterations. Most self-administered
                                                              plaque control programs are ineffective unless
     Gingivitis can be prevented through regular oral         periodic professional reinforcement also is
     hygiene that includes daily brushing and ossing.         provided. (17)
     (33) Hydrogen peroxide, saline, alcohol, or
     chlorhexidine mouthwashes may also be                    The discussion of periodontitis presents a further
     employed. In a 2004 clinical study, the bene cial        discussion of dental plaque and its relationship to
     effect of hydrogen peroxide on gingivitis has been       gingival in ammation. Research has shown that
     highlighted.(34) The use of oscillation-type brushes     few individuals have the physical skills and
     might reduce the risk of gingivitis compared to          motivation necessary to obtain and maintain
     manual brushing.(35)                                     ultimate oral hygiene.
     Rigorous plaque control programs along with
     periodontal scaling and curettage also have proved       Mechanical removal of dental plaque can be aided
     to be helpful, although according to the American        by the use of numerous chemical agents, such as
     Dental Association, periodontal scaling and root         mouth rinses with chlorhexidine or essential oils,
     planing are considered as a treatment for                or dentifrices containing triclosan with 2.0%
     periodontal disease, not as a preventive treatment       Gantrez copolymer. In this vein, studies have
     for periodontal disease.(36) In a 1997 review of         evaluated the addition of these chemo-preventative
     effectiveness data, the U.S. Food and Drug               agents to typical oral hygiene efforts and shown a
     Administration (FDA) found clear evidence                statistically signi cant positive response to these
     showing that toothpaste containing triclosan was         products in controlling plaque and gingivitis.
     effective in preventing gingivitis.(37)
                                                              On occasion, hyperplastic and brotic gingiva may
                                                              have to be re-contoured surgically to allow total
     TREATMENT AND PROGNOSIS                                  resolution of the pathosis after improved hygiene.
                                                              If the gingivitis does not resolve after improved
                                                              plaque control and elimination of obvious
     Although periodontitis always is preceded by             contributing factors, then the patient should be
     gingivitis, most areas of gingivitis remain stable       evaluated for underlying systemic disorders that
     for years, and the number of affected sites that         could be contributing to the process. (38)
     convert to periodontitis is small. In spite of this,
     optimal gingival health should be the goal of all
     clinicians and their patients. In a 26-year study of a
     cohort receiving state-of-the-art dental care, the
     prevalence of localized tooth loss increased 46
                                                                           CONCLUSION
     times in areas associated with gingiva that
     consistently bled on probing during routine              Gingivitis can have multiple origins and can be the
     examinations. Even when attachment loss is not           manifestation of a wide range of systemic diseases.
     evident and the alterations appear restricted to the     Gingival tissue in ammation is one of the most
     gingival soft tissues, proactive interventions are       common lesions encountered in the clinical setting
     recommended to eliminate these areas of persistent       and may be the rst symptom in many types of
     pathosis during the early stages of disease.             disease. Gingivitis may therefore have important
                                                              diagnostic relevance, and it is vital for clinicians to
                                                              be aware of its different possible causes to ensure a
     Treatment of gingivitis consists of elimination (if
                                                              correct diagnosis and treatment.
     possible) of any known cause of increased
     susceptibility and improvement in oral hygiene to
                                                                                                                   7
fl
         fl
               fi
                    fi
                         fl
                              fi
                                          fl
                                               fi
                                         References
1. Parameter on Plaque-Induced Gingivitis". Journal of             I. Role of gingivitis. J Clin Periodontol 30:887–901.
   Periodontology. 71 (5 Suppl): 851–2. 2000. doi:10.1902/         doi:10.1034/j.1600-051X.2003.00414.x. [PubMed]
   jop.2000.71.5-S.851. PMID 10875689.                             [CrossRef]
2. Petersen PE, Bourgeois D, Ogawa H, Estupinan-Day S,         13. Batchelor P. 2014. Is periodontal disease a public health
   Ndiaye C. 2005. The global burden of oral diseases and          problem? Br Dent J 217:405–409. doi:10.1038/
   risks to oral health. Bull World Health Organ 83:661–           sj.bdj.2014.912. [PubMed] [CrossRef]
   669. [PMC free article] [PubMed]
                                                               14. Jeffcoat MK, Reddy MS. 1991. Progression of probing
3. Li X, Kolltveit KM, Tronstad L, Olsen I. 2000. Systemic         attachment loss in adult periodontitis. J Periodontol
   diseases caused by oral infection. Clin Microbiol Rev           62:185–189. doi:10.1902/jop.1991.62.3.185. [PubMed]
   13:547–558. doi:10.1128/CMR.13.4.547-558.2000.                  [CrossRef]
   [PMC free article] [PubMed] [CrossRef]
                                                               15. Haffajee AD, Socransky SS. 1986. Attachment level
4. Yu Y-H, Chasman DI, Buring JE, Rose L, Ridker PM.               changes in destructive periodontal diseases. J Clin
   2015. Cardiovascular risks associated with incident and         Periodontol 13:461–475. doi:10.1111/
   prevalent periodontal disease. J Clin Periodontol 42:21–        j.1600-051X.1986.tb01491.x. [PubMed] [CrossRef]
   28. doi:10.1111/jcpe.12335. [PMC free article]
   [PubMed] [CrossRef]                                         16. Mdala I, Olsen I, Haffajee AD, Socransky SS, Thoresen
                                                                   M, de Blasio BF. 2014. Comparing clinical attachment
5. Ide M, Papapanou PN. 2013. Epidemiology of                      level and pocket depth for predicting periodontal disease
   association between maternal periodontal disease and            progression in healthy sites of patients with chronic
   adverse pregnancy outcomes—systematic review. J                 periodontitis using multi-state Markov models. J Clin
   Periodontol 84:S181–S194. doi:10.1902/                          Periodontol 41:837–845. doi:10.1111/jcpe.12278. [PMC
   jop.2013.134009. [PubMed] [CrossRef]                            free article] [PubMed] [CrossRef]
6. Hajishengallis G. 2015. Periodontitis: from microbial       17. Newman MG, Takei H, Carranza FA et al: Clinical
   immune subversion to systemic inflammation. Nat Rev             periodontology, ed 10, Philadelphia, 2006, WB
   Immunol 15:30–44. doi:10.1038/nri3785. [PMC free                Saunders.
   article] [PubMed] [CrossRef]
                                                               18. Research, Science and Therapy Committee of the
7. Baelum V, Scheutz F. 2002. Periodontal diseases in              American Academy of Periodontology (2001).
   Africa. Periodontol 2000 29:79–103. doi:10.1034/                "Treatment of Plaque-Induced Gingivitis, Chronic
   j.1600-0757.2002.290105.x. [PubMed] [CrossRef]                  Periodontitis, and Other Clinical Conditions". Journal of
                                                                   Periodontology. 72 (12): 1790–1800. doi:10.1902/
8. Van Dyke TE. 2008. The management of inflammation               jop.2001.72.12.1790. PMID 11811516.
   in periodontal disease. J Periodontol 79:1601–1608.
   doi:10.1902/jop.2008.080173. [PMC free article]             19. Kistler, James O.; Booth, Veronica; Bradshaw, David J.;
   [PubMed] [CrossRef]                                             Wade, William G.; Glogauer, Michael (14 August 2013).
                                                                   "Bacterial Community Development in Experimental
9. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent             Gingivitis". PLoS ONE. 8 (8): e71227.
   RL. 1998. Microbial complexes in subgingival plaque. J          Bibcode:2013PLoSO...871227K. doi:10.1371/
   Clin Periodontol 25:134–144. doi:10.1111/                       journal.pone.0071227. PMC 3743832. PMID 23967169.
   j.1600-051X.1998.tb02419.x. [PubMed] [CrossRef]
                                                               20. Horning GM: Necrotizing gingivostomatitis-NUG to
10. Jiao Y, Hasegawa M, Inohara N. 2014. The role of oral          noma, Compend Contin Educ Dent 17:951-962, 1996.
    pathobionts in dysbiosis during periodontitis
    development. J Dent Res 93:539–546.                        21. Jiménez LM, Duque FL, Baer PN et al: Necrotizing
    doi:10.1177/0022034514528212. [PMC free article]               ulcerative periodontal diseases in children and young
    [PubMed] [CrossRef]                                            adults in Medel- lín, Columbia, 1965-2000, J Int Acad
                                                                   Periodontol 7:55-63, 2005.
11. Wade WG. 2013. The oral microbiome in health and
    disease. Pharmacol Res 69:137–143. doi:10.1016/            22. American Academy of Periodontology: Informational
    j.phrs.2012.11.006. [PubMed] [CrossRef]                        paper. Drug-associated gingival enlargement, J
                                                                   Periodontol 75:1424- 1431, 2004.
12. Schätzle M, Löe H, Bürgin W, Anerud A, Boysen H,
    Lang NP. 2003. Clinical course of chronic periodontitis.
                                                                                                                           8
23. Botha PJ: Drug-induced gingival hyperplasia and its             Shaw, William C (2010-12-08). "Cochrane Database of
    management—a literature review, J Dent Assoc S Afr              Systematic Reviews". The Cochrane Database of
    52:659-664, 1997.                                               Systematic Reviews (12): CD004971.
                                                                    doi:10.1002/14651858.cd004971.pub2.
24. Brunet L, Miranda J, Farré M et al: Gingival                    PMID 21154357.
    enlargement induced by drugs, Drug Saf 15:219-231,
    1996.                                                       36. American Dental Hygienists’ Association Position Paper
                                                                    on the Oral ProphylaxisArchived 2012-06-26 at the
25. Umadevi M, Adeyemi O, Patel M, Reichart PA,                     Wayback Machine, Approved by the ADHA Board of
    Robinson PG. (2006) (B2) Periodontal diseases and               Trustees April 29, 1998
    other bacterial infections. Adv Dent Res. 2006 Apr
    1;19(1):139-45                                              37. FDA Triclosan: What Consumers Should Know
                                                                    Accessed 2010-08-12
26. Tovaru S, Parlatescu I, Tovaru M, Cionca L, Arduino
    PG. (2010) Recurrent intraoral HSV-1 infection: a           38. Stoeken, Judith E.; Paraskevas, Spiros; Van Der Weijden,
    retrospective study of 58 immunocompetent patients              Godefridus A. (2007). "The Long-Term Effect of a
    from Eastern Europe. Med Oral Patol Oral Cir Bucal.             Mouthrinse Containing Essential Oils on Dental Plaque
    2010 Aug 15.                                                    and Gingivitis: A Systematic Review". Journal of
                                                                    Periodontology. 78 (7): 1218–28. doi:10.1902/
27. Stanford TW, Rivera-Hidalgo F. (2000) Oral mucosal              jop.2007.060269. PMID 17608576.
    lesions caused by infective microorganisms. II. Fungi
    and parasites. Periodontol 2000. 1999 Oct;21:125-44.
28. Kerr DA, McClatchey KD, Regezi JA: Allergic
    gingivostomatitis (due to gum chewing), J Periodontol
    42:709-712, 1971.
29. MacLeod RL, Ellis JE: Plasma cell gingivitis related to
    the use of herbal toothpaste, Br Dent J 166:375-376,
    1989.
30. Taichman LS, Eklund SA. (2005).Oral contraceptives
    and periodontal diseases: rethinking the association
    based upon analysis of National Health and Nutrition
    Examination Survey data. J Periodontol. 2005
    Aug;76(8):1374-85.
31. Demirer S, Ozdemir H, Sencan M, Marakoglu I. (2007)
    Gingival hyperplasia as an early diagnostic oral
    manifestation in acute monocytic leukemia: a case
    report. Eur J Dent. 2007 Apr; 1(2):111-4.
32. Ryan ME, Carnu O, Kamer A. (2003) The influence of
    diabetes on periodontal tissues. J Am Dent Assoc. 2003
    Oct; 134 Spec No:34S-40S.
33. Sambunjak, D.; Nickerson, J. W.; Poklepovic, T.;
    Johnson, T. M.; Imai, P.; Tugwell, P.; Worthington, H. V.
    (2011). Johnson, Trevor M, ed. "Flossing for the
    management of periodontal diseases and dental caries in
    adults". The Cochrane Library (12): CD008829.
    doi:10.1002/14651858.CD008829.pub2.
    PMID 22161438.
34. Hasturk, Hatice; Nunn, Martha; Warbington, Martha;
    Van Dyke, Thomas E. (2004). "Efficacy of a Fluoridated
    Hydrogen Peroxide-Based Mouthrinse for the Treatment
    of Gingivitis: A Randomized Clinical Trial". Journal of
    Periodontology. 75 (1): 57–65. doi:10.1902/
    jop.2004.75.1.57. PMID 15025217.
35. Deacon, Scott A; Glenny, Anne-Marie; Deery, Chris;
    Robinson, Peter G; Heanue, Mike; Walmsley, A Damien;
                                                                                                                          9
   View publication stats