3 Means of diagnosis and therapy of common dental diseases 3.1 Dental Caries When talking about dentistry, one must instantly think about dental caries, as it is the most common chronic disease in the human body. Epidemiologic studies show us that caries occur all over the world with a higher tendency in Latin American countries, countries in the Middle East, and South Asia, and least prevalent in China. The prevalence of this disease exceeds 70% based on research that had started in 2001 in USA, Philippines, China, Taiwan, Brazil, Argentina, Mexico, Uk, Norway and Armenia. Dental caries affects people of all ages (4) (33) (34).
This disease is a basically a continuous destructive process in all the hard tissues of teeth, that usually start on an intact tooth surface and there are several factors contributing to this result. These factors are divided to endogenous and exogenous. Both type of factors are needed to complete the mechanism and pathophysiology of this process. The exogenous factors are hereditary, sexual, hormonal, radiation, general diseases or anything that else that may affect saliva, the shape of the teeth, their position, their histological and biochemical composition. The edogenous factors are: microorganisms, saccharides taken from food and drinks and time. Combining the factors leads to the microorganism that are found in the mouth are fermenting the saccharides of food remaining in the oral cavity, for their needs in growth and replication and promote a release of acids as their waste products, usually lactic acid. These acids demineralize the hard hard tissue of the tooth creating an acidic environment and weaken the surface, making it more susceptible to bacterial colonization and growth. Saliva on the other hand, has buffering activity due to the neutral pH it contains, and antimicrobial activities because it contains Immunoglobulin A, Lactoferrin, Peroxidase andLysozyme and therefore balances the acidic environment, along with destroying the microorganisms and preventing them from growing, as
part of the process called remineralization. Dental caries will occur over time, as demineralization overcomes its opponent remineralization. Usually the predilected location where caries are formed, are those that lack the sufficient passage of saliva (4) (35) (36) (37).
Dental caries were classified under several criteria, with the most popular classification being the one created by Greene Vardiman Black according to the location of the caries lesion (4), with 1 being the most common and 5 being the less common. In the previous chapter the anatomy of the teeth was explained and this will help in better understanding this and most classification systems that will be mentioned (4).
3.1.1 Classification of dental caries Black classes are described as following: when the cavity originates in the pits and fissures of molar and premolar teeth, or foramen ceacum of lateral incisor and lower first molar, we grade it as the first class of Black classification, or Black 1. In Black 2 the caries lesion originates in occlusal and approximal surfaces of molar and premolar teeth. The next class, Black 3, deals with the anterior teeth, where the lesion originates in their approximal Figure 1 Dental caries on occlusal surface. Notice the depth of the fissure, which suits to be an ideal predilected location for dental caries (Source: DentistryGo) surfaces without altering their incisal edge. Black 4 is on the anterior teeth as well, but in this case the lesion affects the incisal edge as well as the approximal surfaces. The last class by G.V.Black deals with every tooth, both dental arches but it is valid only when the lesion originates in the cervical one third of the crown. A sixth class has been added as well, but not by G.V.Black and describes caries that originated only in the cusps of molar and premolar teeth (4) (38).
Figure 2 Black Classification with surfaces affected: L- Lingual, B - Buccal, F - Frontal (Source: TeethGeek) Another major classification of dental caries is the G. J. Mount’s classification, where it describes caries according to the site of the lesion, and the size. The first site classification is similar to Black 1, as it describes a lesion located in pits, fissures or smooth surfaces. The second site is similar to Black classes 3, 4 and 5 as it describes lesions below contact areas and finally the third site, similarly to Black 4, describes the lesion close to gingival margins, or deeply in the cervical area of the crown after the gingival have been pathologically destroyed and exposed that site (39). The size classes in Mount’s classification use the dentine as checkpoint, where class 1 mentions minimal involvent of dentine in the lesions, moderate involvement in class 2, enlarged involvement, where an ordinary tooth filling treatment is likely to fail and excessive loss of tooth in class 4 (39). Other ways of classifying dental caries are according to various parameters of the lesion such as: the topography and tissue affected, for example crown – enamel, dentine or mixed, or root – cementum, dentine, mixed -the site on teeth is another parameter used for classifying and the sites which are commonly involved are the pits and fissures, the approximal surfaces, the smooth surfaces and the gingival third of the crowns, the dental hard tissue which is affected, the intactness of tissue on which it appears where primary caries appear on a surface previously not affected by caries, secondary caries appear next to filling or next to its margins, recurrent caries, which appear under a filling of a previous cavity and stopped caries, a caries process which started but was stopped, as the process of remineralization had a higher influence than demineralization, - the speed the leasion spreads and progresses where acute caries progresses very quickly and destroys a big amount of dental hard tissue very soon and chronic caries which spreads very slowly and defensive reactions may stop the spread, - the proximity to pulp where superficial caries is the lesion located only in enamel, caries media is located in the proximal half of dentin, deep caries, the lesion is on the distal part of dentin, caries profunda pulpae proximae describes the lesion being very close to the pulp and caries profunda ad pulpam penetrance where the lesion penetrated the pulp chamber and has reached the dental pulp, -the shape and spread in dentine where dental caries undermine is a small lesion in enamel and extensively large
in dentine and dental caries penetrance where the lesion moves from enamel to dentine toward the pulp (39). Special types of dental caries are, for example, rampant caries where multiple active caries lesion are seen in the same patient and it frequently involves surfaces that are normally unaffected by caries, bottle caries, the lesions caused when babies frequently suck sweet drinks from nursing bottles and these types of lessions usually appear on the palatal surfaces of upper incisors and radiation caries as a result excessive radiation towards the head and the neck, by any source, causing reduced saliva production and therefore loss of its defensive functions (39).
3.2 Pulpal Diseases In the morphology of the tooth, we described the dental pulp, the inner most structure of the tooth located in the pulp chamber and also the structure responsible for the vascular supply and innervations of the tooth. When the pulp is affected by any pulpal disease, the state of vitality must be understood in order to make a correct diagnosis and treatment plansto choose the most suitable approach for a successful treatment. Those states are usually classified as following: Healthy –vital- pulp, reversibly damaged pulp, irreversibly damaged pulp – dyingand necrotic pulp –dead (40) (41). There are several methods when it comes to identifying the state of vitality of the pulp. The most commonly used are applying heat or cold, electric current, radiography and drilling the tooth without anesthesia, however no single method has been proven to be the best and this usually forces the practitioner to use a combination of the aforementioned methods (40) (42). When applying cold on the tooth, usually ethyl chloride is used by soaking a cotton wool in it, or just plain ice formed as a stick after we have made sure that the surface is dry. A normal response to this is a fast painful response in the frontal teeth and a slower to the posterior teeth due to their grater mass. Unusual responses to cold vary from no response, suggesting that the pulp is necrotic, exaggerated response, suggesting that the pulp is inflamed, or prolonged response suggesting that the pulp when traumatized. Heat usually gives similar responses, but care must be taken in order to properly heat the tooth. For application of heat, a heated guttapercha cone is used – a material that is primarily being used for filling root canals- and again the surface of the tooth must be dried using the triple syringe (40).
A more advanced method of assessing the vitality state is the electric pulp tester. This device is battery operated and its electrode must touch the tooth to be tested along with using a conducting paste. When it comes to choosing which surface the tester should be touching, there no proof of one surface being the best and usually the dentist proceeds based on his experience or with the instruction of the manufacturer of the device. The circuit completes after placing the ground electrode on the patients lip. The test begins with the lowermost current, gradually increasing until the patient feels a sensation, the current that elicited the sensation is recorded and the neighboring teeth are tested as well (40). Radiographic investigation is done to visualize any evidence that suggest a change in the pulp or adjacent structure morphology. A periapical radiograph is the first radiographic method of choice, as it provides a quality image of both coronal and apical parts of the pulp. The image is examined to identify whether or not the pulp is irritated by dental caries, or if radiolucencies are present in the periapical region, pulp resorption and to assess reparative dentine. Finally when all the methods fail to give an impression of the state of vitality, the tooth suspected of pulpal disease is drilled without anesthesia. If the patient doesn’t feel any pain when dentine is drilled, it means that the pulp is necrotic. If a sensation is felt then the pulp us vital, however there is still no answer to whether the pulp is damaged or not (40). A percussion test helps identifying whether there is inflammation, by gently hitting the tooth on the occluding parts and vestibular surface with the opposite side of a dental probe, however this test does not provide evidence of pulpal necrosis (40) (43). For a pulpal disease to emerge, several factors may cause it to undergo changes. More commonly, these factors are microbial. Microbes may enter the dental pulp through dental caries, through a lesion around the apex of the root– periapical lesion, or via the bloodstream. Microbial factors contribute to approximately an 80% of the cases of patients suffering from an abnormal dental pulp. Less commonly, the causes may an electrical current form source, thermal conduction by food, dissimilar metallic filling, chemical, barometric changes (30) (40). The pulpal diseases are classified as reversible, a case where the damaged may be controlled and the dental pulp may be healed, or irreversible the case where the damage to the dental pulp cannot be controlled anymore and the pulp has to be removed in order to prevent any further pathologies. From reversible to irreversible, there is a continuous process that starts from a healthy dental pulp that will eventually lead to pulpal necrosis (30) (40).
3.2.1 Hyperemia Hyperemias a condition characterized by increased blood pressure throughout the dental pulp, but the pulp is usually not irreversibly damaged. Histologically, the capillaries on the inner side of odontoblasts dilate and erythrocytes move through those capillaries to pulp, great numbers. Also, the pulp is infiltrated by many cells such as leukocytes, plasma cells and macrophages, and the nuclei of endothelial cells separate from each other. The odontoblasts move towards the dentinal tubules as a defensive response and the pulp becomes swollen (44) (45). Clinically, the patient feels pain only due to pressure, where in other cases of pulpal disease, if pain exists it may be felt spontaneously. Pain in hyperemia lasts as long as the reason it was provoked, exists or even slightly after that and it is felt as a short, sharp, shock. What may provoke the pain usually comes from eating, things like heat, cold, sweet, sour and pressure. The tooth affected, appears to have a lesion or a very big restoration close to where the dental pulp is situated. Therefore, this type of pain it is also possible even without a caries lesion, in cases were a new restoration was placed, after root planning or curettage or after the tooth has been prepared for a prosthetic crown. The tooth is vital and the percussion test comes negative, as no inflammation is present on the periapical area. Hyperemia is treated by indirect pulp capping (44) (45).
3.2.2 Acute serous pulpitis Theoretically is classified as partial and total, though clinically is nearly impossible to assess. Histologically acute serous pulpitis has similar features with hyperemia, as the dilation of the capillaries, the swelling and the invasion of cells happen in acute serous pulpitis too, though the main cells that infiltrate in this occasion, are the polymorphonucleocytes. The different features are the serous exudations the pulp and the destruction of especially at the site of exposure (45) (46). Clinically the pain may arise spontaneously and to a cold stimulus as well. In partial pulpitis the pain arises usually in intervals, where in total, the pains is continuous and the patient feels pain in other areas of the side affected, for example the eyes. The pain gets stronger while the disease is progressing. The patient is unable of saying which tooth hurts and usually complains about being unable to sleep due to the pain that is felt. Another complain of the
patients is that typical painkillers did not alleviate the pain, but in partial pulpitis they might be helpful. Usually the vitality test shows a hypersensitivity to cold and the percussion test is positive because of the periapical inflammation. What frequently causes this condition is a very big lesion near or over the dental pulp or a very big restoration near the dental pulp. This disease is treated by an endodontc treatment (45).
3.2.3 Acute purulent pulpitis Histologically this condition is similar to acute serous pulpitis, except the fact that there is purulent exudation and there may be parts where the pulp appears necrotic. Clinically the pain may arise spontaneously or to hot stimuli, as cold usually removes the pain, it is persisting and pulsating and may appear any time in the day or night. Patients may complain also in this condition of inability to sleep and that the painkillers were ineffective and they might have fever and enlarged lymph nodes. The tooth is vital and the percussion test is positive. A large
Figure 3 Abscess formation in apical periodontitis
restoration or dental caries close to or exposing the pulp may cause this disease. To treat this disease, the pulp chamber is trepanated and after two weeks, approxiamtely an endodontic treatment follows (45) (46).
3.2.4 Acute apical periodontitis Acute apical periodontitis is a disease in the periapical region of the toot’s root, where inflammation is present, and it is associated with extreme pain. The cource of this disease is divided into four stages, the periodontal stage, the endosseus stage, the subperiosteal stage and the submucous stage. In the periodontal stage, there is hyperemia of blood vessels and oedema, thing seen histologically, adn clinicallt the tooth is painful to pressure when eating, and there is a feeling that that tooth is slightly elevated in relation to the neighbouring teeth. In the endosseus stage, the bone is involved first by hyperemia of vessels then by leukocytic infiltration and finally by pus formation and clinically intensive pain, continuous and pressing pain and a stronger feeling of an elevated tooth. In the subperiosteal stage, beneath the periosteum leading to subperiosteal abscess and clinicallt the pain increases in intensity and the tooth becomes extremly sensitive to touch. Finally in the submucous stage, pus in soft tissue forming a submucous abcsess and the symptms of pain decrease. This disease usually caused after a pulp became necrotic, but other factors may cause it suchs as bacteria or bacterial toxins found after a pulpal disease, trauma of teeth, leading to formation of cracks thus allowing bacteria or chemical irritants to enter the dental pulp (45) (47). The treatment of this disease is more complex that other diseases, due to formation of abscess and a great amount of bacteria, therefore the patient must visit the dentist four times, if everything goes according to the treatment plan. The treatment for acute apical periodontitis in the first and second stages is as following: In the first visit, the dentist will enter the pulp chamber to drain the root canal and insert intracanal medicaments, with antibiotics in cases where an abscess has been formed and temporarily fill the tooth for approximately 2 weeks. In the second visit, an endodontic treatment is performed only in the coronal two thirds of the root canal and the tooth is filled temporarily. In third visit the whole canal is prepared, intracanal medication is inserted and the tooth is filled temporarily for the last time, because in the fourth and final visit, the tooth will restored with a permanent restoration (45) (47). In cases were this disease is in the third or fourth stage, the treatment plan is different and it is as following: in the first visit an incision and drainage are made to the abscess location and trepanation of pulp chamber. In the second visit, the root canals are prepared and intracanal medication is inserted. In the third visit the root canals are filled and finally in the fourth visit, the tooth is permanently restored (45) (47).
3.2.5 Chronic apical periodontitis Chronic apical periodontitis can be either of initial chronic development or as an outcome of a change from acute to chronic nature. It is usually associated with long standing restorations such as prosthetic crowns, extensive bridges, composite or amalgam filling or with bruxism, incorrectly occluding filling and dental caries. Typically, the lesion is located at the root apex, but communications may exist at various levels along the root surface, and lesions may develop at lateral locations. Chronic apical periodontitis shows replacement of adjacent tissue with an inflammatory cells which produce granulation tissues for repair of damaged area. In addition to the inflammatory cells, it typically contains fibrous tissue and often cholesterol crystals, as well as proliferating strands of epithelium derived from the cells of Malassez. It may develop a cyst cavity, which is lined in part or in full by epithelium (45) (47). Clinically, the patient is usually found without any symptoms except the case of an acute exacerbation, or very mild symptoms such as light pain. A small swelling may be present with formation. Usually the color of the tooth changes, the vitality is negative and the tooth might be a bit tender to percussion. Treatment is usually complete endodontic therapy. To treat this disease, one visit can be enough for root canal therapy and permanent restoration of the tooth by in cases of acute exacerbation several visits may be needed, or other procedures should be performed, such as apicoectomy and resection of the root (45; 47).
3.2.6 Chronic puplitis Chronic pulpitis is considered to be an asymptomatic type of pulpal disease. It produces a mild, poorly localized pain that sometimes comes and goes over a period of weeks or even months. If left untreated the pulp usually dies causing the symptoms of chronic pulpitis to disappear; however, symptoms of periapical changes may appear later. This type of pulpits is classified into closed or open, according to the state of the pulp chamber. The closed forms are “clausa”, “granulomatosa interna” and “a tergo”, while the open forms are “aperta ulcerosa” and “aperta hypertrophica” (45).
3.2.6.1 Chronic closed pulpitis-“clausa” Chronic close pulpitis is histologically similar to other forms of pulpitis as necrosis of parts of the pulp occur also, along with cell infiltration and formation of crhonic abscess.
Clinically, there is mild pain but usuallt no pain at all. Usally this occurs when theres a caries lesion next to the pulp chamber or a big restoration next to pulp. Vitality is negative or hyposensitive and percussion test is negative (45).
3.2.6.2 Chronic closed retrograde pulpitis Chronic closed retrograde pulpitis - atergo describes the pulpitis in which the source of infection enters the pulp chamber throgh the root canal from deep periodontal pockets, hence, the first morphological changes are in the root part of the pulp. Clinically, no pain also but deep periodontal pockets exist. Tooth may otherwise be completely healthy, without caries. Treatment of the periodontal pocket and endodontic therapy are essential in this disease (45).
3.2.6.3 Chronic granulomatous pulpitis Chronic granulomatous pulpitis- granulomatosa interna, also might produce mild or no pain at all and what is typical about this disease is there is a granuloma on the pulp and if it is located on the coronal part of the tooth, is shines through its mass and looks like a pink spot (45).
Figure 4 A pink spot on the permanent upper left central incissor is shown, as a result of chronic granulomatous pulpitis (Source: DrChetan)
3.2.6.4 Chronic open ulcerous pulpitis Chronic open ulcerous pulpitis -aperta ulcerosa, in this condition ulcers appear in the superficial parts of the pulp, mainly cause by mechanical or chemical irritation of the pulp. A large restoration near or over the pulp is responsible, dental caries. Pain in this case, may only be associated with irritation of the ulcer. Though in chronic pulpitis the percussion test is generally negative, in ulcerous pulpitis is positive, just because the ulcer is irritated when the tooth is be hit (45).
3.2.6.5 Chronic open hypertrophic pulpitis Chronic open hypertrophic pulpitis - aperta hypertrophica, an uncommon condition, usually found in children and young people affecting a tooth with caries. It is characterized by a soft tissue mass growth out of the affected pulp wich bleeds on mechanical irritation (45).
Figure 5 A clinical picture of a tooth, where a hypertrophic mass extends form its crown (Source: )
3.2.7 Necrosis of the dental pulp Necrosis of the pulp is when inflammatory changes in the pulp eventually progress to pulpal necrosis. The pulp chamber and root canals are closed organs, unable to accommodate
Figure 6 A clinical picture of a necrotic permanent upper left cental incissor, which shows loss trasperancy and discoloration (Source: )
swelling; when the tissue is edematous enough pressure on the blood vessels occludes them; this causes the pulp to die eventually from lack of blood supply. Necrosis can be simple necrosis where there are no evident changes in pulpal structure, or coagulative necrosis where an albumin
rich fluid is found in the pulp. Necrosis is generally a painless condition, but the tooth is discolored and its transperacy is lost. A large restoration or large lesion is responsible for the formation of this lesion (45).
3.2.8 Gangrene of the dental pulp Gangrene of the dental pulp occurs when a necrotic pulp is infected with microorganisms. Histologically, gangrenes is divided to dry gangrene in which there is a breakdown of cell elements and wet gangrene in which the dental pulp has changed to a liquid substance with a large amount of microorganisms. Clinically gangrene is divided to closed, where pulp chamber is closed and open. Gangrene is generally a painless condition, as pain may only occur in closed gangrene and only for hot stimuli. In this condition also the tooth’s color changes and its transperacy is lost. A large restoration or large lesion is responsible for the formation of this lesion (45).
3.3 Periodontal diseases 3.3.1 Pockets formation A gingival pocket, is a pathologic space that develops as a consequence of gingival hyperplasia, therefore the junctional epithelium is not damaged. It is the space between hyperplastic gingival tissue and enamel surface. This process of the pocket formation is reversible. Depth of gingival sulcus is more than 2mm and the soft base of the junctional epithelium is felt and it measure as the distance from the tip of the probe to the gingival margin. A periodontal pocket is a pathologic space that develops after destruction of the junctional epithelium. It is the space bordered by root cementum and alveolar bone and gingival mucosa that is based by inflamed granular tissue. This process is irreversible. It is measured for the tip of the probe to the junvction between enamel and cementum where the rough surface of cementum and Alveolar bone are felt (48) (49).
3.3.2 Gingival recession Gingival recession is the apical movement of gingiva, that causes exposure roots the juctional epithelium is not damaged and it move along with the rest of the gingival tissue making the neck of the tooth and parts of roots of teeth, visible. This may be cause by a number of hereditary predisposing factors such as abnormal position of teeth, thin gingival narrow attached gingival, or by othe acquired factors such as: meachanical irritation during toothbrushing, with ir without a hard toothbrush , bad habits that involve putting fingers or other objects in the mouth, such as pens, piercings, inflammatory changes (49) (50).
3.3.3 Periodontitis Periodontitis is the inflammatory condition of the periodntium and there are several types of this condition with different etiology and onset time. Chronic periodontitis is most common in adults although the onset (first clinical signs) of the disease is during or after puberty The disease progresses in a relatively slow rate and it is associated with plaque, which accumulates in the oral cavity due to bad oral hygiene. Over time bacteria influence the periodontal tissues and cause their destruction, this is why this disease usually manifests in a later age. Microbes of chronic periodontitis are over seventy five percent Gram positive. Clinically in crhonic periodontitis usually entails a long - term bleeding and most likely during tooth brushing. Periodontal pockets are found in the patient, usually on approximal surfaces and sometimes a purulent exudation with fetor ex-ore is presesent. Refractory periodontitis, a condition of which the etiology was unknown for 30 years, but microbiologically is found to be the bacterium aggregatibacter actinomycetemcomitans. Patients with high concentration of this bacterium, also have a higher serum saliva and gingival exudate antibodies against this bacteria but the disease is successfully treated only when the bacterium is removed from periodontal pockets (49) (51) (52). Aggregatibacter actinomycetemcomitans may not the cause of all periodontal diseases, but it is always present in microbial samples of periodontal disease. This bacterium is able of adhering to host tissues, it is able to grow and reproduce in host environment, damage of host defense mechanism and damaging of host tissue (49) (51).
Figure 7 The lower jaw of a patient with gingival recesion, due to periodontitis (Source: Colgate Professional)
3.3.4 Gingivitis Chronic gingivitis results from chronic inflammation with hyperemia, edema, and celllar inflammatory infiltration. The inflammatory reaction, which is visible microscopically and clinically, represents the host’s response to bacteria and its products. These bacteria are: Actinomyces species, Streptococcus species, Veiolonella species, Fusobacterium species, Treponema species, Prevotella intermedia (main bacteria responsible for gingival inflammation). Clinically chronic gingivitis ranges between small bleeding spots to advanced gingivitis. Attached gingiva is not affected unless a systemic disease is present. There are 4 clinical phases to the development of chronic gingivitis: the first phase consists of bleeding on probing of gingiva even thought their texture appears to be normal and the patient notices that during toothbrushing. In the second phase the marginal gingiva and interdental pailla become more red than pink and the papilla has a rounded tip, and bleeding and swelling are present. In the third phase there is more intensive redness, edema and enlargement of the interdental papilla with a shiny surface. The stippling texture is lost, the gingival bleed it is for possible pus formation and exudation to exist when the interdental papilla is pressed. In the fourth and final phase, gingival
hyperplasia occurs and intensive bleeding that may be spontaneous.Chronic gingivitis is not associated with pain (49) (52). Complex forms of gingivitis appear when bad oral hygiene lead to excessive plaque accumulation and there is presence of local or systemic risk factor such as: mouth breathing, usually due to a nasal polyp obstructing the nose, pregnancy, puberty, leukemia, drugs, hereditary, AIDS (49).
Figure 8 Various stages of periodontal diseases (Source: OraMD)