CLINICAL FEATURES OF GINGIVITIS
CONTENTS Introduction to inflammation Course and duration Components of Gingival Inflammation Experimental gingivitis Prevalence Distribution Stages of inflammation Bleeding from gingiva Color changes in gingiva Changes in Gingival consistency Changes in Gingival Surface texture Changes in Gingival Position Changes in Gingival Contour Conclusion References
INTRODUCTION TO INFLAMMATION Inflammation is defined as an observable alteration in tissues associated with changes in vascular permeability and dilation, often with the infiltration of leukocytes into affected tissues. (Rushton Parker 1910) These changes result in rubor, tumor, calor, dolor, and loss of function being the cardinal signs of inflammation (Celsus 1st centaury AD, Virchow) Typically inflammation can progress through three stages: - Acute - Sub-Acute and - Chronic. Steps involved in inflammation can be remembered in 5 (R) Recognition of the injurious agent. Recruitment of leukocytes. Removal of the agent. Regulation (control) of the responses. Resolution(repair)
Represents early body reaction , usually followed by repair. ACUTE INFLAMMATION: It is a rapid response to injury or microbes and other foreign substances that is designed to deliver leukocytes and plasma proteins to sites of injury( Robbins) short duration. Represents early body reaction , usually followed by repair. CHRONIC INFLAMMATION: Is defined as a prolonged process in which tissue destruction , inflammation & healing occurs at the same time In contrast to acute inflammation, chronic inflammation is characterized by infiltration of macrophages, lymphocytes , plasma cells. LEWIS EXPERIMENT: LEWIS induced the changes in the skin of inner aspect of forearm by firm stroking with a blunt point. Triple response or redline response consist of- RED LINE- with in a few seconds-vasodilation FLARE-reddish appearance surrounding the redline-vasodilation of adjacent arterioles. WHEAL-swelling of the surrounding skin-transudation
COURSE AND DURATION Gingivitis can occur with sudden onset and short duration and can be painful. A less severe phase of this condition can also occur. Recurrent gingivitis reappears after having been eliminated by treatment or disappearing spontaneously. Chronic gingivitis is slow in onset and of long duration. Painless, unless complicated by acute/sub acute exacerbations, and is the type most often encountered Fluctuating disease in which inflammation persists or resolves and normal areas become inflamed. (Hoover DR et al 1965, Larato DC et al 1969)
COMPONENTS OF GINGIVAL INFLAMMATION Gingival inflammation has two components: the acute inflammatory component, with vasodilation, edema, and polymorphonuclear infiltration, and the the chronic inflammatory component, with B and T lymphocytes and capillary proliferation forming a granulomatous response. Each gingival region can have varying amounts of the acute or chronic component.
EXPERIMENTAL GINGIVITIS Despite extensive research, we still cannot distinguish definitively between normal gingival tissue and the initial stage of gingivitis. Most biopsies of clinically normal human gingiva contain inflammatory cells consisting predominantly of T cells, with very few B cells or plasma cells. In 1965, Loe et al demonstrated that in students with clinically healthy gingivae. Clinical symptoms of gingivitis developed within 2 to 3 weeks if dental plaque was allowed to accumulate freely. Once adequate tooth cleaning was resumed, the gingival inflammation subsided within a week
EXPERIMENTAL GINGIVITIS The thickness of the gingival plaque gradually increased during the 3-week experimental period. For the first few days: gram-positive cocci and rods, representing the indigenous micro flora of the tooth surface. After 4 to 5 days: filamentous organisms and gram-negative cocci as well as rods Gradually, non attaching spirochetes appeared in the gingival sulcus, while the assortment of microorganisms in the gingival biofilm increased continuously.
CHARACTERISTICS OF PLAQUE INDUCED GINGIVITIS (Mariotti,1999) Plaque present at gingival margin 2 Disease begins at the gingival margin 3 Change in gingival color 4 Change in gingival contour 5 Sulcular temperature change 6 Increased gingival exudate 7 Bleeding upon provocation 8 Absence of attachment loss* 9 Absence of bone loss* 10 Histological changes including an inflammatory lesion 11 Reversible with plaque removal
PREVALANCE The prevalence of gingivitis is evident worldwide. Higher prevalence of gingivitis is reported for children and adolescents. (Albander JM, Brown LJ et al 1996) A significant percentage of adults also show signs of gingivitis; more than half the U.S. adult population estimated to exhibit gingival bleeding, and other populations show even higher levels of gingival inflammation. (Albander JM, Kingman A et al 1999) In children on average 6% of sites measured showed bleeding on probing. (Albander JM, Tinoco EM 2002)
DISTRIBUTION Localized gingivitis is confined to the gingiva of a single tooth or group of teeth, whereas generalized gingivitis involves the entire mouth. Marginal gingivitis involves the gingival margin and may include a portion of the contiguous attached gingiva. Papillary gingivitis involves the interdental papillae and often extends into the adjacent portion of the gingival margin. Papillae are involved more frequently than the gingival margin, and the earliest signs of gingivitis often occur in the papillae. Diffuse gingivitis affects the gingival margin, the attached gingiva, and the interdental papillae. (Glickman 1953)
GINGIVAL DISEASE IN INDIVIDUAL CASES IS DESCRIBED BY COMBINING THE PRECEDING TERMS AS FOLLOWS: Localized marginal gingivitis is confined to one or more areas of the marginal gingiva Localized diffuse gingivitis extends from the margin to the mucobuccal fold in a limited area Localized papillary gingivitis is confined to one or more interdental spaces in a limited area Generalized marginal gingivitis involves the gingival margins in relation to all the teeth. The interdental papillae are usually affected Generalized diffuse gingivitis involves the entire gingiva. The alveolar mucosa and attached gingiva are affected, so the mucogingival junction is sometimes obliterated. Systemic conditions can be involved in the cause of generalized diffuse gingivitis and should be evaluated if suspected as an etiologic cofactor.
STAGES OF GINGIVAL INFLAMMATION
Gingival alterations which occurred during a 28-day period of plaque accumulation and gingivitis development in beagles. (a) Normal gingiva. (b) Day 4. (c) Day 7. (d) Day 14. (e) Day 21. (f) Day 28 of undisturbed plaque accumulation. Note the gradually developing plaque on the tooth surfaces and the inflammatory changes in the gingiva.
Pristine gingiva: without any bacteria…0%. seen only in infants… Pristine gingiva: without any bacteria…0%...seen only in infants….goal of treatment…to achieve pristine gg…bt impossible…
Stage I Gingivitis : The Initial Lesion - SUBCLINICAL GINGIVITIS. Lindhe , Hamp et al 1973- beagle dogs Dilation of capillaries & increase in blood flow. Initial inflammatory changes in response to microbial activation of resident leukocytes, subsequent stimulation of endothelial cells. Clinically- initial response of gingiva to bacterial plaque(sub clinical gingivitis)- not apparent. Changes in JE and perivascular connective tissue- detected
Perivascular connective tissue matrix-altered STAGE I GINGIVITIS Perivascular connective tissue matrix-altered Exudation & deposition of fibrin in affected area Accumulation of lymphocytes Increase in migration of leukocytes and accumulation within gingival sulcus corelated with increase in flow of gingival fluid into sulcus.
STAGE I GINGIVITIS Character and intensity of host response determines whether initial lesion resolves rapidly with restoration of tissue to normal state or into chronic inflammatory lesion. Inflammatory lesion- infiltrate of macrophages and lymphoid cells appears within few days.
Changes in blood vessel morphologic features (e. g Changes in blood vessel morphologic features (e.g., widening of small capillaries or venules) Some classic features of acute inflammation seen in connective tissue beneath the junctional epithelium. MICROSCOPICALLY
Adherence of neutrophils to vessel walls (margination) occur within 1 week and sometimes as early as 2 days after plaque has been allowed to accumulate. Leukocytes, mainly polymorphonuclear neutrophils (PMNs), leave the capillaries by migrating through the walls - increased quantities in the connective tissue, junctional epithelium, and the gingival sulcus Exudation of fluid from gingival sulcus and extravascular proteins present.
Human biopsy sample, experimental gingivitis Human biopsy sample, experimental gingivitis. After 4 days of plaque accumulation, the blood vessels immediately adjacent to the junctional epithelium are distended and contain polymorphonuclear leukocytes ( PMNs, neutrophils). Neutrophils have also migrated between the cells of the junctional epithelium. OSE, Oral sulcular epithelium.
STAGE II GINGIVITIS : THE EARLY LESION (Payne , Page et al 1975,1991) Early lesion evolves from the initial lesion within 1 week after beginning of plaque accumulation. Clinically may appear as early gingivitis & overlaps with and evolves from the initial lesion with no clear-cut dividing line. As time goes, clinical signs of erythema may appear, mainly because of proliferation of capillaries and increased formation of capillary loops between rete pegs.
Bleeding on probing- evident. (Amato R, Caton J, Polson A et al 1986) Gingival fluid flow and numbers of transmigrating leukocytes reach their maximum between 6 and 12 days after onset of clinical gingivitis. (Lindhe J, Hamp, Loe H et al 1973)
Amount of collagen destruction increases; 70% - collagen is destroyed around the cellular infiltrate. The main fiber groups affected appear to be the CIRCULAR and DENTOGINGIVAL fiber assemblies. Alterations in blood vessel morphologic features and vascular bed patterns.
PMNs that have left the blood vessels in response to chemotactic stimuli from plaque components travel to the epithelium, cross basement lamina, and are found in the epithelium, emerging in pocket area. PMNs are attracted to bacteria and engulf them in the process of phagocytosis. PMNs release their lysosomes in association with ingestion of bacteria. Fibroblasts show cytotoxic alterations, with decreased capacity for collagen production.
MICROSCOPIC: Microscopic examination of the gingiva reveals a leukocyte infiltration in the connective tissue beneath the junctional epithelium, consisting mainly of lymphocytes (75% with the majority T cells) (Payne WA, Page RC, Ogilvie AL et al 1975 and Schroeder HE, Page RC 1973) Also composed of some migrating neutrophils, as well as macrophages, plasma cells, and mast cells.
All the changes seen in the initial lesion continue to intensify with the early lesion. The junctional epithelium- densely infiltrated with neutrophils, as does the gingival sulcus, and the junctional epithelium may begin to show development of rete pegs.
Scanning electron micrograph of leukocyte emerging to pocket wall and covered with bacteria and extracellular lysosomes. EC, Epithelial cells; B, bacteria; L, lysosomes.
STAGE III GINGIVITIS : THE ESTABLISHED LESION Over time, the established lesion evolves Characterized by a predominance of plasma cells B lymphocytes in conjunction with the creation of a small gingival pocket lined with a pocket epithelium (Schroeder HE et al 1975) The B cells - predominantly of immunoglobulin G1 (IgG1) and G3 (IgG3) subclasses (Page RC 1986)
In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of plaque accumulation, blood vessels- engorged and congested, venous return- impaired, blood flow - sluggish. Bluish hue on the reddened gingiva (Hanioka T et al 1991) Extravasation of erythrocytes into the connective tissue and breakdown of hemoglobin into its component pigments can also deepen the color of the chronically inflamed gingiva. The established lesion can be described as moderately to severely inflamed gingiva.
The predominance of plasma cells is thought to be a primary characteristic of the established lesion. Increases in the proportions of plasma cells were evident with long-standing gingivitis, but the time for the development of the classic "established lesion" may exceed 6 months. Inverse relationship exist between the number of intact collagen bundles and the number of inflammatory cells. Collagenolytic activity is increased in inflamed gingival tissue
TWO TYPES : (Lovdal A et al 1958, Mori M et al 1961,Sumoi JD, Smith LW et al 1971) Some remain stable and do not progress for months or years Others become more active and convert to progressively destructive lesions.
HISTOLOGIC SECTIONS Intense, chronic inflammatory reaction. A key feature that differentiates the established lesion is the increased number of plasma cells, which become the preponderant inflammatory cell type. Plasma cells invade the connective tissue not only immediately below the junctional epithelium, but also deep into the connective tissue, around blood vessels, and between bundles of collagen fibers
The junctional epithelium reveals widened intercellular spaces filled with granular cellular debris, including lysosomes derived from disrupted neutrophils, lymphocytes, and monocytes Lysosomes contain acid hydrolases - destroy tissue components. The junctional epithelium develops rete pegs or ridges that protrude into the connective tissue, and the basal lamina is destroyed in some areas. In the connective tissue, collagen fibers are destroyed around the infiltrate of intact and disrupted plasma cells, neutrophils, lymphocytes, monocytes, and mast cells
Established gingivitis in a human subject Established gingivitis in a human subject. Area of crevicular epithelium exhibiting enlarged intercellular spaces with numerous microvilli and desmosomal junctions. Several lymphocytes, both small and large, are seen migrating through the epithelial layer. (x3000.)
STAGE IV GINGIVITS : THE ADVANCED LESION Extension of the lesion into alveolar bone characterizes a fourth stage known as the advanced lesion. Gingivitis -> periodontitis only in individuals who are susceptible.
MICROSCOPICALLY: Fibrosis of the gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. Plasma cells continue to dominate the connective tissues, and neutrophils continue to dominate the junctional epithelium and gingival crevice
CLINICAL FEATURES In evaluating the clinical features it is necessary to be systematic. The clinician should focus on subtle tissue alterations because these may be of diagnostic significance. A systematic clinical approach requires an orderly examination of the gingiva for color, contour, consistency, position, and ease and severity of bleeding and pain.
The two-earliest signs of gingival inflammation preceding established gingivitis are (1) Increased gingival crevicular fluid production rate and (2) Bleeding from the gingival sulcus on gentle probing Raised sulcus temperature has also been shown to be a feature of plaque induced inflammation (Haffajee et al 1992, Loe et al 1965, Poison and Goodson 1985) Increase in leucocytes seen in gingival fluid associated with increased GCF (Payne et al 1975, Page and Schroeder 1976)
BLEEDING ON PROBING It is detected clinically and therefore is of value for the early diagnosis and prevention of more advanced gingivitis. It has been shown that bleeding on probing appears earlier than a change in color or other visual signs of inflammation; in addition, the use of bleeding rather than color changes to diagnose early gingival inflammation is advantageous in that bleeding is a more objective sign that requires less subjective estimation by the examiner. Therefore, bleeding on probing is widely used by clinicians and epidemiologists to measure disease prevalence and progression, to measure outcomes of treatment, and to motivate patients with their home care.
Gingival bleeding on probing is an important diagnostic factor –as it is associated with inflammation and ulceration of the epithelium lining the gingival sulcus. Presence of plaque for only 2 days initiate gingival bleeding on probing, whereas once established, it may take 7 days or more after continued plaque control and treatment to eliminate gingival bleeding. Absence of plaque and presence of gingival bleeding may indicate improvement in plaque control that may have occurred immediately before the examination. Presence of bleeding is an indication of active gingival inflammation, and until it is controlled, the patient is at a risk of continuing periodontal disease and tissue destruction.
In general, gingival bleeding on probing indicates an inflammatory lesion both in the epithelium and in the connective tissue that exhibits specific histologic differences compared with healthy gingiva. Even though gingival bleeding on probing may not be a good diagnostic indicator for clinical attachment loss, its absence is an excellent negative predictor of future attachment loss.(Lang et al 1990) Therefore the absence of gingival bleeding on probing is desirable and implies a low risk of future clinical attachment loss.
Numerous studies show that current cigarette smoking suppresses the gingival inflammatory response, and smoking was found to exert a strong, chronic, dose dependent suppressive effect on gingival bleeding on probing in the third National Health and Nutrition Examination Survey (NHANES III) (Dietrich et al 2004) In addition, recent research reveals an increase in gingival bleeding on probing in patients who quit smoking. (Nair P, Palmer RM et al 2003)
EXAMINATION FOR BOP ERRORs Histopathologic alterations abnormal bleeding dilation and engorgement of capillaries, thinning/ulceration of sulcular epithelium thus capillaries are closer to surface and thinned degenerated epithelium is less protective, stimuli that are normally innocuous cause rupture of capillaries and bleeding Walking probe technique Done with short upward and downward movement A tooth is probed at 6 sites- MB, mid B, DB, and corresponding lingual sites Working force should not be more than 20gms Pain during probing is indicative of too heavy probing force
INDICES USED SULCUS BLEEDING INDEX Muhlemann H R ,Son S 1971- locate areas of gingival sulcus bleeding upon gentle probing and recognize presence of early gingival inflammation 1 => healthy looking papillary and marginal gingiva, bleeding on probing 2 => bleeding on probing and color change in gingiva 3 => bleeding on probing, color change, slight edema 4 => bleeding on probing, color change, obvious edema 5 => spontaneous bleeding, color change, marked edema or ulceration. As early as 1958 a Sulcus Bleeding Index was introduced and termed the PM Index in which bleeding after gentle probing was the leading symptom (Muhlemann & Mazor 1958). To avoid confusion from the earlier PMA Index, the initials describing this index were changed to SBI. (Muhlemann & Son 1971), In this system, 0 = healthy looking papillary and marginal gingiva, no bleeding on probing; 1 =healthy looking papillary and marginal gingiva, bleeding on probing; 2 = bleeding on probing and color change in gingiva; 3 = bleeding on probing, color change, slight edema; 4 = bleeding on probing, color change, obvious edema; 5 = spontaneous bleeding, color change, marked edema or ulceration. SBI was modified and reported as the papillary bleeding index (Muhlemann 1977). This modificadon resulted in the PBI Index based on bleeding following gentle probing of the interdental papilla: 0 = no bleeding; 1 = only one bleeding point present; 2 = several isolated bleeding points on a small area of blood; 3 = interdental triangle filled with blood; 4 = profuse bleeding spreading toward the marginal gingiva.
Modification – discarded A unit MODIFIED PMA Muhlemann and Mazor Modification – discarded A unit
1 => only one bleeding point present PAPILLARY BLEEDING INDEX Muhlemann H R 1977 modification of SBI This modificadon resulted in the PBI Index based on bleeding following gentle probing of the interdental papilla 0 => no bleeding 1 => only one bleeding point present 2 = > several isolated bleeding points on a small area of blood 3 = > interdental triangle filled with blood 4 => profuse bleeding spreading toward the marginal gingiva.
GINGIVAL BLEEDING INDEX Carter H G, Barnes G P 1974- presence/absence of gingival inflammation as determined by bleeding from interproximal gingival sulci MODIFIED SULCULAR BLEEDING INDEX/MODIFIED SULCUS BLEEDING INDEX- A Mombelli, M A Van Oosten, E Schurch, N P Land 1987 EASTMAN INTERDENTAL BLEEDING INDEX- Abrams K, Caton J, Polson A 1984
Presence/absence of bleeding determined by gentle probing of crevice BLEEDING POINT INDEX Lenox and Kopczyk Determines presence/absence of bleeding interproximally on facial and lingual surfaces Probe is drawn horizontally through crevice and gingiva is examined for bleeding after 30 sec GINGIVAL BLEEDING INDEX Ainamo and Bay Presence/absence of bleeding determined by gentle probing of crevice Appearance of bleeding within 10 sec indicates a positive score expressed as a percentage of total no of gingival margins examined
INTERDENTAL BLEEDING INDEX Catson and Polson Utilizes a triangular shaped toothpick made of soft pliable wood to stimulate interproximal gingival tissue Interproximal cleaner inserted horizontally bertwwn teeth from facial surface depressing papilla by 2mm Wooden cleaner inserted and removed 4 times Presence/absence of bleeding within 15 secs is noted score = no of bleeding sites/no of sites evaluated
CHRONIC AND RECURRENT BLEEDING: The most common cause of abnormal gingival bleeding on probing is chronic inflammation. (Milne AM 1967) The bleeding is chronic and recurrent and is provoked by mechanical trauma (eg. from tooth brushing, toothpicks, or food impaction) or by biting into solid foods such as apples. The severity of the bleeding and the ease of its provocation depend on the intensity of the inflammation. After the vessels are damaged and ruptured, interrelated mechanisms induce hemostasis. (Stefanini M, Dameshek W 1962)
The vessel walls contract, and blood flow is diminished; blood platelets adhere to the edges of the tissue; and a fibrous clot is formed, which contracts and results in approximation of the edges of the injured area. Bleeding recurs when the area is irritated. In cases of moderate or advanced periodontitis, the presence of bleeding on probing is considered a sign of active tissue destruction. In gingival inflammation, histopathology alterations that result in abnormal gingival bleeding include dilation and engorgement of the capillaries and thinning or ulceration of the sulcular epithelium. Because the capillaries are engorged and closer to the surface, and the thinned, degenerated epithelium is less protective, stimuli that are normally innocuous cause rupture of the capillaries and gingival bleeding.
Microscopic view of interdental space in a human autopsy specimen Microscopic view of interdental space in a human autopsy specimen.Inflammatory infiltrate and thinned epithelium in area adjacent to the tooth, as well as collagenous tissue in outer half of the section. Sites that bleed on probing have a greater area of inflamed connective tissue (i.e., cell-rich, collagen-poor tissue) than sites that do not bleed. In most cases the cellular infiltrate of sites that bleed on probing is predominantly lymphocytic (a characteristic of stage II, or early, gingivitis). (Amato, Catson, Polson 1986)
ACUTE BLEEDING Acute episodes of gingival bleeding are caused by injury and can occur spontaneously in gingival disease. Laceration of the gingiva by toothbrush bristles during aggressive tooth brushing or by sharp pieces of hard food can cause gingival bleeding even in the absence of gingival disease. Gingival burns from hot foods or chemicals increase the ease of gingival bleeding. Spontaneous bleeding or bleeding on slight provocation can occur in acute necrotizing ulcerative gingivitis. In this condition, engorged blood vessels in the inflamed connective tissue are exposed by ulceration of the necrotic surface epithelium.
GINGIVAL BLEEDING ASSOCIATED WITH SYSTEMIC CHANGES In some systemic disorders, gingival hemorrhage occurs spontaneously or after irritation and is excessive and difficult to control. These hemorrhagic diseases represent a wide variety of conditions that vary in etiologic factors and clinical manifestations. Such conditions have the common feature of a hemostatic mechanism failure and result in abnormal bleeding in the skin, internal organs, and other tissues, including the oral mucosa. (Sodeman WA 1985)
Vascular abnormalities: Hemorrhagic disorders in which abnormal gingival bleeding is encountered include Vascular abnormalities: vitamin C deficiency or allergy, e.g., Schonlein-Henoch purpura, Platelet disorders thrombocytopenic purpura, hypoprothrombinemia (vitamin K deficiency), Other coagulation defects hemophilia, leukemia, Christmas disease, Deficient platelet thromboplastic factor (PF3) resulting from uremia, Multiple myeloma and Post rubella purpura.
The effects of hormonal replacement therapy, oral contraceptives, pregnancy, and the menstrual cycle are also reported to affect gingival bleeding. (Payne, Maze 1999) In addition, changes in androgenic hormones have long been established as significant modifying factors in gingivitis, especially among adolescents. Several reports have shown notable effects of fluctuating estrogen/progesterone levels on the periodontium, starting as early as puberty. (Addy M et al 1994) Among pathologic endocrine changes, diabetes is an endocrine condition with a well-characterized effect on gingivitis. (Tatakis DN et al 1994)
Several medications have also been found to have adverse effects on the gingiva. For example, anticonvulsants, antihypertensive calcium channel blockers, and the immunosuppressant drugs are known to cause gingival enlargement, which secondarily can cause gingival bleeding. The American Heart Association has recommended over the counter aspirin as a therapeutic agent for cardiovascular disease, and aspirin is often prescribed for rheumatoid arthritis, osteoarthritis, rheumatic fever, and other inflammatory joint diseases. (Hennekens CH et al 1997) Thus it is important to consider aspirin's effect on bleeding during a routine dental examination to avoid false-positive readings, which could result in an inaccurate patient diagnosis
COLOUR CHANGES IN GINGIVA The color of the gingiva is determined by several factors, including the number and size of blood vessels, epithelial thickness, quantity of keratinization, arid pigments within the epithelium (Tal H, Tal M 2003)
COLOR CHANGES IN CHRONIC GINGIVITIS Change in color is an important clinical sign of gingival disease. The normal gingival color is "coral pink" and is produced by the tissue's vascularity and modified by the overlying epithelial layers. For this reason, the gingiva becomes red when vascularization increases or the degree of epithelial keratinization is reduced or disappears. The color becomes pale when vascularization is reduced (in association with fibrosis of the corium) or epithelial keratinization increases.
Chronic inflammation intensifies the red or bluish red color because of vascular proliferation and reduction of keratinization. Venous stasis will contribute a bluish hue. The gingival color changes with increasing chronicity of the inflammatory process. The changes start in the interdental papillae and gingival margin and spread to the attached gingiva. Proper diagnosis and treatment require an understanding of the tissue changes that alter the color of the gingiva at the clinical level.
COLOR CHANGES IN ACUTE GINGIVITIS Color changes in acute gingival inflammation differ in both nature and distribution from those in chronic gingivitis. Color changes may be marginal, diffuse, or patch like, depending on the underlying acute condition. In ANUG, the involvement is marginal; in herpetic gingivostomatitis, it is diffuse; and in acute reactions to chemical irritation, it is patch like or diffuse. Color changes vary with the intensity of the inflammation. Initially, there is an increase in erythema. If the condition does not worsen, this is the only color change until the gingiva reverts to normal. In severe acute inflammation, the red color gradually becomes a dull, whitish gray. The gray discoloration produced by tissue necrosis is demarcated from the adjacent gingiva by a thin, sharply defined erythematous zone.
METALLIC PIGMENTATION Heavy metals (bismuth, arsenic, mercury, lead and silver) absorbed systemically from therapeutic use or occupational or household environments may discolor the gingiva and other areas of the oral mucosa. These changes are rare but still should be ruled out in suspected cases. Typically, metals produce a black or bluish line in the gingiva that follows the contour of the margin. The pigmentation may also appear as isolated black blotches involving the interdental marginal and attached gingiva. This differs from the tattooing produced by the accidental embedding of amalgam or other metal fragments. Lead Produces a bluish red or deep blue linear pigmentation of the gingival margin (Burtonian line) Exposure to silver - a violet line accompanied by a diffuse bluish grey discoloration in throughout the oral mucosa (Argyria) METALLIC PIGMENTATION
Gingival pigmentation from systemically absorbed metals results from perivascular precipitation of metallic sulfides in the sub-epithelial connective tissue. Gingival pigmentation is not a result of systemic toxicity. It occurs only in areas of inflammation, where the increased permeability of irritated blood vessels permits seepage of the metal into the surrounding tissue. In addition to inflamed gingiva, mucosal areas irritated by biting or abnormal chewing habits (e.g., inner surface of lips, cheek at level of occlusal line, lateral border of tongue) are common sites of pigmentation. Pigmentation can be eliminated by treating the inflammatory changes without necessarily discontinuing the metal containing medication.
Bismuth gingivitis.linear black discoloration of the gingiva in a patient receiving bismuth therapy. Discoloration of the gingiva caused by embedded metal particles (amalgam).
COLOR CHANGES ASSOCIATED WITH SYSTEMIC FACTORS Many systemic diseases may cause color changes in the oral mucosa, including the gingiva. In general, these abnormal pigmentations are nonspecific and needs further diagnostic efforts or referral to the appropriate specialist. Endogenous oral pigmentations can be caused by melanin, bilirubin, or iron. Melanin oral pigmentations can be normal physiologic pigmentations and are often found in highly pigmented ethnic groups. Diseases that increase melanin pigmentation include the following: Addison’s disease is caused by adrenal dysfunction and produces isolated patches of discoloration varying from bluish black to brown. Peutz-Jeghers syndrome produces intestinal polyposis and melanin pigmentation in the oral mucosa and lips. Albright’s syndrome (polyostotic fibrous dysplasia) and Von Recklinghausen's disease (neurofibromatosis) produce areas of oral melanin pigmentation.
Skin and mucous membranes can also be stained by bile pigments. The deposition of iron in hemochromatosis may produce a blue-gray pigmentation of the oral mucosa. Several endocrine and metabolic disturbances, including diabetes and pregnancy, may result in color changes. Blood dyscrasias such as anemia, polycythemia, and leukemia may also induce color changes. Exogenous factors capable of producing color changes in the gingiva include atmospheric irritants, such as coal and metal dust, and coloring agents in food or lozenges. Tobacco causes hyperkeratosis of the gingiva and also may induce a significant increase in melanin pigmentation of the oral mucosa. Localized bluish black areas of pigment are often caused by amalgam implanted in the mucosa
PHYSIOLOGIC PIGMENTATION: Dummet et al 1946 proposed the following explanation for gingival pigmentation. The color of healthy gingiva is variable ranging from a pale pink to a deep bluish purple hue. Between these limits of normalcy are a large number of pigmentation mosaics which depend primarily upon the intensity of melanogenesis, depth of epithelial cornification and arrangement of gingival vascularity. More over color variation may not be uniform and may exists as unilateral, bilateral, mottled, macular or blotched and may involve gingival papillae alone or extend throughout the gingiva on to other soft tissues.
Most pigmentation is caused by five primary pigments Most pigmentation is caused by five primary pigments. These include: melanin, melanoid, oxyhemoglobin, reduced haemoglobin, and carotene. Others are caused by bilirubin and iron. Alex A Farnoosh 1990 said that melanin deposits mainly in basal and suprabasal cell layers of epithelial. The degree of pigmentation is attributed to melanoblastic activity and density of melanophores in gingiva. In gingiva number of melanophores in the epithelium and the subepithelial connective tissue gradually decreases starting from the free gingival groove area towards the gingival crest in the free gingiva & towards the muco-gingival junction in attached gingiva. In addition, the total number of melanophores in attached gingiva (3230) approximately is 16 times greater than in free gingiva (198).
Melanin is a non-hemoglobin derived brown pigment. It is responsible for the normal pigmentation of the skin, gingiva and remainder of the oral mucosa. It is more prominent in the oral cavity of black individuals. According to Dummett et al 1946, the distribution of oral pigmentation in black individuals is as follows: gingiva:- 60% hard palate:- 61% mucous membrane:- 22% tongue:- 15% Gingival pigmentation occurs as a diffuse, deep- purplish discoloration or as irregularly shaped brown and light brown patches. It may appear as early as 3 hours after birth.
DUMMET PROPOSED THE DUMMET ORAL PIGMENTATION INDEX (DOPI) ASSESSMENT 1964 Score 0 : Pink tissue (No clinical pigmentation) Score 1 : Mild light brown color (Mild clinical pigmentation) Score 2 : Medium brown or blue black tissue (Heavy clinical pigmentation) Score 3 : Deep brown or blue black tissue (Heavy clinical pigmentation)
DEPIGMENTATION Traditionally, gingival depigmentation has been carried out using nonsurgical and surgical procedures, such as chemical, cryosurgical, and electrosurgical techniques. However, those techniques were met with skepticism because of varying degrees of success. More recently, lasers have been used to ablate cells producing the melanin pigment; a nonspecific laser beam destroys the epithelial cells, including those at the basal layer. In addition, selective ablation using a laser beam with a wavelength that is specifically absorbed in melanin effectively destroys the pigmented cells without damaging the non-pigmented cells. In both cases, radiation energy is transformed into ablation energy, resulting in cellular rupture and vaporization with minimal effect on surrounding tissue.
CHANGES IN CONSISTENCY OF THE GINGIVA Both chronic and acute inflammations produce changes in the normal firm and resilient consistency of the gingiva. As previously noted, in chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative predominance. In chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative predominance
CALCIFIED MASSES IN THE GINGIVA Calcified microscopic masses may be found in the gingiva. (Box HK 1950) They can occur alone or in groups and vary in size, location, shape, and structure. Such masses may be calcified material removed from the tooth and traumatically displaced into the gingiva during scaling, root remnants, cementum fragments, or cementicles Chronic inflammation and fibrosis, and occasionally foreign body, giant cell activity, occur in relation to these masses. They are sometimes enclosed in an osteoid-like matrix. Crystalline foreign bodies have also been described in the gingiva, but their origin has not been determined.
TOOTH BRUSHING Tooth brushing has various effects on the consistency of the gingiva, such as promoting keratinization of the oral epithelium, enhancing capillary gingival circulation, and thickening alveolar bone. (Mackenzie IC et al 1972, Tanaka M et al 1998) In animal studies, mechanical stimulation by tooth brushing was found to increase the proliferative activity of junctional basal cells in dog gingiva by 2.5 times compared with using a scaler. (Yamamoto T 2002)
CHANGES IN SURFACE TEXTURE OF THE GINGIVA The surface of normal gingiva usually exhibits numerous small depressions and elevations, giving the tissue an orange peel appearance referred as stippling. (Bergstrom J 1984) Stippling is restricted to the attached gingiva and is predominantly localized to the sub-papillary area, but it extends to a variable degree into the interdental papilla. (Orban B 1948) Although the biologic significance of gingival stippling is not known, some investigators conclude that loss of stippling is an early sign of gingivitis.
However, its pattern and extent vary in different mouth areas, among patients, and with age. In chronic inflammation the gingival surface is either smooth and shiny or firm and nodular, depending on whether the dominant changes are exudative or fibrotic. Smooth surface texture is also produced by epithelial atrophy in atrophic gingivitis, and peeling of the surface occurs in chronic desquamative gingivitis. Hyperkeratosis results in a leathery texture, and drug-induced gingival overgrowth produces a nodular surface.
Gingival biopsy demonstrating alternate elevations and depressions in the attached gingiva responsible for stippled appearance.
TRAUMATIC LESIONS One of the unique features of the most recent gingival disease classification is the recognition of non-plaque induced traumatic gingival lesions as distinct gingival conditions. (Armitage GC 1999) Traumatic lesions, whether chemical, physical, or thermal, are among the most common lesions in the mouth. Sources of chemical injuries include aspirin, hydrogen peroxide, silver nitrate, phenol, and endodontic materials. Physical injuries can include lip, oral, and tongue piercing, which can result in gingival recession. Thermal injuries can result from hot drinks and foods..
In acute cases, the appearance of slough (necrotizing epithelium), erosion, or ulceration and the accompanying erythema are common features. In chronic cases, permanent gingival defects are usually present in the form of gingival recession. Typically, the localized nature of the lesions and the lack of symptoms readily eliminate them from the differential diagnosis of systemic conditions that may be present with erosive or ulcerative oral lesions. (Rawal SY et al 2004)
POSITION OF GINGIVA Gingival recession is a common finding. The prevalence, extent, and severity of gingival recession increase with age and are more prevalent in males. (Albander JM, Kingman A 1999) By clinical definition, recession is exposure of the root surface by an apical shift in the position of the gingiva. Gingival recession is defined as the apical migration of the junctional epithelium with exposure of root surfaces.(Kassab MM, Cohen RE 2003) Gingival recession is the apical shift of the marginal gingiva from its normal position on the crown of the tooth to levels on the root surface beyond the cemento enamel junction (Loe H 1992) To understand recession, it helps to distinguish between the actual and apparent positions of the gingiva.
In periodontal disease, the inflamed pocket wall covers part of the denuded root; thus some of the recession is hidden, and some may be visible. The total amount of recession is the sum of the two. Recession refers to the location of the gingiva, not its condition. Receded gingiva can be inflamed but may be normal except for its position. Recession may be localized to one tooth or a group of teeth, or it may be generalized throughout the mouth. The actual position is the level of the epithelial attachment on the tooth, whereas the apparent position is the level of the crest of the gingival margin. The severity of recession is determined by the actual position of the gingiva, not its apparent position.
THEORY The most accepted theory to explain the origin of gingival recession is based on inflammation of the connective tissue of free gingiva and its consequent destruction, where the gingival epithelium migrates into the connective tissue and gets destroyed, while the gingival epithelial basement membrane and sulcus epithelium reduce the thickness of the connective tissue between them, thus reducing the blood flow by impairing the repair of the initial injury. As the lesion progresses, the connective tissue disappears and fusion occurs between the gingival epithelium and the sulcular and union epithelia, which will subsequently withdraw due to lack of blood flow (Susin et al)
ETIOLOGIC FACTORS Gingival recession increases with age; the incidence varies from 8% in children to 100% after age 50 years. (Woofter C 1969) This has led some investigators to assume that recession may be a physiologic process related to aging. However, no convincing evidence has been presented for a physiologic shift of the gingival attachment. (Loe H 1967) The gradual apical shift is most likely the result of the cumulative effect of minor pathologic involvement and repeated minor direct trauma to the gingiva. In some populations without access to dental care, however, recession may be the result of increasing periodontal disease. (Hirschfeld I 1923, Loe H 1967)
The following etiologic factors have been implicated in gingival recession: faulty tooth brushing technique (gingival abrasion), tooth malposition, friction from soft tissues (gingival ablation), gingival inflammation, abnormal frenum attachment, and iatrogenic dentistry. Trauma from occlusion has been suggested in the past, but its mechanism of action has never been demonstrated. For example, a deep overbite has been associated with gingival inflammation and recession. Excessive incisal overlap may result in a traumatic injury to the gingiva. Orthodontic movement in a labial direction in monkeys has been shown to result in loss of marginal bone and connective tissue attachment, as well as in gingival recession.
Standard oral hygiene procedures, whether tooth-brushing or flossing, may lead to a frequent transient and minimal gingival injury. Although tooth brushing is important for gingival health, faulty tooth brushing technique or brushing with hard bristles may cause significant injury. This type of injury may present as lacerations, abrasions, keratosis and recession, with the facial marginal gingiva most affected. Thus, in these cases, recession tends to be more frequent and severe in patients with clinically healthy gingiva, little bacterial plaque, and good oral hygiene.
Susceptibility to recession is also influenced by the position of teeth in the arch, the root-bone angle, and the mesiodistal curvature of the tooth surface. On rotated, tilted, or facially displaced teeth, the bony plate is thinned or reduced in height. Pressure from mastication or moderate tooth brushing damages the unsupported gingiva and produces recession.
The effect of the angle of the root in the bone on recession is often observed in the maxillary molar area. If the lingual inclination of the palatal root is prominent or the buccal roots flare outward, the bone in the cervical area is thinned or shortened, and recession results from repeated trauma of the thin, marginal gingiva.
RESTORATIONS AND RECESSION The health of the gingival tissue also depends on properly designed and placed restorative materials. Pressure from a poorly designed partial denture, such as ill-fitting denture clasp, can cause gingival trauma and recession. Overhanging dental restorations have long been viewed as a contributing factor to gingivitis because of plaque retention. (Zlataric DK, Celebic A et al 2002) In addition, there is general agreement that placing restorative margins within the biologic width frequently leads to gingival inflammation, clinical attachment loss, and eventually, bone loss. Clinically, the violation of biologic width typically manifests as gingival inflammation, deepened periodontal pockets, or gingival recession. (Bjorn et al 1969, Garguilo et al 1961) RESTORATIONS AND RECESSION
A relationship may exist between smoking and gingival recession. The multifactorial mechanisms may include reduced gingival blood flow and altered immune response but are not, as yet, conclusive. (Gunsolley JC, Tew J et al 1998) CLINICAL SIGNIFICANCE Several aspects of gingival recession make it clinically significant. Exposed root surfaces are susceptible to caries. Abrasion or erosion of the cementum exposed by recession leaves an underlying dentinal surface that can be sensitive. Hyperemia of the pulp and associated symptoms may also result from excessive exposure of the root surface. (Merritt AA 1993) Interproximal recession creates oral hygiene problems and resulting plaque accumulation. SMOKING AND RECESSION
CLASSIFICATION An early study of recession associated with mandibular incisor teeth used the descriptive terms “narrow,” “wide,” “shallow” and “deep” to classify recession into four groups (Sullivan HC, Atkins JH-1968) Another study classified gingival recession into “shallow-narrow” defects as less than 3 mm in both dimensions, and “deep-wide” defects as more than 3 mm in both dimensions (Mlinek A, Smukler H, Buchner A 1973)
The Index of Recession, or IR, was introduced by Smith(1997). Recession was described by two digits separated by a dash (for example, F2-4) and the prefixed letter F or L denotes whether the recession is on the facial or lingual aspects of the tooth. The digits describe the horizontal and vertical components of a recession site in that order. If an asterisk were present, it would denote involvement of the mucogingival junction. The horizontal component is expressed as a whole number value (from the range 0-5) depending on what proportion of the CEJ is exposed on either the facial or lingual aspects of the tooth, between the mesial and distal midpoints.
MAHAJAN'S MODIFICATION An outline of classification system including the above mentioned changes is presented: Class I: GRD not extending to the MGJ. Class II: GRD extending to the MGJ/beyond it. Class III: GRD with bone or soft-tissue loss in the interdental area up to cervical 1/3 of the root surface and/or malpositioning of the teeth. Class IV: GRD with severe bone or soft tissue loss in the interdental area greater than cervical 1/3rd of the root surface and/or severe malpositioning of the teeth.
PROPOSED CLASSIFICATION OF GINGIVAL RECESSION [ASHISH KUMAR, SUJATA SURENDRA MASAMATTI- 2013] This classification can be applied for facial surfaces of maxillary teeth and facial and lingual surfaces of mandibular teeth. Interdental papilla recession can also be classified according to this new classification. Class I deals with marginal tissue recession with no loss of interdental bone or soft-tissue. Class II and III deal with the loss of interdental bone/soft-tissue with/ without marginal tissue recession.
Class I: There is no loss of interdental bone or soft-tissue. This is sub-classified into two categories: Class I-A: Gingival margin on F/L aspect lies apical to CEJ, but coronal to MGJ with attached gingiva present between marginal gingiva and MGJ. Class I-B: Gingival margin on F/L aspect lies at or apical to MGJ with an absence of attached gingiva between marginal gingiva and MGJ. Either of the subdivisions can be on F or L aspect or both (F and L)
Class II-A: There is no marginal tissue recession on F/L aspect. Class II: The tip of the interdental papilla is located between the interdental contact point and the level of the CEJ midbuccally/ mid-lingually. Interproximal bone loss is visible on the radiograph. This is sub-classified into three categories: Class II-A: There is no marginal tissue recession on F/L aspect. Class II-B: Gingival margin on F/L aspect lies apical to CEJ but coronal to MGJ with attached gingiva present between marginal gingiva and MGJ. Class II-C: Gingival margin on F/L aspect lies at or apical to MGJ with an absence of attached gingiva between marginal gingiva and MGJ Either of the subdivisions can be on F or L aspect or both (F and L).
Class III: The tip of the interdental papilla is located at or apical to the level of the CEJ mid-buccally/mid-lingually. Interproximal bone loss is visible on the radiograph. This is sub-classified into two categories: Class III-A: Gingival margin on F/L aspect lies apical to CEJ, but coronal to MGJ with attached gingiva present between marginal gingiva and MGJ. Class III-B: Gingival margin on F/L aspect lies at or apical to MGJ with an absence of attached gingiva between marginal gingiva and MGJ. Either of the subdivisions can be on F or L aspect or both (F and L).
CLASSIFICATION OF PALATAL GINGIVAL RECESSION The position of interdental papilla remains the basis of classifying gingival recession on palatal aspect. The criteria of sub-classifications have been modified to compensate for the absence of MGJ. PR-I deals with marginal tissue recession on palatal aspect with no loss of interdental bone or soft-tissue. PR-II and PR-III deal with the loss of interdental bone/soft tissue with marginal tissue recession on palatal aspect.
Palatal recession-I There is no loss of interdental bone or soft-tissue. This is sub-classified into two categories: PR-I-A: Marginal tissue recession ≤3 mm from CEJ. PR-I-B: Marginal tissue recession of >3 mm from CEJ.
Palatal recession-II The tip of the interdental papilla is located between the interdental contact point and the level of the CEJ mid-palatally. Interproximal bone loss is visible on the radiograph. This is sub-classified into two categories: PR-II-A: Marginal tissue recession ≤3 mm from CEJ. PR-II-B: Marginal tissue recession of >3 mm from CEJ
Palatal recession-III The tip of the interdental papilla is located at or apical to the level of the CEJ mid-palatally. Interproximal bone loss is visible on the radiograph. This is sub-classified into two categories: PR-III-A: Marginal tissue recession ≤3 mm from CEJ. PR-III-B: Marginal tissue recession of >3 mm from CEJ.
LIST OF DIFFERENT SURGICAL TECHNIQUES USED IN ROOT COVERAGE PROCEDURES.
CHANGES IN GINGIVAL CONTOUR Changes in gingival contour are primarily associated with gingival enlargement, but such changes may also occur in other conditions. Of historical interest are the descriptions of indentations of the gingival margin referred to as Stillman's clefts and the McCall festoons. A gingival cleft is a vertical fissure Stillmans cleft ( PR Stillman 1871-1945) american periodontologist: is a narrow slit like or triangular shaped fissure of gingival tissue extending from gingival margin Semilunar shaped enlargement of marginal gingiva primarily on labial surface of anterior and premolar teeth described by JOHN OPPIE Mc CALL in 1922…believed to be caused by occlusal traumatism but has not been confirmed by later studies (ref: oxford medical terms overview)
STILLMAN'S CLEFTS Used to describe a specific type of gingival recession consisting of a narrow, triangular shaped gingival recession. As the recession progresses apically, the cleft becomes broader, exposing the cementum of the root surface. When the lesion reaches the mucogingival junction, the apical border of oral mucosa is usually inflamed because of the difficulty in maintaining adequate plaque control at this site.
Originally described by Stillman PR 1921 and considered to be the result of occlusal trauma These clefts were subsequently described by Box HK 1950 as pathologic pockets in which the ulcerative process had extended to the facial surface of the gingiva. The clefts may repair spontaneously or persist as surface lesions of deep periodontal pockets that penetrate into the supporting tissues. Their association with trauma from occlusion has not been substantiated.
The clefts are divided into simple clefts: in which cleavage occurs in a single direction (the most common type), and compound clefts: in which cleavage occurs in more than one direction. The clefts vary in length from a slight break in the gingival margin to a depth of 5 to 6 mm or more.
Mc CALL’s FESTOONS (John Oppie Mc Call 1922) Used to describe a rolled, thickened band of gingiva usually seen adjacent to the cuspids when recession approaches the mucogingival junction. Initially, Stillman's clefts and McCall festoons were attributed to traumatic occlusion, and the recommended treatment was occlusal adjustment. However, this association was never proved, and these indentations merely represent peculiar inflammatory changes of the marginal gingiva.
CONCLUSION Establish a proper diagnosis based on clinical findings….. Proper management…phase I… Prevention of periodontitis….
REFERENCES Clinical Periodontology- Carranza’s 10th edition Clinical Periodontalogy and implant dentistry- Jan Lindhe 5th edition. Oral history- Antonio Nanci Ten Cate’s Essential Pathology – Harsh Mohan 3rd edition The gingival tissues: the architecture of periodontal protection. Periodontology 2000, vol. 13, 1997, 91-120. REFERENCES
Page RC, Gingivitis. J Clin Periodontol 1986;13: 345-355. Richard R. Ranney, Discussion: Pathogenesis of gingivitis. J Clin Periodontol 1986;13: 356-359. William, Roy et al, Histopathologic features of the initial and early stages of experimental gingivitis in man. J. Periodonlal Res1975;10:51-64. Monitoring disease during supportive periodontal treatment by bleeding on probing. Periodontology 2000, vol. 12, 1996, 4448