Perio Pre-Final Lecture Notes on Gingival Defense Mechanisms (PDF)

CHAPTER 13: DEFENSE MECHANISMS OF THE GINGIVA CHAPTER 14: GINGIVAL INFLAMMATION CHAPTER 15: CLINICAL FEATURES OF GINGIVITIS Angeli Mangahas-Saldon, DMD  TOPIC OUTLINE: GCF Sulcular fluid Saliva Gingival inflammation Stage I: Initial...

CHAPTER 13: DEFENSE MECHANISMS OF THE GINGIVA CHAPTER 14: GINGIVAL INFLAMMATION CHAPTER 15: CLINICAL FEATURES OF GINGIVITIS Angeli Mangahas-Saldon, DMD  TOPIC OUTLINE: GCF Sulcular fluid Saliva Gingival inflammation Stage I: Initial lesion Stage II: Early lesion Stage III: Established lesion Stage IV: Advanced lesion Clinical features of Gingivitis The gingival tissue is constantly subjected to mechanical and bacterial aggressions. The saliva, the epithelial surface, and the initial stages of the inflammatory response provide resistance to these actions.  GINGIVAL CREVICULAR FLUID Pioneer research by Waerhaug (1950) focused on the anatomy of sulcus and its transformation into a gingival pocket during the course of periodontitis. Brill et al (1950) → laid the foundation of understanding the physiology of gingival crevicular fluid as an indicator of periodontal disease. Loe et al (1965) → used gingival crevicular fluid as an indicator of periodontal disease. Goodson → thoroughly studied major issues in gingival crevicular fluid flow rate and its method of collection. Egelberg → focused the studies on dentogingival blood vessels and their permeability as they relate to the gingival crevicular fluid flow.  SULCULAR FLUID Also known as: gingival crevicular fluid (GCF) Its composition and possible role in oral defense mechanisms were elucidated by the pioneering work of Waerhaug and Bill and Krasse (1958) How? Introduction of filter paper into the gingival sulci of dogs that had been previously been injected IM with fluorescein; within 3 mins, the fluorescent material was recovered on the paper strips. This indicated the passage of fluid from the bloodstream through the tissues & the exiting of fluid via the gingival sulcus.  IS GCF A TRANSUDATE OR EXUDATE? Brill (1959) → confirmed the presence of GCF in humans and considered it a “transudate” However, others demonstrated that GCF is an inflammatory exudate , nota continuous transudate. In strictly normal gingiva, little or no fluid can be collected. Alfano (1974) and Pashley (1976) → suggested that the initial fluid which appears in the crevice as a result of osmotic gradient. This initial, proinflammatory fluid was earlier considered to be transudate, and on stimulation it changes to an exudate. MODEL BY PASHLEY (1976)  Exert antibody activity in defense of gingiva Possesses anti-bacterial Functions Cleanses materials from the of sulcus Properties GCF Contains plasma proteins that may improve adhesion of epi. To tooth METHODS OF COLLECTION Absorbing paper strips Placement of twisted threads around & into the sulcus Micropipettes Intercrevicular washings  ABSORBENT FILTER PAPER STRIPS The most common method of collection These are pre-sterilized filter paper strips of standard size that can absorb fluid volumes of up to approximately 1.2µl. Methods of placement: → Intrasulcular (within sulcus) → Extrasulcular (at its entrance) *** Periopaper strips are typically inserted no more than 1- 2mm into the sulcus/pocket to permit absorption of gingival crevicular fluid from the site, with gentle placement until mild resistance is felt. *** The periopaper is held in place for a fixed period of time (typically 30s)  BRILL’S LOE & HOLM- TECHNIQUE PEDERSON TECHNIQUE The strip is To minimize the inserted until irritation, they placed resistance is felt the filter paper strip just at the entrance of the But this induces a pocket or over the degree of irritation pocket entrance. of the In this way, the fluid Sulcular epithelium, seeping out is picked up that can itself by the strip, but the Trigger oozing of sulcular epithelium will fluid. not be in contact with the paper.  PREWEIGHED TWISTED THREADS This method was used by Weinstein et al. Threads were placed in the gingival crevice around the tooth and the amount of fluid collected was estimated by weight of sample thread. The threads were weighed before collection within a sealed microcentrifugation plastic tube and the weighing was repeated immediately after the collection. MICROPIPETTES/ CAPILLARY TUBINGS Krasse and Egelberg (1962) →were first to utilize capillary tubing. This permits the collection of fluid by capillary action. This is not a practicable technique in subjects with clinically normal gingiva. Disadvantages: Long collection period Difficult due to the viscosity of fluid makes the aspiration difficult. Difficult to remove the complete sample from the tubing. Advantages: Provides an undiluted sample of native GCF whose volume can be accurately assessed.  CREVICULAR WASHINGS → can be used to study GCF from clinically normal gingiva. →One method involves the use of an appliance that consists of a hard acrylic plate that covers the maxilla, with soft borders and a groove that follows the gingival margins; it is connected to four collection tubes. → The washings are obtained by rinsing the crevicular areas from one side to the other with the use of a peristaltic pump  COMPOSITION OF GCF → can be characterized according to individual proteins, specific antibodies, antigens and enzymes of several specificities. The GCF also contains cellular elements. → So far, more than 40 compounds found in GCF have been analyzed. Cellular Elements Electrocytes Organic Compounds Bacteria Potassium Glucose hexosamine Desquamated epithelial Sodium Hexuronic acid cells Calcium Metabolic and bacterial products Leukocytes (PMN’s, (lactic acid, urea, hydroxyproline, lymphocytes, monocytes & endotoxins, cytotoxic substances, macrophages) hydrogen sulfide & antibacterial factors  CLINICAL SIGNIFICANCE OF GCF TO REMEMBER GCF is an inflammatory exudate Circadian Periodicity GCF is greater when inflammation is Increased from 6am to 10pm present Sex hormones Production is NOT increased by trauma Pregnancy, ovulation & hormonal contraceptives from occlusion but is ↑ by: increase GCF production →mastication of coarse foods Mechanical Stimulation → toothbrushing & gingival Chewing, vigorous gingival brushing stimulate flow. massage Smoking → ovulation ↑ GCF flow → hormonal contraceptives Periodontal Therapy → prosthetics ↑ in production during healing after perio surgery. → smoking  SALIVA Functions: maintain the oral tissues in physiological state. Mechanically cleansing the exposed oral surfaces by buffering produced bacteria and by controlling bacterial activity. Coagulation factors that protect wounds from bacterial invasion.  ANTIBACTERIAL FACTORS Inorganic factors includes: Organic factors includes: Ions and gases Lysozyme – targets Veillonella sp. & Aa Bicarbonate Lactoferrin – targets Actinobacillus sp. Sodium Myeloperoxidase – released by leukocytes also targets Potassium Actinobacillus sp. Phosphates Lactoperoxidase – targets strains of Lactobacillus & Streptococcus by preventing accumulation Calcium of lysine & glutamic acid. Fluorides and agglutinins such as glycoproteins, mucins, β2- Ammonium macroglobulins, fibronectins and antibodies. Carbon dioxide  Salivary Antibodies Enzymes Immunoglobulins present: IgA Derived from: salivary glands, leukocytes, (preponderant) , IgG and IgM oral tissues and ingested substances However, IgG is more prevalent in GCF. Major enzyme: parotid amylase Gibbons and colleagues suggested that saliva contains antiproteases that inhibit antibodies in secretions may impair the cysteine proteases such as cathepsins ability of bacteria to attach to mucosal and antileukoproteases that inhibit or dental surfaces. elastase. Another antiprotease, which has been identified as a tissue inhibitor of matrix metalloproteinase, has been shown to inhibit the activity of collagen- degrading enzymes  ROLE IN PERIODONTAL THERAPY Has a major influence on plaque Xerostomia may result from: initiation, maturation and →Sialolithiasis metabolism. →Sarcoidosis, In humans, an increase in →Sjögren syndrome, inflammatory gingival diseases, dental caries, and rapid tooth →Mikulicz disease, destruction that is associated with →irradiation, cervical or cemental caries is →the surgical removal of the partially a consequence of salivary glands, decreased salivary gland secretion (xerostomia). → and other factors  GINGIVAL INFLAMMATION  INTRODUCTION The sequence of events that culminates in clinically apparent gingivitis is categorized as the initial, early, and established stages of disease, with periodontitis designated as the advanced stage. One stage evolves into the next, with no clear-cut dividing lines.  STAGE I GINGIVAL INFLAMMATION: THE INITIAL LESION The first manifestations of gingival inflammation are vascular changes that consist of: → dilated capillaries and → increased blood flow This occur in response to the microbial activation of resident leukocytes and the subsequent stimulation of endothelial cells.  STAGE II GINGIVAL INFLAMMATION: THE EARLY LESION The early lesion evolves from the initial lesion within about 1 week after the beginning of plaque accumulation. Clinically, the early lesion may appear as early gingivitis. Bleeding on probing may also be evident. Gingival fluid flow and the numbers of transmigrating leukocytes reach their maximum between 6 and 12 days after the onset of clinical gingivitis. Leukocyte infiltration beneath the junctional epithelium consists mainly of lymphocytes (particularly T cells) There is a ↑ in collagen destruction (about 70%) Main fiber group affected: Circular & Dento-gingival  STAGE III GINGIVAL INFLAMMATION: THE ESTABLISHED LESION It is characterized by a predominance of plasma cells and B lymphocytes, and it is probably in conjunction with the creation of a small gingival pocket lined with a pocket epithelium. occurs 2 to 3 weeks after the beginning of plaque accumulation, the blood vessels become engorged and congested, venous return is impaired, and the blood flow becomes sluggish. The result is localized gingival anoxemia, which superimposes a somewhat bluish hue on the reddened gingiva.  STAGE IV GINGIVAL INFLAMMATION: THE ADVANCED LESION known as the advanced lesion or phase of periodontal breakdown. Gingivitis will progress to periodontitis only in individuals who are susceptible. Patients who had sites with consistent bleeding (gingival index = 2) had 70% more attachment loss as compared with sites that were not inflamed consistently (gingival index = 0).  CLINCIAL FEATURES OF GINGIVITIS  INTRODUCTION In general, clinical features of gingivitis may be characterized by the presence of any of the following clinical signs: redness and sponginess of the gingival tissue, bleeding on provocation, changes in contour, and the presence of calculus or plaque with no radiographic evidence of crestal bone loss. Main etiologic agent of gingivitis: Plaque  COURSE AND DURATION Gingivitis can occur with sudden onset and short duration, and it can be painful. Chronic gingivitis is slow in onset and of long duration. It is painless, unless it is complicated by acute or subacute exacerbations, and it is the type that is most often encountered. Recurrent gingivitis reappears after having been eliminated by treatment or disappearing spontaneously.  DESCIPTION LOCALIZED GENERALIZED MARGINAL PAPILLARY DIFFUSE GINGIVITIS GINGIVITIS GINGIVITIS GINGIVITIS GINGIVITIS confined to the involves the involves the involves the affects the gingival gingiva of a entire mouth. gingival margin, interdental margin, the attached single tooth or and it may papillae, and it gingiva, and the group of teeth include a often extends into interdental papillae. portion of the the adjacent contiguous portion of the attached gingiva gingival margin EARLIEST sign of gingivitis occur in the papillae. 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 the attached gingiva are affected, so the mucogingival junction is sometimes obliterated.  GINGIVAL BLEEDING ON PROBING The two earliest signs of gingival inflammation that precede established gingivitis are as follows: (1) increased gingival crevicular fluid production rate; and (2) (2) bleeding from the gingival sulcus on gentle probing Gingival bleeding varies with regard to severity, duration, and ease of provocation. In general, gingival bleeding on probing indicates an inflammatory lesion both in the epithelium and in the connective tissue that exhibits specific histologic differences as compared with healthy gingiva people who are committed to a smoking cessation program should be informed about the possibility of an increase in gingival bleeding associated with smoking cessation.  GINGIVAL BLEEDING CAUSED BY LOCAL FACTORS 1. Anatomic and 6. Mouth breathing developmental tooth 7. Overhangs variations 8. Partial dentures 2. Caries 9. Lack of attached gingiva 3. Frenum pull 10.Recession 4. Iatrogenic factors 11.Orthodontics treatments 5. Malpositioned teeth and fixed retainers  CHRONIC & RECURRENT BLEEDING The most common cause of abnormal gingival bleeding on probing is chronic inflammation. it is provoked by mechanical trauma (e.g., from toothbrushing, toothpicks, or food impaction) or by biting into solid foods (e.g., apples). The severity of bleeding and the ease of its provocation depend on the intensity of the inflammation. In cases of moderate or advanced periodontitis, the presence of bleeding on probing is considered a sign of active tissue destruction Spontaneous bleeding or bleeding on slight provocation can occur with acute necrotizing ulcerative gingivitis  COLOR CHANGES IN THE GINGIVA Normally, gingiva appears to be coral pink. The factors that are responsible for this are tissue vascularity, degree of keratinization and thickness of the epithelium. When there is increased vascularity or reduced epithelial keratinization, the gingiva becomes more red. The color becomes pale when vascularization is reduced or epithelial keratinization increases. Venous statis gives a bluish hue to the gingiva. Systemically absorbed heavy metals may also cause gingival pigmentation, e.g. bismuth, arsenic, mercury, lead and silver. Abnormal melanin pigmentation of the gingiva may be observed in conditions like Addison’s disease, Peutz- jeghers syndrome, Addison’s disease and Von Recklinghausen's disease.  Peutz-jeghers syndrome  CHANGES IN CONSISTENCY Changes in the consistency of gingiva Normal gingiva exhibits a firm and resilient consistency. Factors that are responsible are cellular and fluid content and collagenous nature of lamina propria. In disease conditions, it can be soggy and edematous or firm; and leathery con SURFACE TEXTURE Under normal conditions, gingiva appears to be stippled(orange peel appearance) due to attachment of gingival fibers to the underlying bone. Microscopically, alternate rounded protuberance and depressions in the gingival layer may rise to stippled appearance. Stippling is absent in disease conditions. Hence, the gingiva may appear smooth and shiny.  GINGIVAL RECESSION Definition: is defines as the exposure of the root surface by an APICAL shift in the position of the gingiva. It can either be localized or generalized in nature. 2 classification systems: 1. According to Sullivan & Atkins → Shallow-narrow, shallow- wide and deep-wide 2. According to PD Miller’s: Class I, Class II, Class III, Class IV.  ETIOLOGY OF GINGIVAL RECESSION Plaque-induced gingival inflammation is the primary etiological factor responsible for gingival recession; next common cause is faulty tooth- brushing (facial and marginal gingiva). Other secondary factors on gingival recession are broadly categorized as i. Anatomic factors ii. Habits iii. Iatrogenic factors iv. Physiologic factors  CLINICAL SIGNIFICANCE OF GINGIVAL RECESSION 1) The exposed root surface may be extremely sensitive. 2) Hyperemia of the pulp may result due to gingival recession. 3) Interproximal recession creates oral hygiene problems thereby resulting in plaque accumulation. 4) Finally, it is aesthetically unacceptable.  CHANGES IN GINGIVAL CONTOUR Normally, marginal gingiva is scalloped and knife edges, 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 the facial and lingual gingival embrasures. In diseased conditions, the marginal gingiva may become rounded or rolled, whereas interdental papilla can become blunt and flat. Stillman’s clefts are apostrophe shaped indentations extending from and into the gingival margin varying distance on the facial surface. There are two types- 1) Simple Cleft: Cleavage in a single direction. 2) 2) Compound Cleft: Cleavage in more than one direction.