Gingivitis refers to the inflammation of soft tissues, surrounding the teeth. Inflammation in gingivitis is restricted to the gingiva unlike periodontitis where inflammation extends to other periodontal tissues like periodontal ligament, cementum and alveolar bone. The primary etiology of gingivitis is dental plaque which comprises predominantly of bacterial communities in a matrix of exfoliated epithelial cells, bacterial and salivary proteins. Gingivitis however could also be caused by systemic diseases, allergies, medications, hormones, viruses and many other factors. Gingivitis starts off by an inflammatory process being triggered by dental plaque. The bacteria and their toxins from the gingival sulcus penetrate through the intercellular gaps in the junctional epithelium to enter the underlying connective tissue. Events leading to the causation and progression of gingivitis are, for the sake of comprehension, divided into three stages. Stage I is referred to as the “Initial lesion”, Stage II is the “Early lesion” and Stage III is the “Established lesion”. Stage I is basically, microorganisms in the dental plaque triggering the inflammatory process. This starts within 2-4 days of plaque accumulation. Bacteria and their toxins after entering the connective tissue stimulate or activate cells like mast cells or neutrophils to produce vasoactive mediators of inflammation, that cause vasodilation of the capillaries and increase blood flow. Along with vasodilation, mediators of inflammation also increase vascular permeability which leads to escape of plasma fluids containing proteins. This is called an exudate. It is this exudate that escapes out via the sulcus as the gingival crevicular fluid! There is margination or adherence of leukocytes in the capillary vessel finally leading to diapedesis or escape of leukocytes, primarily neutrophils. Escaped neutrophils via a process called chemotaxis, migrate to the area of insult and accumulate in the connective tissue below the sulcular and junctional epithelium. Neutrophils also penetrate the epithelium. Clinically, this stage may not show any symptoms but may present with exudation of gingival crevicular fluid. Persisting inflammation may result in the health status of gingiva deteriorating and disease progressing to the next stage of gingivitis. Now, stage II of gingivitis may start within 4-7 days and persisting inflammation leads to further recruitment of leukocytes like lymphocytes, monocytes as well as macrophages. Also present are plasma cells and mast cells. However, this stage is characterised by the predominant accumulation of lymphocytes. Apart from vasodilation of vessels caused by vasoactive substances, lymphocytes and macrophages produce growth factors which help in angiogenesis and further proliferation of capillaries. Junctional epithelium at this stage becomes densely infiltrated with neutrophils. Under the microscope, neutrophils can be seen engulfing bacteria in the sulcular area. Now, there are some important events that happen as a result of this dense inflammation. So, after accumulation of inflammatory cells in the connective tissue, the cells in an attempt to destroy invading bacteria also cause collateral damage to the surrounding tissues. On ingestion of bacteria, leukocytes produce numerous enzymes and free radicals to degrade bacterial agents. However, the enzymes are also released extra-cellularly, causing damage to surrounding tissues, especially vascular tissue and collagen. As a result, 70% of collagen is damaged, predominantly the circular fibres and dento-gingival fibres. Also, the inflammation may trigger proliferation of the junctional epithelium which starts to show development of rete ridges. The increased capillary density and vasodilation of capillaries in this stage are responsible for the erythema and bleeding on probing that may appear clinically. Stage III is when gingivitis has become chronic and is moderately to severely inflamed. Now, persistent inflammation, vasodilation and continuous leak of plasma proteins or exudate from the vessels lead to an increased viscosity of blood. This leads to a slow and almost stagnant blood flow. Red blood cells escape to the connective tissue and hemoglobin is broken down into pigments which may further redden the already erythematous gingiva. It's important to note that this stage is characterised by the intense chronic inflammation predominated by plasma cells. Proliferation of rete ridges from junctional epithelium into the connective tissue is pronounced and there is further destruction of collagen. Clinically, the chronically inflamed gingiva is edematous, boggy and is deep red or bluish red. The bluish hue is due to the sluggish blood flow which may cause anoxemia or a deficiency of oxygen in blood. Gingiva easily bleeds and exudate can be seen oozing out of the gingival sulcus.