GINGIVITIS CONTENT l INTRODUCTION l STAGES OF GINGIVITIS

GINGIVITIS

CONTENT l INTRODUCTION l STAGES OF GINGIVITIS l TYPES OF GINGIVITIS l CLINICAL FINDINGS

INTRODUCTION DEFNITION: INFLAMATION OF THE GINGIVA IS TERMED AS GINGIVITIS. THE MICRO ORGANISM IN PLAQUE CAN EXERT ITS EFFECT ON PERIODONTIUM BY RELEASING CERTAIN PRODUCTS WHICH CAN CAUSE DAMAGE TO THE EPITHELIUM AND CONNECTIVE TISSUE CONSTITUENTS. THE INTER CELLULAR SPACES BETWEEN THE JUNCTIONAL EPITHELIAL CELLS ARE DESTROYED AND MAY PERMIT THE BACTERIAL PRODCTS OR BACTERIA THEMSELVES TO GAIN ACCESS INTO THE CONNECTIVE TISSUE. THE SEQUENCE OF EVENTS DURING THE DEVELOPMENT OF GINGIVITIS CAN OCCUR IN FOUR DIFFERENT STAGES

STAGE I GINGIVITIS: THE INITIAL LESION l CLINICALLY NO VISIBLE CHANGES ARE SEEN EXCEPT PRESENCE OF EXUDATION OF FLUID FROM THE GINGIVAL SULCUS , HENCE THIS CONDITION IS CALLED SUBCLINICAL GINGIVITIS FEATURES. 1. CLASSIC VASCULITIS OF VESSELS SUBADJACENT TO THE JUNCTIONAL EPITHELIUM 2. EXUDATION OF FLUID FROM GINGIVAL SULCUS 3. CHANGES IN THE CORONAL MOST PART OF THE JUNCTIONAL EPITHELIUM 4. INCREASED MIGRATION OF THE LEUKOCYTES INTO THE JUNCTIONAL EPITHELIUM AND GINGIVAL SULCUS. 5. PRESENCE OF SERUM PROTEINS 6. LOSS OF PERIVASCULAR COLLAGEN

STAGE II GINGIVITIS: THE EARLY LESION l l 1. 2. 3. 4. 5. CLINICALLY ERYTHEMATOUS GINGIVA AND BLEEDING ON PROBING MAY BE EVIDENT. FEATURES ALL THE CHANGES SEEN IN THE INITIAL LESIONS CONTINUE TO INTENSIFY THE JUNCTIONAL EPITHELIUM MAY BEGIN TO SHOW THE DEVELOPMENT OF RETE PEGS OR RIDGES. ACCUMULATION OF LYMPHOCYTES (T CELLS) BENEATH THE JUNCTIONAL EPITHELIUM. FURTHER LOSS OF COLLAGEN FIBRE NETWORK SUPPORTING THE MARGINAL GINGIVA FIBROBLASTS SHOW CYTOTOXIC ALTERATION WITH A DECREASED CAPACITY FOR COLLAGEN PRODUTION

STAGE III GINGIVITIS: THE ESTABLISHED LESION CLINICAL FEATURES 1. A BLUISH HUE ON THE REDDENDED GINGIVA DUE TO IMPAIRED VENOUS RETURN 2. GINGIVA APPEARS TO BE MODERATELY TO SEVERLY INFLAMMED l MICROSCOPICALLY 1. PREDOMINANT INFLAMATORY CELLS TYPE ARE PLASMA CELLS, WHICH INVADES EPITHELIUM AND ALSO DEEP INTO THE CONNECTIVE TISSUE, AROUND THE BLOOD VESSELS AND BETWEEN THE BUNDLES OF COLLAGEN FIBRES. 2. PROLIFERATION, APICAL MIGRATION AND LATERAL EXTENSION OF THE JUNCTIONAL EPITHELIUM IS SEEN. EARLY POCKET FORMATION MAY OR MAY NOT BE PRESENT. 3. FURTHER COLLAGEN DESTRUCTION AND CONTINUING LOSS OF CONNECTIVE TISSUE SUBSTANCE SEEN IN THE EARLY LESION. 4. THE FOLLOWING ENZYME LEVELS ARE SAID TO BE ELEVATED IN CHRONICALLY INFLAMMED GINGIVA: ACID AND ALKALINE PHOSPHATES, B-GLUCORONIDASE etc

STAGE IV GINGIVITIS: THE ADVANCED LESION IS ALSO KNOWN AS PHASE OF ADVANCED PERIODAONTAL BREAKDOWN l FEATURES 1. PERSISTENCE OF FEATURES DESCRIBED IN THE ESTABLISHED LESION 2. EXTENSION OF THE LESION INTO THE ALVEOLAR BONE AND PERIODONTAL LIGAMENT LEADING TO SIGNIFICANT AMOUNT OF BONE LOSS. 3. CONTINUED LOSS OF COLLAGEN 4. FORMATION OF PERIODONTAL POCKETS. 5. CONVERSION OF BONE MARROW INTO FIBROUS TISSUE 6. PRESENCE OF ALMOST ALL THE TYPES OF INFLAMMATORY CELLS l

STAGES OF GINGIVITIS STAGES TIME BLOOD (DAYS) VESSEL JUNCTINAL PREDOM AND SULCULAR INANT EPITHELIUM IMMUNE COLLAGEN CLINICAL FINDINGS CELLS INITIAL LESION 2 -4 VASCULAR DILATION VASCULITIS INFILTRATED BY PMNs PERIVASCULAR LOSS GINGIVAL FLUID FLOWS EARLY LESION 4 -7 VASCULAR PROLIFERATION SAME AS STAGE I RETE PEGS FORMATION ATROPHIC AREAS LYMPHOCYTES INCREASED LOSS ERYTHEMA BLEEDING ON PROBING SAME AS STAGE II, PLUS BLOOD STASIS SAME AS STAGE II BUT MORE ADVANCED PLASMA CELLS CONTINUED LOSS CHANGES IN COLOUR, SIZE, TEXTURE ESTABLI- 14 - 21 SHED LESION

TYPES OF GINGIVITIS DEPENDING UPON THE COURSE AND DURATION l DEPENDING ON DISTRIBUTION l

DEPENDING ON COURSE AND DURATION 1. ACUTE GINGIVITIS IT IS A PAINFUL CONDITION THAT COMES ON SUDDENLY AND IS OF SHORT DURATION 2. SUB ACUTE GINGIVITIS IT IS A LESS SEVERE PHASE OF AN ACUTE CONDITION 3. RECUURENT GINGIVITIS APPEARS AFTER HAVING BEEN ELIMINATED BY TREATMENT OR DISAPPEARS SPONTANEOUSLY AND THEN REAPPEARS 4. CHRONIC GINGIVITIS COMES ON SLOWLY, IS OF LONG DURATION AND IS PAINLESS UNLESS COMPLICATED BY ACUTE/SUB ACUTE EXACERBATION

DEPENDING ON DISTRIBUTION 1. LOCALISED GINGIVITIS IS CONFINED TO GINGIVA IN RELATION TO A SINGLE TOOTH OR GROUP OF TEETH 2. GENERALISED GINGIVITIS INVOLVES THE ENTIRE MOUTH 3. MARGINAL GINGIVITITIS INVOLVES THE GINGIVAL MARGIN BUT MAY INCLUDE A PORTION OF THE CONTIGEOUS ATTACHED GINGIVA 4. PAPILLARY GINGIVITIS INVOLVES THE INTER DENTAL PAPILLAE AND OFTEN EXTENDS INTO THE ADJACENT PORTION OF THE GINGIVAL MARGIN 5. DIFFUSE GINGIVITIS AFFECTS THE MARGIN, ATTACHED GINGIVA AND THE INTER DENTAL PAPILLAE PAPILLARY, MARGINAL AND DIFFUSE GINGIVITIS CAN OCCUR AS LOCALISED OR GENERALISED CONDITIONS

CLINICAL FINDINGS WHILE EXAMINING THE GINGIVA CLINICALLY ONE MUST ADOPT A SYSTEMATIC APPROACH WHILE CLOSE ATTENTION SHOULD BE GIVEN TO ANY TISSUE ALTERATION BECAUSE THEY CONTRIBUTE TO DIAGNOSIS. THE GINGIVA IS EXAMINED FOR: COLOUR, CONTOUR, CONSISTENCY, SIZE, POSITION, SEVERITY OF BLEEDING, SURFACE TEXTURE.

GINGIVAL BLEEDING THE TWO EARLIEST SYMPTOMS 1. INCREASED GINGIVAL FLUID PRODUTION RATE 2. BLEEDING FROM THE GINGIVAL SULCUS ON GENTLE PROBING GINGIVAL BLEEDING VARIES IN SEVERITY, DURATION AND THE EASE WITH WHICH IT IS PROVOKED. BLEEDING ON PROBING IS EASILY DETECTABLE CLINICALLY AND HENCE IT IS OF GREAT VALUE FOR EARLY DIAGNOSIS AND PREVENTION. IT IS ONE OF THE TWO EARLIEST VISUAL SIGNS OF INFLAMMATION. IT CAN APPEAR EARLIER THAN COLOUR CHANGES. IT ALSO REQUIRE LESS SUBJECTIVE EXAMINATION GINGIVAL BLEEDING ON PROBING DETERMINES IF THE LESION IS OF ACTIVE OR INACTIVE STATE –LITTLE BLEEDING/NO BLEEDING ON PROBING ACTIVE LESION –BLEEDS MORE READILY ON PROBING THE SEVERITY AND EASE WITH WHICH BLEEDING CAN BE PROVOKED INDICATES THE INTENSITY OF INFLAMMATION

GINGIVAL BLEEDING CAUSED BY LOCAL FACTORS l CHRONIC AND RECURRENT BLEEDING THE MOST COMMON CAUSE OF ABNORMAL GINGIVAL BLEEDING IS CHRONIC INFLAMMATION. THE BLEEDING IS CHRONIC OR RECCURENT AND IS PROVOKED BY MECHANICAL TRAUMA, OR BY BITING INTO SOLID FOODS. SITES THAT BLEED ON PROBING HAVE A GREATER AREA OF INFLAMED CONNECTIVE TISSUE THAN THE SITES THAT DO NOT BLEED. IN MOST CASES THE CELLULAR INFILTRATE OR SITES THAT BLEED ON PROBING IS PREDOMINANTELY LYMPHOCYTE. SEVERITY OF BLEEDING AND THE EASE WITH WHICH IT IS PROVOKED DEPENDS ON INTENSITY OF THE INFLAMMATION. AFTER THE VESSELS RUPTURE, A COMPLEX OF MECHANISM INDUCES HEMOSTASIS. IN CASES OF MODERATE OR ADVANCED PERIODONTITIS THE PRESENCE OF BLEEDING ON PROBING IS CONSIDERED A SIGN OF ACTIVE TISSUE DESTRUCTION.

l ACUTE BLEEDING: ACUTE EPISODES OF GINGIVAL BLEEDING ARE CAUSED BY INJURY OR OCCUR SPONTANEOUSLY IN ACUTE GINGIVAL DISEASE. GINGIVAL BURNS FROM HOT FOODS OR CHEMICALS INCREASE THE EASE OF GINGIVAL BLEEDING. SPONTANEOUS BLEEDING OR BLEEDING ON SLIGHT PROVOCATION OCCURS IN ACUTE NECROTIZING ULCERATIVE GINGIVITIS. ENGORGED BLOOD VESSELS IN THE INFLAMED CONNECTIVE TISSUE ARE EXPOSED BY ULCERATION.

COLOUR CHANGES IN GINGIVA COLOUR OF THE GINGIVA IS AN IMPORTANT CLINIACAL SIGN OF GINGIVAL DISEASE. NORMALLY GINGIVA APPEARS TO BE CORAL PINK. ENDOGENEOUS ORAL PIGMENTATIONS CAN BE DUE TO MELANIN, BILIRUBIN OR IRON. MELANIN IS COMMONLY FOUND IN DARKER RACES. DISEASE THAT INCREASES MELANIN PIGMENTATION INCLUDE ADDISON’S DISEASE (ADRENAL DYSFUNCTION) WHICH PRODUCES ISOLATED PATCHES OF DISCOLOURATION VARYING FROM BLUISH BLACK TO BROWN.

PEUTZ JEGHERS SYNDROME (PRODUCES INTESTINAL POLYPOSIS) AND MELANIN PIGMENTATION IN ORAL MUCOSA AND LIPS; AND ALBRIGHT’S SYNDROME AND VON RECKLING HAUSEN’S DISEASE BOTH OF WHICH PRODUCE AREAS OF ORAL MELANIN PIGMENTATION. SKIN AND MUCOUS MEMBRANES CAN ALSO BE STAINED BY BILE PIGMENTS. JAUNDICE IS BEST DETECTED BY EXAMINATION OF SCLERA, BUT THE ORAL MUCOUSA ALSO ACQUIRES A YELLOWISH COLOUR. THE DEPOSITION OF IRON IN HAEMOCHROMATOSIS MAY PRODUCE A BLUE GREY PIGMENTATION OF THE ORAL MUCOSA

SEVERAL ENDOCRINE AND METABOLIC DISTURBANCES, INCLUDING DIABETES AND PREGNANCY, MAY RESULT IN COLOUR CHANGES. BLOOD DYSCRASIS SUCH AS ANEMIA, POLYCYTHEMIA AND LEUKEMIA MAY ALSO INDUCE COLOUR CHANGES. EXOGENEOUS FACTOR PRODUCING COLOUR CHANGES INCLUDE ATMOSPHERIC IRRITANTS SUCH AS COAL AND METAL DUST AND COLOURING AGENTS IN FOOD OR LOZENGES. TOBACCO CAUSE A GREY HYPER KERATOSIS OF THE GINGIVA. LOCALISED BLUISH BLACH AREAS OF PIGMENT ARE NORMALLY DUE TO AMALGAM IMPLANTED IN THE MUCOSA.

SILVER PIGMENTATION VIOLET MARGINAL LINE. BISMITH, ARSENIC, MERCURY PIGMENTATION BLACK LINES FOLLOWING THE CONTOUR OF MARGINAL GINGIVA LEAD PIGMENTATION BLUISH RED OR DEEP BLUE LINEAR PIGMENTATION (BURTONIAN LINE)

CHANGES IN THE CONSISTENCY OF THE GINGIVA NORMAL GINGIVA EXHIBITS FIRM AND RESILIENT CONSISTENCY. FACTORS THAT ARE RESPONSIBLE ARE CELLULAR AND FLUID CONTENT AND COLLAGENOUS NATURE OF LAMINA PROPRIA. IN DISEASE CONDITION IT CAN BE SOGGY AND EDEMATOUS OR FIRM AND LEATHERY IN CONSISTENCY.

CHANGES IN SURFACE TEXTURE UNDER NORMAL CONDITION GINGIVA APPEARS TO BE STIPPLED (ORANGE PEEL APPEARANCE) DUE TO ATTACHMENT OF GINGIVAL FIBRES TO THE UNDERLYING BONE. LOSS OF STIPPLING IS AN EARLY SIGN OF GINGIVITIS. IN CHRONIC INFLAMATION THE SURFACE IS EITHER SMOOTH AND SHINY OR FIRM OR NODULAR. SMOOTH SURFACE TEXTURE IS ALSO PRODUED BY EPITHELIAL ATROPHY IN SENILE ATROPHIC GINGIVITIS AND PEELING OF THE SURFACE OCCURES IN CHRONIC DESQUAMATIVE GINGIVITIS. HYPER KERATOSIS RESULTS IN LEATHERY TEXTURE AND NON INFLAMATORY GINGIVAL HYPERPLASIA PRODUCES A MINUTELY NODULAR SURFACE.

CHANGES IN THE SIZE OF GINGIVA NORMAL SIZE DEPENDS ON SUM OF THE BULK OF CELLULAR AND INTERCELLULAR ELEMENTS AND THEIR VASCULAR SUPPLY. IN DISEASE THE SIZE IS INCREASED WHICH CAN BE TERMED AS GINGIVAL ENLARGEMENTS. THE FACTOR RESPONSIBLE FOR THIS ARE INCREASE IN FIBRES AND DECREASE IN CELLS AND AS IN NON INFLAMATORY TYPE. WHERE AS IN INFLAMATORY TYPE THERE WILL BE INCREASE IN CELLS AND DECREASE IN FIBRES.

CHANGES IN THE POSITION OF GINGIVA ACTUAL AND APPARENT POSITION. RECESSION IS EXPOSURE OF THE ROOT SURFACE BY AN APICAL SHIFT IN THE POSITION OF THE GINGIVA. ACTUAL POSITION IS THE LEVEL OF EPITHELIAL ATTACHMENT ON THE TOOTH. APPARENT POSITION IS THE LEVEL OF CREST OF THE GINGIVAL MARGIN. THE SEVERITY OF RECESSION IS DETERMINED BY THE ACTUAL POSITION OF THE GINGIVA AND

TWO TYPES OF RECESSION 1. VISIBLE-WHICH IS CLINICALLY OBSERVABLE 2. HIDDEN- IT IS COVERED BY GINGIVA AND CAN BE MEASURED ONLY BY INSERTING A PROBE TO THE LEVEL OF EPITHELIAL ATTACHMENT. THE TOTAL AMOUNT OF RECESSION IS THE SUM OF THE TWO. RECESSION MAY BE LOCALISED ONE TOOTH OR A GROUP OF TEETH OR MAY BE GENERALISED THROUGH OUT THE MOUTH.

CLASSIFICATION OF GINGIVAL RECESSION l TWO CLASSIFICATION SYSTEMS ARE AVAILABLE 1. ACCORDING TO THE SULLIVAN AND ATKINS SHALLOW NARROW SHALLOW WIDE DEEP NARROW DEEP WIDE

2. ACCORDING TO P. D MILLER’S CLASS I : MARGINAL TISSUE RECESSION THAT DOES NOT EXTEND TO THE MUCO GINGIVAL JUNCTION. THERE IS NO LOSS OF BONE OR SOFT TISSUE IN THE INTERMEDIATE AREA. THIS CAN BE NARROW OR WIDE. CLASS II : MARGINAL TISSUE RECESSION THAT EXTENDS TO OR BEYOND THE MUCOGINGIVAL JUNCTION. THERE IS NO LOSS OF BONE OR SOFT TISSUE IN THE INTERDENTAL AREAS. THIS CAN BE NARROW OR WIDE. CLASS III : MARGINAL TISSUE RECESSION THAT EXTENDS TO OR BEYOND THE MUCO GINGIVAL JUNCTION. IN ADDITION THERE IS LOSS OF BONE/ SOFT TISSUE IN THE INTER DENTAL AREAS OR THERE IS MALPOSITIONING OF THE TOOTH. CLASS IV : MARGINAL TISSUE RECESSION THAT EXTENDS TO OR BEYOND THE MUCOGINGIVAL JUNCTION WTH SEVERE LOSS OF BONE AND SOFT TISSUE INTERDENTALLY. SEVERE MALPOSITIONING OF THE TOOTH IS SEEN.

PROGNOSIS CLASS I AND II IS GOOD TO EXCELLENT CLASS III ONLY PARTIAL COVERAGE CAN BE EXPECTED CLASS IV POOR PROGNOSIS

ETIOLOGY OF GINGIVAL RECESSION PLAQUE INDUCED GINGIVAL INFLAMMATION IS THE PRIMARY ETIOLOGICAL FACTOR RESPONSIBLE FOR GINGIVAL RECESSION; NEXT MOST COMMON CAUSE IS FAULTY TOOTH BRUSHING. OTHER SECONDARY OR CONTRIBUTING FACTORS OF GINGIVAL RECESSION ARE BROADLY CATEGORISED AS: A) B) C) D) ANATOMIC FACTORS HABITS IATROGENIC FACTORS PHYSIOLOGICAL FACTORS

ANATOMIC FACTORS INCLUDE 1. 2. 3. 4. TOOTH MALPOSITION OR POSITION OF THE TOOTH IN THE ARCH. A TOOTH IN LABIAL ASPECT WILL BE INVARIABLY THIN. WHEN THIS IS EXPOSED TO ANY KIND OF TRAUMA OR FRACTIONAL FORCES, GINGIVAL RECESSION RESULTS. PRESENCE OF DEHISCENCE AND FENESTRATIONS. GINGIVAL ABRATION FROM SOFT TISSUE LIKE LIPS etc. ROOT BONE ANGLE AND MESIODISTAL CURVATURE OF THE TOOTH SURFACE. IN ROTATED AND FACIALLY DISPLACED TEETH, BONY PLATES ARE EITHER THINNED OR SHORTENED AND RECESSION RESULTS FROM REPEATED TRAUMA TO THE THIN PERIODONTAL TISSUES.

HABITS FAULTY TOOTH BRUSHING OR BRUSHING WITH HARD BRISTLES MAY LEAD TO GINGIVAL RECESSION. RECENTLY IT HAS BEEN NOTED THAT THERE MAY BE POSITIVE RELATIONSHIP BETWEEN SMOKING AND RECESSION

IATROGENIC FACTOR PRIMARY TRAUMA FROM OCCLUSION HAS BEEN REPORTED TO CAUSE GINGIVAL RECESSION. ORTHODONTIC MOVEMENT IN THE LABIAL DIRECTION AND IMPROPER RESTORATION CAN LEAD TO GINGIVAL RECESSION.

PHYSIOLOGICAL FACTORS GINGIVAL RECESSION WAS THOUGHT TO BE A PHYSIOLOGIC PROCESS RELATED TO AGING. HOWEVER THIS IDEA WAS DISCARDED BECAUSE THERE WAS NO CONVINCING EVIDENCE FOR A PHYSIOLOGIC SHIFT OF THE GINGIVAL ATTACHMENT.

CLINICAL SIGNIFICANCE OF GINGIVAL RECESSION 1. 2. 3. 4. THE EXPOSED ROOT SURFACE MAY BE EXTREMELY SENSITIVE. HYPEREMIA OF THE PULP MAY RESULT DUE TO GINGIVAL RECESSION INTERPROXIMAL RECESSION CREATES ORAL HYGEINE PROBLEMS THEREBY RESULTING IN PLAQUE ACCUMULATION FINALLY IT IS AESTHETICALLY UNACCEPTABLE

CHANGES IN GINGIVAL CONTOUR NORMALLY, MARGINAL GINGIVA IS SCALLOPED AND KNIFE EDGED WHEREAS INTERDENTAL PAPILLA IN THE ANTERIOR REGION IS PYRAMIDAL AND POSTERIORLY TENT SHAPED. THE FACTORS THAT MAINTAIN NORMAL CONTOUR ARE SHAPE OF THE TEETH AND ITS ALIGNMENT IN THE ARCH, LOCATION AND SIZE OF THE PROXIMAL CONTACT AND DIMENSIONS OF FACIAL AND LINGUAL EMBRASURES. IN DISEASED CONDITIONS, THE MARGINAL GINGIVA MAY BECOME ROUNDED OR ROLLED WHERE AS INTERDENTAL PAPILLA CAN BECOME BLUNT AND FLAT

STILLMAN’S CLEFTS ARE APOSTROPHE-SHAPED INDENTATIONS EXTENDING FROM/AND INTO THE GINGIVAL MARGIN FOR VARYING DISTANCES. THE CLEFTS GENERALLY OCCUR ON THE FACIAL SURFACE. ONE OR TWO MAY BE PRESENT IN RELATION TO A SINGLE TOOTH. THE MARGINS OF THE CLEFTS ARE ROLLED UNDERNEATH THE LINEAR GAP IN THE GINGIVA, AND THE REMINDER OF THE GINGIVAL MARGIN IS BLUNT INSTEAD OF KNIFE EDGED CAUSED BY OCCLUSAL TRAUMA. THE CLEFTS MAY REPAIR SPONTANEOUSLY OR PERSISIT AS SURFACE LESIONS OF DEEP PERIODONTAL POCKETS THAT PENETRATE INTO THE SUPPORTING TISSUE. CLEFTS ARE DIVIDED INTO SIMPLE AND COMPOUND CLEFT. THE CLEFTS VARY IN LENGTH FROM A SLIGHT BREAK IN THE GINGIVAL MARGIN TO A DEPTH OF 5 -6 mm OR MORE.

Mc CALL’S FESTOONS ARE LIFE PRESERVER- SHAPED ENLARGEMENTS OF THE MARGINAL GINGIVA THAT OCCUR MOST FREQUENTLY IN THE CANINE AND PRE MOLAR AREAS ON THE FACIAL SURFACE. IN THE EARLY STAGES, THE COLOUR AND THE CONSISTENCY OF THE GINGIVA ARE NORMAL. HOWEVER, ACCUMULATION OF FOOD DEBRIS LEADS TO SECONDARY INFLAMMATORY CHANGES.

CONCLUSION: IT BECOMES NECESSARY TO EDUCATE PEOPLE ABOUT THE IMPORTANCE OF VARIOUS RISK FACTORS, INORDER TO MAINTAIN A HEALTHY ORAL CONDITION. EVEN A SMALL GINGIVAL INFLAMMATION WHICH IS OFTEN NEGLECTED IS OF TREMENDOUS IMPORANCE IN CASE OF A DISEASE PROGRESSION.

REFERENCES 1. 2. CLINICAL PERIODONTOLOGY BY FERMIN. A. CARRANZA WIKIPEDIA