Cross section of a tooth. Non-dentin layer is covered by enamel or cementum and gingiva. An odontoblast cell showing odontoblast process (not in proportion – in reality this process is far longer than the body of the cell). The real cause of<unk>  is controversial. There have been several theories put forward to try and explain the cause of<unk> . These include the odontoblastic transduction theory, the neural theory and the hydrodynamic theory. The most commonly accepted model is called the hydrodynamic or fluid movement theory proposed by Brannstrom in 1964. According to this theory, when the exposed<unk> e surface is subjected to thermal, chemical, tactile or evaporative stimuli, the flow of the fluid within the tubules will be increased. Fluid movement inside the<unk> al tubules may be away from or towards the pulp.<unk> e contains many thousands of microscopic tubular structures that radiate outwards from the pulp; these<unk> al tubules are typically 0.5-2 micrometres in diameter. Changes in the flow of the plasma-like biological fluid present in the<unk> al tubules can trigger mechanoreceptors present on nerves located at the pulpal aspect, thereby eliciting a pain response. This hydrodynamic flow can be increased by cold, (air pressure), drying, sugar, sour (dehydrating chemicals), or forces acting on to the tooth. Hot or cold food or drinks, and physical pressure are typical triggers in those individuals with teeth sensitivity. Movement of<unk> al fluid away from the pulp can be caused by triggers such as cold and drying and movement towards the pulp can be caused by heat. Research has shown that triggers causing<unk> al fluid to move away from the pulp elicit more of a painful response. The odontoblastic transduction theory was suggested by Rapp et al. and puts forward the idea that odontoblasts act as receptor cells, and conduct impulses via synaptic junctions to the end of the nerves and therefore cause the feeling of pain. However, there is not much evidence to support this theory. The neural theory proposes that thermal or mechanical stimuli can directly influence nerve endings within the<unk> al tubules via direct communication with the nerve endings of the pulp. There are two common ways in which<unk> e can be exposed; gingival recession and tooth wear. The main cause of DH is gingival recession (receding gums) with exposure of root surfaces, loss of the cementum layer and smear layer. Receding gums can be a sign of long-term trauma from excessive or forceful toothbrushing or abrasive toothpaste (dental abrasion), or a sign of chronic periodontitis (gum disease). A less common cause is acid erosion, which is the loss of hard dental tissues due to acids e.g. related to gastroesophageal reflux disease, bulimia or excessive consumption of acidic foods and drinks. Repeated exposures to a low pH cause the mineral content of the teeth on the outer layer of enamel to dissolve therefore leaving the<unk> e exposed and leading to<unk> . Other causes include dental bleaching, smoking tobacco (which can lead to recession and therefore sensitivity) cracked teeth and abfraction or grinding of teeth. Evidence of abfraction may be shown by wedge shaped defects that are developed at the cervical region of the teeth known as abfraction lesions. There is no direct relationship between abfraction lesions and diet, periodontal disease or abrasion. Most experts on this topic state that the pain of DH is in reality a normal, physiologic response of the nerves in a healthy, non-inflamed dental pulp in the situation where the insulating layers of gingiva and cementum have been lost; i.e.,<unk>  is not a true form of allodynia or hyperalgesia. To contradict this view, not all exposed<unk>  surfaces cause DH. Others suggest that due to the presence of patent<unk> al tubules in areas of hypersensitive<unk> , there may be increased irritation to the pulp, causing a degree of reversible inflammation.
Dentin hypersensitivity
Dentin dysplasia
Tooth ankylosis
Ligamentous laxity
Zaspopathy
Radiosensitivity
Accessory nerve disorder
Enthesopathy