Studies have also suggested that psychological/psychiatric factors, diabetes, gastrointestinal diseases and haematological disorders may predispose to GT however, more studies with a larger cohort are needed to determine if GT could be an oral manifestation of a systemic disease. There is strong evidence to support a high prevalence of celiac disease and iron-deficiency anaemia in patients with GT. Oral candidiasis and caries are commonly reported in patients with GT, however this can be explained by saliva of a lower pH which will promote the cariogenic process. Most common areas in which GT can be found include; the lateral border of the tongue, followed by the anterior dorsum of the tongue and ventral surface. Diagnosis
Diagnosis of Geographic Tongue (GT) mainly relies on clinical, intraoral findings. As GT is usually asymptomatic in the mouth it does not require treatment. A differential diagnosis between oral candidiasis and GT, two similar looking conditions, can be established through a careful and thorough examination. GT is a keratotic lesion which can be described as a round or irregular shaped white plaque, cannot be scraped off and is normally self-resolving. These lesions are known to reoccur within variable periods. Although rare, cytological techniques and biopsies can be done to aid in a clinical diagnosis. The cytological description can define the disease due to its inflammatory characteristics, with its main characteristic being nuclear demarcation. Furthermore, it is important to be aware that GT may be related to other extraoral and intraoral conditions.
Endocytic PRRs on phagocytes reflect these molecular patterns, with C-type lectin receptors binding to mannans and β-glucans, and scavenger receptors binding to LPS. Upon endocytic PRR binding, actin-myosin cytoskeletal rearrangement adjacent to the plasma membrane occurs in a way that endocytoses the plasma membrane containing the PRR-PAMP complex, and the microbe. Phosphatidylinositol and Vps34-Vps15-Beclin1 signalling pathways have been implicated to traffic the endocytosed phagosome to intracellular lysosomes, where fusion of the phagosome and the lysosome produces a phagolysosome. The reactive oxygen species, superoxides and hypochlorite bleach within the phagolysosomes then kill microbes inside the phagocyte. Phagocytic efficacy can be enhanced by opsonization. Plasma derived complement C3b  and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens. As well as endocytic PRRs, phagocytes also express opsonin receptors Fc receptor and complement receptor 1 (CR1), which bind to antibodies and C3b, respectively. The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the lysosomal elimination of the infective agent. Cell-derived mediators
* non-exhaustive list

Morphologic patterns
Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved. Granulomatous inflammation: Characterised by the formation of granulomas, they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, sarcoidosis, and syphilis. Fibrinous inflammation: Inflammation resulting in a large increase in vascular permeability allows fibrin to pass through the blood vessels.