Understanding Gingival Crevicular Fluid (GCF): Its Role in Inflammation and Diagnosis
Host Response Basic Concept
Question 1. GCF is an inflammatory exudate. Justify?
Answer. Waerhaug, Brill and Krasse (1950) introduced fiter paper in the gingival sulci of dogs that had previously been injected IM with florescein, within 3 minutes florescent material was recovered on the paper strips. This indicated a passage of fluid from the bloodstream through the tissues and exiting via the gingival sulcus.
- Brill (1959, 1969) confirmed the presence of GCF in humans and considered it a transudate. Brill technique places paper strips into the pocket until resistance is encountered. This method introduces a degree of irritation of the sulcular epithelium that can by itself trigger the oozing of the fluid.
- Protective effect of gingival fluid was suggested by Brill (1959) using charcoal and bacteria Serratia marcescens. Serratia marcescens and Flavobacterium Lutescens are chromogenic organisms responsible for orange stains on both facial and lingual surfaces of anterior teeth, Substances that can penetrate sulcular epithelium include albumin, endotoxin, thymine, histamine, phenytoin and horseradish peroxidase this indicates that GCF is an inflammatory exudate.
Question 2. Write short note on modes of collection of sulcular fluid.
Answer. Following are the modes of collection of sulcular fluid, i.e. the use of absorbing paper strips, twisted threads placed around and into the sulcus, micropipetts, and intracrevicular washings.
- The absorbing paper strips are placed within the sulcus (intrasulcular method) or at its entrance (extrasulcular method). The placement of the filter paper strip in relation to the sulcus or pocket is important.
- Preweighed twisted threads were used. The threads were placed in the gingival crevice around the tooth, and the amount of fluid collected was estimated by weighing the sample thread.
- The use of micropipetts permits the collection of fluid by capillarity. Capillary tubes of standardized length and diameter are placed in the pocket, and their content is centrifuged and analyzed.
Read And Learn More: Periodontics Question And Answers
- Crevicular washings can be used to study GCF from clinically normal gingiva. One method uses an appliance consisting of a hard acrylic plate covering the maxilla with soft borders and a groove following 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, using a peristaltic pump.
- A modification of the previous method uses two injection needles fitted one within the other such that during sampling, the inside (ejection) needle is at the bottom of the pocket, and the outside (collecting) needle is at the gingival margin. The collection needle is drained into sample tube by continuous suction.
Question 3. Write short note on functions of leukocytes.
Answer. Following are the function of leukocytes:
Question 4. Discuss inflammation in periodontal disease.
Answer. Inflammation is a physiologic series of responses generated by the host in response to infection or injury.
- The initial events of inflammation are initiated by vascular reactions at the site of injury leading to extravasation of fluid and plasma proteins and recruitment of leucocytes to the site of injury.
- Inflammation is a natural beneficial response confirming the injury or infection, and serves as the first step in the initiation of the immune response.
- Ideally, the innate immune or inflammatory response is sufficient to eliminate the infection, allowing for healing and return to homeostasis.
- If the innate immune response fails, chronic inflammation ensues.
- In the case of chronic inflammation, the persistence of the response leads to host tissue self-destruction and may result in irreversible pathological changes.
- Various cell types including mast cells, platelets and leukocytes generate inflammatory mediators (chemokines and cytokines).
- Elevated levels of these molecules promote inflammation and amplify the response.
- Proteins-including cytokines and chemokines. low molecular weight lipids derived from arachidonic acid, nitric oxide and carbon monoxide, reactive oxygen species, and nucleotides are recognized as inflammatory mediators.
- Neutrophils are the most abundant white blood cells recruited to the early inflammatory periodontal lesion.
- The early response that initiates the inflammatory cascade begins with expression of cell adhesion molecules on endothelial cells and secretion of various cytokines such as lL-8 and MCP-l in response to the bacterial stimulus that recruits neutrophils to the site of invasion.
- If the first line of defense fails to clear the bacteria, the lesion matures as described histologically by Page and Schroeder, the established chronic gingivitis lesion exhibiting all the components of an immune lesion with T-cells, B-cells and antibody-secreting plasma cells. The trigger for transition from the established (stable) gingivitis lesion to the advanced or progressing periodontitis lesion remains elusive, but it is known that it is characterized by a continuous and uncontrolled response by neutrophils. Interestingly, it would appear that in the progressing immune lesion of periodontitis, there is continuous neutrophil activation leading to ‘neutrophil-mediated tissue injury’.
Question 5. Discuss host modulation therapy in periodontal disease management.
Answer. Concept of host modulation was first introduced by William (1990) and Golub et al (1992).
- William introduces the concept of NSAIDs and host modulation with tetracycline while Golub et al introduce chemically modified analogues.
- Here term ‘modulation’ refers to the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment.
- Concept of host modulation in periodontics is the treatment concept which aims to decrease tissue destruction and also the regeneration of periodontium by modifying the destructive aspects of the host response and upregulating protective or regenerative process.
- For fighting against the pathogenic bacteria, normal defensive immune-inflammatory reaction is essential but ameliorating excessively elevated inflammatory process to enhance the opportunities for wound healing is the host modulation therapy.
- Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes which involve in the physiological degradation of extracellular matrix and basement membrane. Other stimulators of bone resorption are parathyroid hormone (PTH), macrophage colony stimulating factor (M-CSF), receptor activator of NFab (RANK), RANK ligand and 1,25-dihydroxy vitamin D3.
- Several inhibitors are there to combat the stimulators of bone resorption; they are interferon gamma (IFN -γ), osteoprotegerin, estrogens, androgens, calcitonin and IL-1ra (receptor antagonist).
- Modulation of such host responses is possible and beneficial. Basically, there are three potential approaches to the host modulation:
- Use of anti-inflammatory drugs for blocking prostaglandins and proinflammatory cytokines.
- Inhibiting MMPs with antiproteinases.
- Inhibiting activation of osteoclast with sparing agents.
Drugs Leading to Host Modulation
- NSAIDs: They play an important role in treatment of periodontal disease. There mechanism of action includes decreased PMNL migration; decrease in vascular permeability and decreased platelet aggregation. Various drugs which are studied are ibuprofen, flurbiprofen, mefenamic acid and naproxen.
- Bisphosphonates: They inhibit bone resorption by disrupting the osteoclastic activity. E.g. alendronate.
- Tetracyclines (Subantimicrobial dose doxycycline): 20 mg of doxycycline is indicated as an adjunct to scaling and root planning. It has anti-collagenase effect. It is taken twice daily for 3 months or till 9 months. It is marketed as periostat.
- Growth factors, bone morphogenic protein and enamel matrix proteins: Currently approved by FDA for adjunctive use during surgery. Most commonly marketed brand is Emdogain.
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