Clinical signs of TRs are often minimal since the discomfort can be minor. However, some authors have described discomfort while chewing, anorexia, dehydration, weight loss, and tooth fracture. The lower third premolar is the most commonly affected tooth.

Clinical appearance is variable with presentation ranging from gray to yellowish brown, but the characteristic features is the translucent or opalescent hue to the teeth.

In Type I, primary teeth are more severely affected compared to the permanent dentition which has more varied features, commonly involving lower incisors & canines. Primary teeth have a more obvious appearance as it has a thinner layer of enamel overlying dentine, hence the color of dentine is more noticeable.

In Type II, both the dentitions are equally affected.

Enamel is usually lost early because it is further inclined to attrition due to loss of scalloping at the dentoenamel junction (DEJ). It was suggested that the scalloping is beneficial for the mechanical properties of teeth as it reinforces the anchor between enamel and dentine. However, the teeth are not more susceptible to dental caries than normal ones.

However, certain patients with dentinogenesis imperfecta will suffer from multiple periapical abscesses apparently resulting from pulpal strangulation secondary to pulpal obliteration or from pulp exposure due to extensive coronal wear. They may need apical surgery to save the involved teeth.

These features are also present in dentine dysplasia and hence, the condition may initially be misdiagnosed.

Type II would mostly cause discolouration to the primary teeth. Affected teeth usually appear as brownish-blue, brown or yellow. Translucent “opalescence” is often one of the characteristics to describe teeth with DD-2. In some cases teeth might show slightly amber coloured but in most of the cases permanent teeth are unaffected and appear normal regardless of colour, shape and size. Dental X-rays is the key to diagnose dentine dysplasia, especially on permanent teeth. Abnormalities of the pulp chamber is the main characteristic to make a definitive diagnosis.

In the primary teeth, coronal dentin dysplasia may appear similar to Dentinogenesis Imperfecta type II (DG-II) but if abnormalities features appear to be more pronounced in the permanent teeth, then consider changing the diagnosis to DGI-II instead of DD-2.

In other words, affect primary teeth usually have abnormal shaped or shorter than normal roots . “Crescent/ half-moon shaped” pulp chamber remnant in permanent teeth can be seen on x-rays. The roots may appear to be darker or radiolucent/ pointy and short with apical constriction. Dentine is laid down abnormally and causes excessive growth within the pulp chamber. This will reduce the pulp space and eventually cause incomplete and total pulp chamber obliteration in permanent teeth. Sometimes periapical pathology or cysts can be seen around the root apex. Most cases of DD associated with peri-apical radiolucency/ pathology have been diagnosed as radicular cysts, but some of them have been as diagnosed peri-apical grauloma instead.

Type I and II have similar radiographic features

- Total obliteration of the pulp chamber and root canals due to deposition of dentine

- Bulbous crowns with apparent cervical constriction

- Reduced root length with rounded apices

Type III shows thin dentin and extremely enormous pulp chamber. These teeth are usually known as "shell teeth".

Periapical radiolucency may be seen on radiographs but may occur without any apparent clinical pathology.

Feline Tooth Resorption (TR) is a syndrome in cats characterized by resorption of the tooth by odontoclasts, cells similar to osteoclasts. TR has also been called "feline odontoclastic resorption lesion" (FORL), neck lesion, cervical neck lesion, cervical line erosion, feline subgingival resorptive lesion, feline caries, or feline cavity. It is one of the most common diseases of domestic cats, affecting up to two-thirds. TRs have been seen more recently in the history of feline medicine due to the advancing ages of cats, but 800-year-old cat skeletons have shown evidence of this disease. Purebred cats, especially Siamese and Persians, may be more susceptible.

TRs clinically appear as erosions of the surface of the tooth at the gingival border. They are often covered with calculus or gingival tissue. It is a progressive disease, usually starting with loss of cementum and dentin and leading to penetration of the pulp cavity. Resorption continues up the dentinal tubules into the tooth crown. The enamel is also resorbed or undermined to the point of tooth fracture. Resorbed cementum and dentin is replaced with bone-like tissue.

Attrition occurs as a result of opposing tooth surfaces contacting. The contact can affect cuspal, incisal and proximal surface areas.

Indications of attrition can include:

- Loss of tooth anatomy: This results in loss of tooth characteristics including rounding or sharpening of incisal edges, loss of cusps and fracturing of teeth. Enamel of molar teeth may appear thin and flat. When in occlusion the teeth may appear the same height which is particularly apparent for anterior teeth.

- Sensitivity or pain: Attrition may be entirely asymptomatic, or there may be dentin hypersensitivity secondary to loss of the enamel layer, or tenderness of the periodontal ligament caused by occlusal trauma.

- Tooth discolouration: A yellow appearance of the tooth surface may be due to the enamel being worn away, exposing the darker yellower dentin layer underneath.

- Altered occlusion due to decreasing vertical height, or occlusal vertical dimension.

- Compromised periodontal support can result in tooth mobility and drifting of teeth

- Loss in posterior occlusal stability

- Mechanical failure of restorations

Acid erosion often coexists with abrasion and attrition. Abrasion is most often caused by brushing teeth too hard.

Any frothing or swishing acidic drinks around the mouth increases the risk of acid erosion.

Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging. Advanced and excessive wear and tooth surface loss can be defined as pathological in nature, requiring intervention by a dental practitioner. The pathological wear of the tooth surface can be caused by bruxism, which is clenching and grinding of the teeth. If the attrition is severe, the enamel can be completely worn away leaving underlying dentin exposed, resulting in an increased risk of dental caries and dentin hypersensitivity. It is best to identify pathological attrition at an early stage to prevent unnecessary loss of tooth structure as enamel does not regenerate.

Abrasion is a pathological, non-carious tooth loss that most commonly affects the premolars and canines. Abrasion frequently presents at the cemento-enamel junction and can be caused by many contributing factors, all with the ability to affect the tooth surface in varying degrees.

Sources of abrasion may arise from oral hygiene habits such as toothbrushes, toothpicks, floss, and dental appliance or may arise from other habits such as nail biting, chewing tobacco or another object. Abrasion can also occur from the type of dentifrice being utilized as some have more abrasive qualities such as whitening toothpastes.

The appearance may vary depending on the aetiology of abrasion, however most commonly presents in a V-shaped caused by excessive lateral pressure whilst tooth-brushing. The surface is shiny rather than carious, and sometimes the ridge is deep enough to see the pulp chamber within the tooth itself.

In order for successful treatment of abrasion to occur, the aetiology first needs to be identified and ceased, e.g. overzealous brushing. Once this has occurred subsequent treatment may involve the changes in oral hygiene or toothpaste, application of fluoride to reduce sensitivity or the placement of a restoration to aid in reducing the progression of further tooth loss.

There are many signs of dental erosion, including changes in appearance and sensitivity. One of the physical changes can be the color of teeth. There are two different colors teeth may turn if dental erosion is occurring, the first being a change of color that usually happens on the cutting edge of the central incisors. This causes the cutting edge of the tooth to become transparent. A second sign is if the tooth has a yellowish tint. This occurs because the white enamel has eroded away to reveal the yellowish dentin. A change in shape of the teeth is also a sign of dental erosion. Teeth will begin to appear with a broad rounded concavity, and the gaps between teeth will become larger. There can be evidence of wear on surfaces of teeth not expected to be in contact with one another. If dental erosion occurs in children, a loss of enamel surface characteristics can occur. Amalgam restorations in the mouth may be clean and non-tarnished. Fillings may also appear to be rising out of the tooth, the appearance being caused when the tooth is eroded away leaving only the filling. The teeth may form divots on the chewing surfaces when dental erosion is occurring. This mainly happens on the first, second, and third molars. One of the most severe signs of dental erosion is cracking, where teeth begin to crack off and become coarse. Other signs include pain when eating hot, cold, or sweet foods. This pain is due to the enamel having been eroded away, exposing the sensitive dentin.

Amelogenesis imperfecta (AI) is a congenital disorder that presents with a rare abnormal formation of the enamel or external layer of the crown of teeth, unrelated to any systemic or generalized conditions. Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it. Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel (ameloblastin, enamelin, tuftelin and amelogenin) as a result of abnormal enamel formation via amelogenesis.

People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey; this disorder can afflict any number of teeth of both dentitions. The teeth have a lower risk for dental cavities and are hypersensitive to temperature changes as well as rapid attrition, excessive calculus deposition, and gingival hyperplasia.

1-increased localised pressure.

2- focal growth retardation and stimulation.

Invaginatus is an anomaly resulting from invagination forming within the enamel organ. Invagination ranges pitting occupying most of the crown and root. Although examination may reveal a fissure on the surface of anterior tooth, radiographic examination is the way.

Tooth wear (also termed non-carious tooth substance loss) refers to loss of tooth substance by means other than dental caries or dental trauma. Tooth wear is a very common condition that occurs in approximately 97% of the population. This is a normal physiological process occurring throughout life, but accelerated tooth wear can become a problem.

Tooth wear is majorly the result of three processes; attrition, abrasion and erosion. These forms of tooth wear can further lead to a condition known as abfraction, where by tooth tissue is 'fractured' due to stress lesions caused by extrinsic forces on the enamel. Tooth wear is a complex, multi-factorial problem and there is difficulty identifying a single causative factor. However, tooth wear is often a combination of the above processes. Many clinicians therefore make diagnoses such as "tooth wear with a major element of attrition", or "tooth wear with a major element of erosion" to reflect this. This makes the diagnosis and management difficult. Therefore, it is important to distinguish between these various types of tooth wear, provide an insight into diagnosis, risk factors, and causative factors, in order to implement appropriate interventions.

Multiple indices have been developed in order to assess and record the degree of tooth wear, the earliest was that by Paul Broca. In 1984, Smith and Knight developed the tooth wear index (TWI) where four visible surfaces (buccal, cervical, lingual, occlusal-incisal) of all teeth present are scored for wear, regardless of the cause.

Enamel infractions are microcracks seen within the dental enamel of a tooth. They are commonly the result of dental trauma to the brittle enamel, which remains adherent to the underlying dentine. They can be seen more clearly when transillumination is used.

Enamel infractions are found more often in older teeth, as the accumulated trauma is greatest.

Enamel infractions can also be found as a result of iatrogenic damage inadvertently caused by instrumentation during dental treatments.

AI can be classified according to their clinical appearances:

- Type 1 - Hypoplastic

Enamel of abnormal thickness due to malfunction in enamel matrix formation. Enamel is very thin but hard & translucent, and may have random pits & grooves. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel differs in appearance from dentine radiographically as normal functional enamel.

- Type 2 - Hypomaturation

Enamel has sound thickness, with a pitted appearance. It is less hard compared to normal enamel, and are prone to rapid wear, although not as intense as Type 3 AI. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel appears to be comparable to dentine in its radiodensity on radiograpshs.

- Type 3 - Hypocalcified

Enamel defect due to malfunction of enamel calcification, therefore enamel is of normal thickness but is extremely brittle, with an opaque/chalky presentation. Teeth are prone to staining and rapid wear, exposing dentine. Condition is of autosomal dominant and autosomal recessive pattern. Enamel appears less radioopaque compared to dentine on radiographs.

- Type 4: Hypomature hypoplastic enamel with taurodontism

Enamel has a variation in appearance, with mixed features from Type 1 and Type 2 AI. All Type 4 AI has taurodontism in common. Condition is of autosomal dominant pattern.

Other common features may include an anterior open bite, taurodontism, sensitivity of teeth.

Differential diagnosis would include dental fluorosis, molar-incisor hypomineralization, chronological disorders of tooth development.

Early Childhood Caries (ECC), formerly known as nursing bottle caries, baby bottle tooth decay, night bottle mouth and night bottle caries, is a disease that affects teeth in children aged between birth and 71 months. ECC is characterized by the presence of 1 or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces in any primary tooth. ECC has been shown to be a very common, transmissible bacterial infection, usually passed from the primary caregiver to the child. The main bacteria responsible for dental caries is Streptococcus mutans (S. Mutans) and Lactobacillus. There is also evidence that supports that those who are in lower socioeconomic populations are at greater risk of developing ECC.

Erosion is chemical dissolution of tooth substance caused by acids, unrelated to the acid produced by bacteria in dental plaque. Erosion may occur with excessive consumption of acidic foods and drinks, or medical conditions involving repeated regurgitation and reflux of gastric acid. derived from the Latin word "erosum", which describes the action ‘to corrode’. This is usually on the palatal (inside) surfaces of upper front teeth and the occluding (top) surfaces of the molar teeth.

- Gastroesophageal reflux disease (GERD)

- Vomiting, e.g. bulimia, alcoholism

- Rumination

- Eructation (burping)

- Dietary - liquids of low pH and high titratable acids.

Early childhood caries (ECC) is a multi-factorial disease, referring to various risk factors that inter-relate to increase risk of developing the disease. These risk factors include but not limited to, cariogenic bacteria, diet practices and socioeconomic factors. Normally after 6 months, deciduous teeth begin to erupt means, they are susceptible to tooth decay or dental caries. In some unfortunate cases, infants and young children have experienced severe tooth decay called ECC. This can result in the child experiencing severe pain, extensive dental restorations or extractions. The good news is that ECC is preventable, however, still remains a large burden particularly towards health care expenditure.

Dentin hypersensitivity (abbreviated to DH, or DHS, and also termed sensitive dentin, dentin sensitivity, cervical sensitivity, and cervical hypersensitivity) is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.

A degree of dentin sensitivity is normal, but pain is not usually experienced in everyday activities like drinking a cooled drink. Therefore, although the terms "dentin sensitivity" and "sensitive dentin" are used interchangeably to refer to dental hypersensitivity, the latter term is the most accurate.

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

The aetiology of dental abrasion can be due to a single stimuli or, as in most cases, multi-factorial. The most common cause of dental abrasion, is the combination of mechanical and chemical wear.

Tooth brushing is the most common cause of dental abrasion, which is found to develop along the gingival margin, due to vigorous brushing in this area. The type of toothbrush, the technique used and the force applied when brushing can influence the occurrence and severity of resulting abrasion. Further, brushing for extended periods of time (exceeding 2-3 min) in some cases, when combined with medium/hard bristled toothbrushes can cause abrasive lesions.

Different toothbrush types are more inclined to cause abrasion, such as those with medium or hard bristles. The bristles combined with forceful brushing techniques applied can roughen the tooth surface and cause abrasion as well as aggravating the gums. Repetitive irritation to the gingival margin can eventually cause recession of the gums. When the gums recede, the root surface is exposed which is more susceptible to abrasion.

Comparatively, electric toothbrushes have less abrasive tendencies.

Types of toothpastes can also damage enamel and dentine due to the abrasive properties. Specific ingredients are used in toothpaste to target removal of the bio-film and extrinsic staining however in some cases can contribute to the pastes being abrasive.

Whitening toothpastes are found to be one of the most abrasive types of toothpastes, according to the RDA Scale, detailed below. In-home and clinical whitening have been proven to increase the likelihood of an individual experiencing dental abrasion. It is believed that dental abrasion due to the whitening process is caused by a combination of both mechanical and chemical irritants, for example, using whitening toothpaste and at home bleaching kits together. However, if an individual is regimented in their after-whitening care then they can avoid loss of dentine minerals and in turn abrasion can be avoided. (that contribute to developing abrasion).

Another factor that can contribute to abrasion is alteration of pH levels in the saliva. This can be sugary/ acidic foods and liquids. The reasoning behind this is that an increase in acidity of saliva can induce demineralization and therefore compromising the tooth structure to abrasive factors such as tooth brushing or normal wear from mastication. When the tooth structure is compromised, this is where the mineral content of the saliva can create shallow depressions in the enamel and thus, when brushed can cause irreparable damage on tooth surface. The dental abrasion process can be further stimulated and accelerated through the effects of dental Acid erosion.

The diagnosis of DH may be challenging. It is a diagnosis of exclusion, reached once all other possible explanations for the pain have been ruled out. A thorough patient history and clinical examination are required. The examination includes a pain provocation test by blasting air from a dental instrument onto the sensitive area, or gentle scratching with a dental probe. If a negative result for the pain provocation test occurs, no treatment for dentinal hypersensitivity is indicated and another diagnosis should be sought, such as other causes of orofacial pain.

Inflammation of the dental pulp, termed pulpitis, produces true hypersensitivity of the nerves in the dental pulp. Pulpitis is classified as "irreversible" when pulpal inflammation will irreversibly progress to pulpal necrosis due to compression of the venous microcirculation and tissue ischemia, and "reversible" when the pulp is still capable of returning to a healthy, non-inflamed state, although usually dental treatment is required for this. Irreversible pulpitis is readily distinguishable from DH. There is poorly localized, severe pain which is aggravated by thermal stimuli, and which continues after the stimulus is removed. There also is typically spontaneous pain without any stimulus. Reversible pulpitis may not be so readily distinguishable from DH, however usually there will be some obvious sign such as a carious cavity, crack, etc. which indicates pulpitis. In contrast to pulpitis, the pain of DH is short and sharp.

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels the nerves and connective tissue inside a tooth and provides the tooth’s blood and nutrients. Pulpitis is mainly caused by bacteria infection which itself is a secondary development of caries (tooth decay). It manifests itself in the form of a toothache.