October 28, 2009 by admin 





1. Simple gingivitis


2. Acute gingival inflammation

a)        Herpes simplex virus

b)        Recurrent apthous ulcers

c)        Acute necrotizing ulcerative gingivitis

d)        Acute candidiasis

e)        Acute bacterial infection


3. Chronic non – specific gingivitis


4. Condition gingival enlargement

a)        Puberty gingivitis

b)        Fibromatosis

c)        Phenytoin induced gingival over growth


5. Scorbutic gingivitis




1. Chronic periodontitis


2. Early onset periodontitis

a)    Localized juvenile periodontitis

b)    Generalized juvenile periodontitis

c)    Pubertal periodontitis

ü    Localized.

ü    Generalized.




 3. Systemic diseases associated with periodontal problems.

a)    Papillion – lefevere syndrome.

b)    Hypophosphates.

c)    Leukocyte adhesion defect.

d)    Down’s syndrome

e)    Neutropenia.

f)     Acute leukemia.

g)    Langerhans cell histeocytosis.

h)    AIDS.

i)     Insulin dependent diabetes mellitus.


 4. Anatomical periodontal problems.

a)    Mucogingival defects.

b)    Localized areas of gingival recession.

c)    High labial frenum attachment




Local irritating factor


Local functioning factor


Systemic factors






a)    Eruption gingivitis

b)    Gingivitis associated with poor oral hygiene



a)    Eruption gingivitis


-       Inflammation around the erupting teeth is known as eruption gingivitis.

-       A temporary type of gingivitis is often observed in young children when the primary teeth are erupting.

-       It is often associated with difficulty in eruption which subsides after the teeth emerged into the oral cavity.

-       The greatest increase in the incidence of gingivitis in children is often seen in the 6-7 year age group.   


This is because

(i). Gingival margin receives no protection from the coronal contour of the tooth during the early stage of active eruption.

(ii).The continual impingement of food on the gingiva causes the inflammatory process:

-       Food debris, material alba and bacterial plaque often collect around and beneath the free tissue partially cover the crown of the erupting tooth and cause the development of an inflammatory process.

-       This inflammation is most commonly associated with the eruption of the first and second permanent molars.

-       This condition can be painful and can develop into a pericoronitis or a pericoronal abscess.                     



-       Mild eruption gingivitis requires no treatment other then improved oral hygiene.

-       Painful pericoronitis may be helped when the area is irrigated with a counter irritant such as peroxyl.

-       Pericoronitis accompanied by swelling and lymph node involvement should be treated with antibiotic therapy.


b. Gingivitis associated with poor oral hygiene


-       The degree of dental cleanliness and the condition of the gingival tissue in children are definitely related.

-       Favorable occlusion and the chewing of coarse detergent type foods such as raw carrots and apples have a beneficial effects or oral cleanliness.

-       Murray pointed the importance of a good standard of oral cleanliness in reducing gingivitis.

-       Gingivitis associated with poor oral hygiene is classified as:


(i). Early (slight)

(ii). Moderate

(iii). Advanced


-       Early gingivitis is reversible

-        Gingivitis is generally less severe in children than in adults with similar plaque levels.



              -    Good oral prophylactic treatment

-       Flossing techniques

-       Instruction in good tooth brushing.




a.  Herpes simplex virus


             -    Herpes virus is one of most wide spread viral infection.

-       Primary infection usually occurs in child under 6 year of age. Who has had no contact with type I herpes simplex virus and therefore no neutralizing antibodies.

-       Infection may also occur in susceptible adults who have not had a primary infection.

-       Primary infection characterized by one or two mild sore on oral mucous membrane which may go unnoticed by parents

-       primary infection may be manifested by acute symptoms(acute  herpetic gingivostomatitis) 

Symptoms (primary tissue)                               


1-                Fiery red gingival tissue

2-                Malaise

3-                Irritability

4-                Headache

5-                Cervical lymphadenopathy

6-                High fever about l05 degree celsius

7-                Pain associated with intake of food, liquid or acid contents.

              (i). Characteristics of acute primary disease is presence of yellow or white liquid filled vesicles.

             (ii). In few days vesicles rupture and form painful ulcer 1-3 mm in diameter covered with whitish grey membrane and have a circumscribed area of inflammation.

            (iii). Ulcers may be observed on mucous membrane including buccal. Mucosa, tongue, lip, hand and soft palate and tonsilar areas.

            (iv).   In healed ulcer scaring is not present



Diagnostic criterion


(i).   Four fold rise in serum antibodies to herpes simplex virus I.

           (ii). Lesion culture will also show positive result for herpes simplex virus I.


-       Primary herpetic infection has been observed on dorsal surface of thumb of pediatric patient when child sucks the thumb acute primary infection sets transmitted to the mouth.

-       The dorsal surface of thumb will be rested on lower incisor teeth apparentally become irritated and inoculations of virus takes place.

-       Oral condition and lesion on thumb subsides in two weeks.


Treatment of acute herpetic gingival stomatitis in children


                It runs a course of 10-14 days.



Antiviral drugs are





-       Another topical anesthetic lidocaine (xylocaine viscous) can be prescribed for the child who can hold 1 tea spoon of anesthetic in mouth for 2-3 min and then expectorate the solution.

-       Alternative to anesthetic, A mixture of equal parts of diphenylhydramine (benadryl) and kaopectate can be given. In this diphenhydramine has mild analgesic and antinflammatory properly. Whereas kaolin – pectin compound Coats the lesion because food juices are irritating to ulcerated area.


Recurrent herpes labialis




           Most effective treatment is of specific systemic antiviral medication.

          This medication should be taken immediately after periodontal symptoms reoccurs.

-       Course of treatment is 5 days.

Topical antiviral agent

            Penciclovir (denavir) cream may be applied to perioral lesion but not intraoral                 lesion.

            Topical 5% acyclovir cream may be prescribed for use 5 times daily for 4 days in children 12 yrs of age and older.

-       Pencyclovir cream is applied every two hrs while awake for 4 days in children 12 yrs of age.


(b). Recurrent apthous ulcer [canker sore]


- Recurrent apthous ulcer also referred as recurrent apthous stomatitis.

- It is painful ulceration on the unattached mucous membrane that occurs in school aged children & adults.

- Peak age – 10-19 year of age

- Characterized by recurrent ulceration on moist mucous membranes of the mouth, in w/h discrete & confluent lesions form rapidly in certain sites and feature.

-       They may appear as attacks of minor or single major or multiple or herpetic form lesion.

-       Lesion persists for 4-12 days and heals uneventfully leaving scars very rarely.

-       Description of referred to apthous ulcer frequency includes canker sore.

-       Major form is recurrent to as periadenitis mucosa necrotica reccurrence and Sutton disease.

-       Recurrent apthous stomatitis is associated with other systemic disease –

Cause of RAU is unknown



Precipitating factors


-       Acc. to Green Span – either non-specific factor (prune) food allergy or specific factor (bacterial and viral infection) trigger imbalance in various cell.

This imbalance upset immune regulation & result in local destruction of oral epithelium and thus ulcerative.


            -    Treatment  is focused on promoting ulcer healing, reducing ulcer duration and patient pain, maintaining patient’s nutritional intake and preventing, reducing the frequency of recurrence of disease.

            –    Topical antinflammatory and analgesic medicines and for systemic                                                                immunomodulity and immunosuppression agents you have been  used for RAU.

            –     Primary line of t / t use topical gels, cream and ointment as anti-     inflammatory agents.

              -     Topical antiflammatory and antiallergic medication in form of  topical paste is effective in reducing pain & accelerating healing of ulcer.

            -     Active ingredient in paste in 5% Amlexanox and available as Apthason.

            –      Past is applied no ulcer 4 time daily after meals & at bed time until ulcer heals.

            -      Topical rinses also helpful for relief of RAU.

            -      Sucralfate is useful by coating the area.

            -      Topical application of tetracycline to ulcer is helpful in reducing pain & shorting the course of disease.

            -      Chlorohexidine mouthwash also alleviate the symptom of RAU.

         -      Swished dexomethesone elixir is useful to treat ulceration in areas of mouth that are difficult to access.


(c).  Acute necrotizing Ulcerative gingivitis


                                 ·        Also called –



  ·        ANUG has been defined as acute recurring gingival infection of complex etiology, characterized by necrosis of tip of gingival papillae, spontaneous bleeding and pain.

 ·        Rare among pre school children, occasionally in 6 – 12 year & common on young adults.

 Etiology of ANUG is not known, but increase in fusiform bacilli and spirochetes are seen in smears from the lesions.

Predisposing factors


             LOCAL                                               SYSTEMIC


Erupting teeth                                              Psychic Conflicts

Inadequate restoration margins                      Emotional stress

Calculus accumulation                                  Stress of drug addiction.

Open contacts                                               Nutrition def. vit. B complex, vit.C

Occlusal trauma                                             Debilitating ds. like blood dyscryasis,

Poor oral hygiene                                          Malnutrition, Down’s Synd., Diabetes


Clinical features  


Clinical course-


Management –


1- Examination –



2- Treatment –


Ist visit-       

                         1. Antibiotics – metronidazole. Pencillin, erythromycin.

                         2. Analgesics – NSAIDS 

                         3. Vit. B & C



IInd visit –   After 2 days




IIIrd visit -   After 5 days


(d).  Acute candidiasis


(Thrush, candidiasis, moniliasis).

Candida (monilia) albicans is a common inhabitant of oral cavity but may multiply & cause pathogenic state when tissue resistance is lower.



   ·        Seen in healthy neonates, when oral micro flora is disturbed by antibiotics, corticosteroids or xerostomia which allow fungus to grow.

   ·        Immune defect, especially HIV infection – immunosuppressive treatment, leukemia & lymphomas, cancer and diabetes predispose to thrush.

 Clinical features


                                 ·        Lesion of oral disease appear as raised, furry, white patches, which can be removed easily to produce bleeding underlying surfaces.

                                 ·        Lesion most commonly on upper buccal vestibule posteriorly and soft palate.

                                 ·        This infection also common in immunosuppressed patient.





                                 ·        Antifungal  antibiotics to control thrush for infants & very young children suspension of 1ml of nystatin (mycostatin) may be dropped in mouth for local action four times a day.  Drug is non-irritating & non toxic.

                                 ·        Clotrimazole suspension (10 mg/ml) 1 -2 ml applied to effected  areas four times daily, is an effective antifungal medication.

                                 ·        Systemic fluconazole suspension (10 mg/ml) is safe to use in infant at total dosage of     6 ml /kg per day.

                                 ·        For children old enough to manage solid medication allowed to dissolve in mouth, clotrimazole troches or nystatin pastilles are recommended coz therapeutic agents remain in saliva longer than liquid medication.

                                 ·        For children old enough to swallow, systemic flucanozole 100mg in 14 days course may be prescribed for patient whose infection has no responded to topical antifungal drug.



(e). Acute bacterial infection


                                 ·        Blake & Trott reported acute streptococcal gingivitis with painful, vivid red gingiva that bleeds easily.

                                 ·        Papilla gets enlarged and gingival abscesses develop.

                                 ·        Culture show predominant hemolytic streptococci.



                                 ·        Broad spectrum antibiotics are recommended if infection is believed to be bacterial in origin.

                                 ·        Improved oral hygiene is important in treating the infection.

                                 ·        Chlorhexidine mouth rinses are also useful.

                                 ·        Placement of dental restoration to restore the adequate function & contour after the reduction of the acute symptom is important




                                 ·        Gingivitis commonly seen during pre teenage and teenage years is referred to as chronic non-specific gingivitis.

                                 ·        This may it localized to anterior region or it may be more generalized.

                                 ·        Rarely painful, and persist for long periods.

                                 ·        Fiery red gingival lesion not accompanied by enlarged interdental labial papillae or closely associated with local irritant.


                                 ·        Inadequate oral hygiene:

                                 ·        Food impaction

                                 ·        Accumulation of material alba & bacterial plaque.


Predisposing factors


                                 ·        Insufficient quantities of fruits & vegetables in diet or sub clinical vit.deficiency.

                                 ·        Malocclusion – prevent adequate function and crowded teeth make oral hygiene & plaque removal more difficult.

                                 ·        Carious lesion with irritating sharp margins as will as faulty restoration with overhanging margins.

                                 ·        Mouth breathing.

                                 ·        Histologic examination tissue section and the use of special stains ruled out a bacterial infection.


                                 ·        Oral prophylaxis

                                 ·        Improved dietary intake of vitamins & use of multiple vitamin supplement.

                                 ·        All the factors should be corrected in treatment





(a) Puberty gingivitis-


                                 ·        Also known hormonal gingivitis.

                                 ·        Distinctive type of gingivitis that develop in children in prepubertal & pubertal period.

                                 ·        Gingival enlargement in anterior segment with regularity in prepubertal & premenarcheal period as well as pubescence.

                                 ·        It is confined to anterior segment and may be present in only one arch. Lingual gingival tissue generally remains unaffected.

                                 ·        Gingival enlargement is marginal, and in presence of local irritants, was characterized by prominent bulbous interproximal papilla for greater gingival enlargement associated with local factor.

                                 ·        Hormonal changes are reported to have a direct effect on periodontal tissue metabolism by increasing the permeability of the vascular system.

                                 ·        In both sexes the prevalence of gingivitis tended to decrease with age.

Treatment –

                                 ·        Improve oral hygiene by controlling plaque by

                                 ·        Means of scaling & curettage.

                                 ·        Removal of all local irritants.

                                 ·        Restoration of carious teeth.

                                 ·        Dietary changes necessary to ensure an adequate nutritional status.

                                 ·        Oral administration of 500 mg of ascorbic acid.

                                 ·        Severe cases of hyperplastic gingivitis that do not respond to local or systemic therapy should be treated by gingivoplasty.

                                 ·        Reccurrence may occur due to poor oral hygiene.


(b) Hereditary Gingival Fibromatosis

                                 ·        Characterized by a slow, progressive, benign enlargement of the gingiva.

                                 ·        Most common genetic form; hereditary gingival fibromatosis has an autosomal dominant mode of inheritance.

                                 ·        Also known elephantiasis gingiva or hereditary hyperplasia of gums but begin to enlarge with the eruption of the primary teeth.

                                 ·        Gingival tissues usually continue to enlarge with eruption of permanent teeth until the tissue essentially cover clinical crown of teeth.

                                 ·        Dense fibrous tissue often causes displacement of teeth & malocclusion.

                                 ·        Tissue enlarges to the extent that it partially covers the surface of molars & becomes traumatized during mastication.

                                 ·        Histologically fibromatosis is described as a moderate hyperplasia of epithelium, with hyperkeratosis and elongation of rete pegs.

                                 ·        Increase in tissue mass is primarily the result of on increase & thickening of the collagenous bundles in connective tissue stroma.

                                 ·        Tissue shows high degree of differentiation and few young fibroblasts are present.









About half of adult population is affected but it can be seen in children and adolescents. Both primary and permanent dentitions are affected and are of slow progression.


Clinical features










                    ·       Early onset periodontitis is used as a generic term to describe a heterogeneous group of periodontal disease occurring in growing individuals who are otherwise healthy.

                    ·       It is viewed in 3 categories.


A)   A localized form (localized juvenile periodontitis)

B)    A generalized form (generalized juvenile periodontitis)

C)    A prepubertal category (localized and generalized prepubertal          periodontitis).


 A) Localized juvenile periodontitis (localized early onset periodontitis)


It occurs in otherwise healthy children and adolescents without clinical evidence of systemic diseases.


Clinical features


                                 ·        It is characterized by the rapid and severe loss of alveolar bone around more than are permanent teeth, usually 1st molar and incisor.

                                 ·        It appears self limiting.

                                 ·        Localized juvenile periodontitis patients have little or no tissue inflammation and very little supragingival dental plaque or calculus.

                                 ·        Progression of bone loss is 3 to 4 times faster than in adult periodontitis.

                                 ·        Most patients with localized juvenile periodontitis manifest abnormalities in peripheral blood neutrophil chemotaxis and in same cases monocytes chemotaxis.





LJP is not through single disease entity. The probable causative microbial species are Porphyromonas gingivalis. Prenotella intermedia, fusobacterium nucleatum and actinobacillus, actinomycetemcomitans.

 B) Generalized juvenile periodontitis (generalized early onset periodontitis)


It occurs at or around puberty in old juvenile and young adults. It often affects the entire periodontal of the dentition.






C). Prepubertal periodontitis-


Prepubertal periodontitis of the primary dentition can occur in a localized form but usually is seem in the generalized form.


ü   Localized prepubertal periodontitis (LPP)

It is localized attachment loss only in the primary dentition in the otherwise healthy child. The exact time of the onset is unknown but it appears to arise around or before 4 years of age, when the bone is usually seen on radiographs around primary molars and incisors.


Clinical feature


                         ·       Abnormal probing depths with minor gingival inflammation.

                         ·       Rapid bone loss and minimal to varying amount of plaque at the affected sites of child dentition. 

                         ·       Abnormalities in host defense (e.g. Leukocyte chemotaxis),

                         ·       As the disease progresses, the childs periodontium show signs of gingival inflammation with gingival cleft and localized ulceration of the gingival margins.


ü   Generalized Prepubertal Periodontitis (GPP)

It is seen during or soon after eruption of the primary teeth.


Clinical feature

                                 ·        It results in severe gingival inflammation

                                 ·        Generalized attachment loss.

                                 ·        Tooth mobility.

                                 ·        Rapid alveolar bone loss with premature exfoliation of teeth.

                                 ·        The gingival tissue show minimum of plaque material

                                 ·        Chronic cases display the presence of clefting  and pronounce recession  with associated acute inflammation

                                 ·        Functional defect of neutrophils and monocytes, absence of neutrophils from gingival tissue and leukocyte adhesion defect are seen in it.

                                 ·        Alveolar bone destruction proceeds rapidly and the primary teeth may be lost by 3 year of age.



                                 ·        Microorganism predominant include

                                 ·        Actinobacillus actinomycetemcomitant (Aa), porphyromonas gingivalis. Bacteroides melaninogenicus, prenotella intermedia, fusobacterium nucleatum.




                                 ·        Early diagnosis, use of antibiotics against the infection microorganism and provision of an infection free environment for healing. Treatment of EOP, both the localized and generalized type, include surgery and the use of tetracycline.

                                 ·        Treatment with antibiotic done, such as a 2 week course of doxycycline (a systemic tetracycline), has been shown to reduce the Aa.

                                 ·        Surgical removal of infection of cravicular epithelium and debridement of root surface during surgery while the patient is a 14 – day course of doxycycline hyclate (1 g per day) is considered the best effective treatment modality.

                                 ·        In a study of deep periodontal lesion, Christersson et al demonstrated that scaling  and root planing alone were ineffective for the elimination of Aa.

                                 ·        Rams, Keges and Wright described the Keges technique as effective in treating localized juvenile periodontitis.

                                 ·        The treatment includes meticulous scaling and root planing of all teeth, with concomitant irrigation to probing depth of saturated inorganic salt solution and 1% chloramines T.

                                 ·        In addition, they recommended administration of systemic tetracycline (1s per day) for 14 days. Patient home care treatment includes daily application of a past of sodium bicarbonate and 3% hydrogen peroxide and inorganic salt irrigation.

                                 ·        Treatment of localized prepubertal periodontitis and generalized prepubertal periodontitis depends on early diagnosis, dental curettage, root planing, prophylaxis, oral hygiene instruction, restoration of decayed teeth, removal of the primary teeth that have lost bony support, and more frequent recalls.

                                 ·        Use of antimicrobial rinses (chlorhexidine) and therapy with broad spectrum antibiotics are effective in eliminating the periodontal pathogens.

                                 ·        Amoxicillin has been used in children (250 mg liquid 3 times a day for 10 days) because tetracycline or a derivative is a effective antibiotic against Aa and other gram –ve anaerobic microorganism, its use should be considered in the treatment of localized prepubertal periodontitis or generalized prepubertal periodontitis.

                                 ·        Treatment of generalized prepubertal periodontal is less successful overall and something requires extraction of all primary teeth.




A) Papillon – lefevre syndrome


                                 ·        It was observed in a 2 1/2  year old child.

                                 ·        The disorder is noted, an autosomal recessive mode of inheritance to chromosome band 11 or 14 or 21.

                                 ·        The primary teeth erupted at the normal time. However, as early as 2 years of age, the child rubbed the gingival tissue and acted as if they were painful.

                                 ·        There was tendency towards gingival bleeding when the teeth were brushed. Hyperkeratosis of the palms and soles was present; the 1st evidence was erythma and scarness noted initially at 8 months of age.

                                 ·        At 2 ½ yrs of age. All the primary teeth showed looseness, and full mouth radiographs revealed severe horizontal bone resorption.

                                 ·        Because of gingival inflammation, patient discomfort, and the presence of infected periodontal pocket’s all the primary teeth were removed by 3 year of age.

                                 ·        Histologic sections of the teeth displayed a premature resorption pattern with essentially normal pulp tissue. Cementum was apparently normal. An accumulation of adherent basophilic plaque, made up of a mass of filamentous microorganism, was noted on almost the entire length of the root surface.





Actinobacillus, actinomycetemcomitans, F. nucleatum, etc.



Complete denture was instructed 3 months after the removal of the primary teeth. The 1st permanent molar and mandibular central incisors erupted at the expected time, and the dentures base was adjusted do allow for the emergence of the teeth.

This regimen may have been responsible for eliminating pathogens and preventing the destruction process from being carried into permanent dentition.


B) Hypophosphatamia Rathbun Syndrome


                         ·       It is a genetic disorder in which four groups are described , perinatal (lethal), infantile, childhood and adult. The earlier the presentation of the symptoms the more severe is the disease.

                         ·       Hypophosphatamia is a familial disorder of the inborn error of metabolism.

                         ·       There is disease result from an autosomal recessive trait, although in other instances dominant inheritance is indicated.



Clinical Features


                                 ·        The disease occurs in severe and mild forms, and at least three types are recognized. The infantile type first appears between birth and 6 months of age. The childhood type appears between the age of 6 and 14 months, and the adult type manifests during childhood and radio graphically osseous radiolucencies are seen. The disease is characterized by abnormal mineralization of bone and dental tissue premature exfoliation of the primary teeth observed. 


                                 ·        Low serum alkaline phosphates, inc. phospho ethanolamine in urine.




Dental management includes extraction of mobile primary teeth to prevent discomfort. For permanent dentition conventional periodontal therapy is advocated. 


C) Leukocyte adhesion defect (LAD).:-


                                 ·        Prepubertal generalized aggressive periodontitis is the oral manifestation of LAD, it is an autosomal recessive defect.


                                 ·        Leukocyte surface glycoprotein defect resulting in poor leukocyte adherence.


                                 ·        Frequent respiratory. Skin, ear and soft tissue bacterial infection are seen.


Clinical Features


Severe gingivitis and periodontitis leads to tooth loss because of periodontal destruction. Early exfoliation of deciduous dentition is seen due to rapid attachment and bone loss after eruption. 




Only bone morrow transplantation can resolve the problem.


 D) Down’s syndrome (Trisomy 21)

 Prevalence of periodontal diseases is 60 – 100% in Down’s syndrome patients.

 Clinical Features

 May be noted in primary dentition with mandibular incisor often being affected. In these patients the occurrence of the periodontal pathogenic microorganism A. actinomycetecomitans in subgingival plaque is more when compared to the control.


 Suggested etiology of periodontitis is poor vascularization of gingival tissue, T cells maturation defect, reduced polymorphonuclear neutrophil (PMN) chemotaxis and phagocytosis and IgG subclass deficiencies.


E) Chediak – Higashi syndrome –


It is a rare autosomal recessive immunodeficiency disorder larger lysosomal granule in granulocytes, neutrophil and monocyte defects are seen. Recurrent and severe infection may be seen.


Clinical Features


                                 ·        Occulocutaneous albinism photo phobia, nystagmus and peripheral neuropathy.


                                 ·        Severe gingivitis and periodontitis tooth loss is due to periodontal destruction. Ulcerations mucosa, tongue and hard palate are seen.



F) Neutropenia:


It is a manifestation of dec. circulating PMN cells. Its severe forms are cyclic neutropenia, chronic bening neutropenia of childhood, chronic idiopathic neutropenia and familial benign neutropenia.


Clinical Feature



G) Acute Leukemia


Gingival enlargement due to infiltration with leukemic cell may be the presenting symptoms, particularly of acute myloblastic (AML)


Clinical Feature

                                 ·        Gingiva appears hyperplastic, edematous and bluish red.

                                 ·        Petechial or mucosal ulceration may be present with any form of leukemia related to thrombocyte and coagulation abnormalities.

                                 ·        Gingival ulceration is common.

                                 ·        Initial diagnosis is carried out by complete blood picture.


H) Langerhan cells histeocytosis


It is a group of disorders with variable symptoms resulting from abnormal proliferation and dissemination of histocyte cells of langerhans system


Clinical feature

                                 ·        Ulcerative necrotizing lesions of the gingiva,

                                 ·        Root exposure

                                 ·        Increase mobility of teeth,

                                 ·        Halitosis

                                 ·        Osteolytic areas of alveolar bone in the radiographic examination giving the appearance of “floating teeth”.

                                 ·        Diagnosis is done by biopsy and histopathological examination.





I) Acquired immunodeficiency syndrome


HIV infection in children is also associated with nerotising ulcerative periodontitis (NUP).


Clinical features

                                 ·        A typical gingival, inflammation around the marginal gingiva,

                                 ·        Linear gingival erythema, is a common feature in HIV infected children. Spontaneous gingival bleeding

                                 ·        Deep  pain is observed.


J) Insulin Dependent Diabetes Mellitus (Type I)

                                 ·        In individuals with type I diabetes mellitus, the fasting blood sugar level more than 120mg/dl .

                                 ·        Incidence increase after puberty and with age.


Clinical features

                                 ·        Decrease function of neutrophils is seen.

                                 ·        Xerostomia and recurrent gingival abscess may be present.

                                 ·        Reduced salivary flow leads to  increase caries risk.



                 1) Mucogingival defects –

                                 ·        Pocket depth exceeds with attached gingiva.

                                 ·        Lower incisors are most commonly involved.

                                 ·        In children the defect may result from labial positioning of tooth erupting

2) Localized areas of gingival recession  (stripping):-

                                 ·        Usually due to labial malposition of tooth.

                                 ·        It is most common in lower incisors.

                                 ·        May lead to mucogingival defects.

3) High labial frenum attachment:-

                                 ·        May exacerbate stripping and mucogingival defects in mandible.

                                 ·        May be esthetically objectionable in maxilla.


                                 ·        Narrow band of attached gingiva can be maintained through effective plaque control.

                                 ·        Gingival graft may be needed to create anatomic contours conducive  to  good plaque control.

                                 ·        Frenectomy may be indicated to relocate frenal attachment



            Gingival & periodontal diseases produce deformities in gingiva that interfere with normal food excursion, collect plaque and food debris & prolong and aggravate the disease process. Deformities include – gingival cleft & craters, shelf line interdental papillae caused by ANUG, gingival enlargement.




Subgingival calculus is usually harder than gingival calculus and is often locked into root irregularities making it more tenacious and difficult to remove.Curette is preferred by most clinicians for subgingival scaling & root planing. Its curved blade, rounded toe and curved back allow the curette to be inserted to the base of pocket and adapt to variations in tooth contour with minimal tissue displacement and trauma.Sickle, hoes, files and ultrasonic instruments also used for subgingival scaling. Subgingival scaling and root planing are accomplished with either universal or area specific (Gracey) curette using the following basic procedure. The curette is held with a modified pen grasp. The correct cutting edge is slightly adapted to the tooth with the lower shank kept parallel to the tooth surface. The lower shank is moved towards the tooth so that face of the blade is nearly flush with the tooth surface. The blade is then inserted under the gingiva and advanced to the base of the pocket by a light exploratory stroke. When the cutting edge reaches the base of the pocket, a working angulations of between 45 degree to 90 degree is established & pressure is applied lateral against the tooth surface.Scaling and root planing strokes should e confined to the portion of the tooth where the calculus or altered cementum is found, this area is k/a instrumentation zone.



ü             Impact zone (where the solution initially contact the area)

ü             Flushing zone (where solution reaches the subgingival calculus).



Periodontal inflammation and resultant loss of attachment results in reduced attached gingiva. Frenal and muscle attachments that encroach on the marginal gingiva distend the gingival sulcus, fastenings plaque accumulation, increase the rate of progression of periodontal recession. In such areas gingival grafts and frenectomy is done to reduce the tissue recession.



Gingivectomy means excision of the gingiva. By removing pocket wall, gingivectomy provides visibility and accessibility for complete calculus removal and through smoothing of roots.




ü             Elimination of supraboney pockets.

ü             Elimination of gingival enlargement.

ü             Elimination of supraboney periodontal abscess.


ü             Need for bone surgery.

ü             Situation in which bottom of pocket is apical to the mucogingival                                                                                                                      junction.

ü             Esthetic consideration.

Surgical Gingivectomy


STEP – 1    Pocket on each surface are explored with periodontal probe and marked with pocket markers.

STEP – 2    Periodontal knives are used for incision on facial and lingual surfaces and those distal to terminal tooth in the arch.

Discontinuous or continuous incision may be used.

Incision should be beveled at approximately 45 degree to tooth surface.

Failure to bevel leaves broad fibrous plate arm that take more time than required to develop physiologic contour.

In the interim plaque & food accumulation may lead to recurrence of pockets.

STEP – 3    Remove the excised pocket wall, clean the area and closely examine root surface.

Most apical zone consist of bend like light zone where tissue were attached and coronally to it calculus remnant, root caries or root resorption may be found.

Granulation tissue may be seen on excised soft tissue.

STEP – 4       Carefully curette the granulation tissue and remove any remaining calculus and necrotic cementum to leave smooth and clear surface.

STEP -5         Cover area with surgical pack.




Similar to gingivectomy, purpose is different. Gingivoplasty is reshaping of gingiva to create physiologic gingival contour, with the sole purpose of recontouring the gingiva in absence of pocket.

It may be done by periodontal knife, scalpel, rotatory coarse diamond stone and electrodes. It consist of procedure that resemble those performed in festooning artificial denture, tapering gingival margin, creating scalloped marginal outline, thinning attached gingiva, creating vertical interdental groove, and shaping interdental papillae to provide sluiceway for passage of food.













Comments are closed.