CS4-4) The Role of Dental Calculus - Yakindogu Üniversitesi

YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Assist. Prof. Dr.Ayşe Çaygür Yoran Learning Outcomes: 1-Will be able to define calculus and distinguish it clinically. 2- Will be able to explain the causes of calculus formation and composition of calculus, list the theories of calculus formation. 3-...

YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Assist. Prof. Dr.Ayşe Çaygür Yoran Learning Outcomes: 1-Will be able to define calculus and distinguish it clinically. 2- Will be able to explain the causes of calculus formation and composition of calculus, list the theories of calculus formation. 3- Will be able to identify oral halitosis and list its causes. 4- Will be able to explain and clinically determine the iatrogenic and other predisposing factors that play a role in periodontal diseases. The Role of Dental Calculus and Other Local Predisposing Factors The primary cause of gingival inflammation is bacterial plaque. Other predisposing factors include calculus, faulty restorations, complications associated with orthodontic therapy, self-inflicted injuries, and the use of tobacco, in addition to several others. These will be discussed in turn. Calculus Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prostheses. Supragingival and Subgingival Calculus Supragingival calculus is located coronal to the gingival margin and therefore is visible in the oral cavity. It is usually white or whitish yellow in color; hard, with a claylike consistency; and easily detached from the tooth surface. After removal, it may rapidly recur, especially in the lingual area of the mandibular incisors. The color is influenced by contact with such substances as tobacco and food pigments. It may localize on a single tooth or group of teeth, or it may be generalized throughout the mouth. The two most common locations for the development of supragingival calculus are the buccal surfaces of the maxillary molars and the lingual surfaces of the mandibular anterior teeth. Saliva from the parotid gland flows over the facial surfaces of the upper molars via the parotid duct, whereas the submandibular duct and the lingual duct empty onto the lingual surfaces of the lower incisors from the submaxillary and sublingual glands, respectively. In extreme cases, calculus may form a bridgelike structure over the interdental papilla of adjacent teeth or cover the occlusal surface of teeth that are lacking functional antagonists. Subgingival calculus is located below the crest of the marginal gingiva and therefore is not visible on routine clinical examination. The location and extent of subgingival calculus may be evaluated by careful tactile perception with a delicate dental instrument such as an explorer. Clerehugh and colleagues used a World HealthOrganization no. probe to detect and score subgingival calculus.Subsequently, these teeth were extracted and visually scored for subgingival calculus. An agreement of 80% was found between these two scoring methods. Subgingival calculus is typically hard and dense; it frequently appears to be dark brown or greenish black in color, and it is firmly attached to the tooth surface. Supragingival calculus and subgingival calculus generally occur together, but one may be present without the other. Microscopic studies demonstrate that deposits of subgingival calculus usually extend nearly to the base of periodontal pockets in individuals with chronic periodontitis but do not reach the junctional epithelium. When the gingival tissues recede, subgingival calculus becomes exposed and is therefore reclassified as supragingival. Thus, supragingival calculus can be composed of both supragingival calculus and previous subgingival calculus. A reduction in gingival inflammation and probing depths with a gain in clinical attachment can be observed after the removal of subgingival plaque and calculus. Composition Inorganic Content. Supragingival calculus consists of inorganic (70% to 90%52) and organic components. The major inor ganic proportions of calculus have been reported as approximately 76% calcium phosphate, (Ca3[PO4]2); 3% calcium carbonate (CaCO3); and traces of magnesium phosphate (Mg3[PO4]2) and other metals. The percentage of inorganic constituents in calculus is similar to that of other calcified tissues of the body. The principal inorganic components have been reported as approximately 39% calcium, 19% phosphorus, 2% carbon dioxide, and 1% magnesium as well as trace amounts of sodium, zinc, strontium, bromine, copper, manganese, tungsten, gold, aluminum, silicon, iron, and fluorine.At least two thirds of the inorganic component is crystalline in structure. The four main crystal forms and their approximate percentages are as follows: hydroxyapatite, 58%; magnesium whitlockite, 21%; octacalcium phosphate, 12%; and brushite, 9%. Two or more crystal forms are typically found in a sample of calculus. Hydroxyapatite and octacalcium phosphate are detected most frequently (i.e., in 97% to 100% of all supragingival calculus) and constitute the bulk of the specimen. Brushite is more common in the mandibular anterior region, and magnesium whitlockite is found in the posterior areas. The incidence of the four crystal forms varies with the age of the deposit. Organic Content. The organic component of calculus consists of a mixture of protein–polysaccharide complexes, desquamated epithelial cells, leukocytes, and various types of microorganisms. Between 1.9% and 9.1% of the organic component is carbohydrate, which consists of galactose, glucose, rhamnose, mannose, glucuronic acid, galactosamine, and sometimes arabinose, galacturonic acid, and glucosamine. All of these organic tion of arabinose and rhamnose. Salivary proteins account for 5.9% to 8.2% of the organic component of calculus and include most amino acids. Lipids account for 0.2% of the organic content in the form of neutral fats, free fatty acids, cholesterol, cholesterol esters, and phospholipids. The composition of subgingival calculus is similar to that of supragingival calculus, with some differences. It has the same hydroxyapatite content, more magnesium whitlockite, and less brushite and octacalcium phosphate. The ratio of calcium to phosphate is higher subgingivally, and the sodium content increases with the depth of periodontal pockets. These altered compositions may be attributed to the origin of subgingival calculus being plasma, whereas supragingival calculus is partially composed of saliva constituents. Salivary proteins present in supragingival calculus are not found subgingivally. Dental calculus, salivary duct calculus, and calcified dental tissues are similar in inorganic composition. Attachment to the Tooth Surface Differences in the manner in which calculus is attached to the tooth surface affect the relative ease or difficulty encountered during its removal. Four modes of attachment have been described.Attachment by means of an organic pellicle on cementum is depicted in, and attachment on enamel is shown in. Mechanical locking into surface irregularities, such as caries lesions or resorption lacunae, is illustrated in Figure 7-8. The fourth mode of attachment consists of the close adaptation of the undersurface of calculus to depressions or gently sloping mounds of the unaltered cementum surface, as shown in, and the penetration of bacterial calculus into cementum. Formation Calculus is mineralized dental plaque. The soft plaque is hardened by the precipitation of mineral salts, which usually starts between the first and fourteenth days of plaque formation. Calcification has been reported to occur within as little as 4 to 8 hours.166 Calcifying plaques may become 50% mineralized in 2 days and 60% to 90% mineralized in 12 days. All plaque does not necessarily undergo calcification. Early plaque contains a small amount of inorganic material, which increases as the plaque develops into calculus. Plaque that does not develop into calculus reaches a plateau of maximal mineral content within 2 days. Microorganisms are not always essential in calculus formation, because calculus occurs readily in germ-free rodents.Saliva is the source of mineralization for supragingival calculus, whereas the serum transudate called gingival crevicular fluid furnishes the minerals for subgingival calculus. The calcium concentration/content in plaque is 2 to 20 times that found in saliva. Early plaque of heavy calculus formers contains more calcium, three times more phosphorus, and less potassium than that of noncalculus formers, thereby suggesting that phosphorus may be more critical than calcium for plaque mineralization. Calcification entails the binding of calcium ions to the carbohydrate–protein complexes of the organic matrix and the precipitation of crystalline calcium phosphate salts. Crystals form initially in the intercellular matrix and on the bacterial surfaces and finally within the bacteria. The calcification of supragingival plaque and in the attached component of subgingival plaque begins along the inner surface adjacent to the tooth. Separate foci of calcification increase in size and coalesce to form solid masses of calculus Calcification may be accompanied by alterations in the bacterial content and staining qualities of the plaque. As calcification progresses, the number of filamentous bacteria increases, and the foci of calcification change from basophilic to eosinophilic. There is a reduction in the staining intensity of groups that exhibit a positive periodic acid–Schiff reaction. Etiologic Significance Distinguishing between the effects of calculus and plaque on the gingiva is difficult, because calculus is always covered with a nonmineralized layer of plaque. A positive correlation between the presence of calculus and the prevalence of gingivitis exists, but this correlation is not as great as that between plaque and gingivitis. The initiation of periodontal disease in young people is closely related to plaque accumulation, whereas calculus accumulation is more prevalent in chronic periodontitis found in older adults. The incidence of calculus, gingivitis, and periodontal disease increases with age. It is extremely rare to find periodontal pockets in adults without at least some subgingival calculus being present, although the subgingival calculus may be of microscopic proportions. Calculus does not contribute directly to gingival inflammation, but it provides a fixed nidus for the continued accumulation of plaque and its retention in close proximity to the gingiva. Subgingival calculus is likely to be the product rather than the cause of periodontal pockets. Plaque initiates gingival inflammation, which leads to pocket formation, and the pocket in turn provides a sheltered area for plaque and bacterial accumulation. The increased flow of gingival fluid associated with gingival inflammation provides the minerals that mineralize the continually accumulating plaque that results in the formation of subgingival calculus. Materia Alba, Food Debris, and Dental Stains Materia alba is an accumulation of microorganisms, desquamated epithelial cells, leukocytes, and a mixture of salivary proteins and lipids, with few or no food particles; it lacks the regular internal pattern observed in plaque. It is a yellow or grayish-white, soft, sticky deposit, and it is somewhat less adherent than dental plaque. The irritating effect of materia alba on the gingiva is caused by- bacteria and their products. Most food debris is rapidly liquefied by bacterial enzymes and cleared from the oral cavity by salivary flow and the mechanical action of the tongue, cheeks, and lips. The rate of clearance from the oral cavity varies with the type of food and the individual. Aqueous solutions are typically cleared within 15 minutes, whereas sticky foods may adhere for more than 1 hour. Dental plaque is not a derivative of food debris, and food debris is not an important cause of gingivitis.Pigmented deposits on the tooth surface are called dental stains. Stains are primarily an aesthetic problem and do not cause inflammation of the gingiva. The use of tobacco products coffee, tea, certain mouthrinses, and pigments in foods can contribute to stain formation. Other Predisposing Factors Iatrogenic Factors Deficiencies in the quality of dental restorations or prostheses are contributing factors to gingival inflammation and periodontal destruction. Inadequate dental procedures that contribute to the deterioration of the periodontal tissues are referred to as iatrogenic factors. Iatrogenic endodontic complications that can adversely affect the periodontium include root perforations, vertical root fractures, and endodontic failures that may necessitate tooth extractio. Margins of Restorations. Overhanging margins of dental restorations contribute to the development of periodontal disease by (1) changing the ecologic balance of the gingival sulcus to an area that favors the growth of disease-associated organisms (predominantly gram-negative anaerobic species) at the expense of the health-associated organisms (predominantly gram-positive facultative species) and (2) inhibiting the patient’s access to remove accumulated plaque. The location of the gingival margin of a restoration is directly related to the health status of the adjacent periodontal tissues.Numerous studies have shown a positive correlation between margins located apical to the marginal gingiva and the presence of gingival inflammation. Subgingival margins are associated with large amounts of plaque, more severe gingivitis, and deeper pockets. Even high-quality restorations, if placed subgingivally, will increase plaque accumulation, gingival inflammation,and the rate of gingival fluid flow. Retained Cement/Periimplantitis. Periimplantitis is an inflammatory disease that affects the tissues around dental implants and that results in progressive bone loss. The prevalence of periimplantitis among implant supported prosthesis/restoration ranges from 28% to 56%.184 The early diagnosis of this condition and its proper management are critical to the longevity of the implant and supported prosthesis. Contours/Open Contacts. Overcontoured crowns and restorations tend to accumulate plaque and handicap oral hygiene measures in addition to possibly preventing the self-cleaning mechanisms of the adjacent cheek, lips, and tongue. Restorations that fail to reestablish adequate interproximal embrasure spaces are associated with papillary inflammation. Undercontoured crowns that lack a protective height of contour do not retain as much plaque as overcontoured crowns and therefore may not be as detrimental during mastication as once thought. Materials. In general, restorative materials are not in themselves injurious to the periodontal tissues. One exception to this may be self-curing acrylics. Plaque that forms at the margins of restorations is similar to that found on adjacent nonrestored tooth surfaces. The composition of plaque formed on all types of restorative materials is similar, with the exception of that formed on silicate. Although surface textures of restorative materials differ with regard to their capacity to retain plaque, all can be adequately cleaned if they are polished and accessible to methods of oral hygiene. Design of Removable Partial Dentures. Several investigations have shown that, after the insertion of partial dentures, mobility of the abutment teeth, gingival inflammation, and periodontal pocket formation all increase. This is because partial dentures favor the accumulation of plaque, particularly if they cover the gingival tissue. Partial dentures that are worn during both night and day induce more plaque formation than those worn only during the daytime. These observations emphasize the need for careful and personalized oral hygiene instruction to avoid the harmful effects of partial dentures on the remaining teeth and the periodontium. The presence of removable partial dentures induces not only quantitative changes in dental plaque but also qualitative changes, thereby promoting the emergence of spirochetal microorganisms. Restorative Dentistry Procedures. The use of rubber dam clamps, matrix bands, and burs in such a manner as to lacerate the gingiva results in varying degrees of mechanical trauma and inflammation. Although such transient injuries generally undergo repair, they are needless sources of discomfort to the patient. The forceful packing of a gingival retraction cord into the sulcus to prepare the subgingival margins of a tooth or for the purpose of obtaining an impression may mechanically injure the periodontium and leave behind impacted debris that are capable of causing a foreign body reaction. Malocclusion The irregular alignment of teeth as found in cases of malocclusion may make plaque control more difficult. Several authors have found a positive correlation between crowding and periodontal disease, whereas other investigators did not find such a correlation. Uneven marginal ridges of contiguous posterior teeth have been found to have a low correlation with pocket depth, loss of attachment, plaque, calculus, and gingival inflammation. Roots of teeth that are prominent in the arch—such as in a buccal or lingual version or that are associated with a high frenal attachment and small quantities of attached gingiva—frequently exhibit recession. Plaque Retention and Composition. Orthodontic appliances tend to retain bacterial plaque and food debris, thereby resulting in gingivitis, and they are also capable of modifying the gingival ecosystem. Gingival Trauma and Alveolar Bone Height. Orthodontic treatment is often started soon after the eruption of the permanent teeth, when the junctional epithelium is still adherent to the enamel surface. Tissue Response to Orthodontic Forces. Orthodontic tooth movement is possible because the periodontal tissues are responsive to externally applied forces. Alveolar bone is remodeled by osteoclasts that induce bone resorption in areas of pressure and by osteoblasts that form bone in areas of tension. Although moderate orthodontic forces ordinarily result in bone remodeling and repair, excessive force may produce necrosis of the periodontal ligament and the adjacent alveolar bone. Habits and Self-Inflicted Injuries Patients may not be aware of their self-inflicted injurious habits that may be important to the initiation and progression of their periodontal disease. Mechanical forms of trauma can stem from the improper use of a toothbrush, the wedging of toothpicks between the teeth, the application of fingernail pressure against the gingiva, pizza burns, and other causes. Trauma Associated with Oral Jewelry. The use of piercing jewelry in the lip or tongue has become more common recently among teenagers and young adults. Toothbrush Trauma. Abrasions of the gingiva as well as alterations in tooth structure may result from aggressive brushing in a horizontal or rotary fashion. The deleterious effect of excessively forceful brushing is accentuated when highly abrasive dentifrices are used. The gingival changes that are attributable to toothbrush trauma may be acute or chronic. The acute changes vary with regard to their appearance and duration, from scuffing of the epithelial surface to denudation of the underlying connective tissue with the formation of a painful gingival ulcer. Chemical Irritation. Acute gingival inflammation may be caused by chemical irritation that results from either sensitivity or nonspecific tissue injury. In allergic inflammatory states, the gingival changes range from simple erythema to painful vesicle formation and ulceration. Severe reactions to ordinarily innocuous mouthwashes, dentifrices, and denture materials are often explainable on this basis. Smokeless Tobacco Snuff and chewing tobacco constitute the two main forms of smokeless tobacco. Snuff is a fine-cut form of tobacco that is available loosely packed or in small sachets. Chewing tobacco is a more coarse-cut tobacco that is available in the form of loose leaves, a solid block, a plug, or as a twist of dried leaves. Breath Malodor In the vast majority, breath malodor originates from the oral cavity. Gingivitis, periodontitis, and especially tongue coating are the predominant causative factors. In general, one can identify two pathways for bad breath. The first one involves an increase of certain metabolites in the blood circulation (e.g., due to a systemic disease), which will escape via the alveoli of the lungs during breathing(blood-breath exchange) and it is commonly referred as “extraoral halitosis.” The second pathway (intraoral halitosis) involves an increase of either the bacterial load or the amount of substrate for these bacteria at one of the lining surfaces of the oropharyngeal cavity, the respiratory tract, or the esophagus. All types of infections, ulcerations, or tumors at one of the previously mentioned areas can thus lead to bad breath. Studies also suggest that oral malodor is associated with the total bacterial load of anaerobic bacteria in both saliva and tongue coating. Intraoral Causes Tongue and Tongue Coating. The dorsal tongue mucosa, with an area of 25 cm2, shows a very irregular surface topography. The posterior part exhibits a number of oval cryptolymphatic units, which roughen the surface of this area. The anterior part is even rougher because of the high number of papillae: the filiform papillae with a core of 0.5 mm in length, a central crater and uplifted borders; the fungiform papillae, 0.5 to 0.8 mm in length; the foliate papillae, located at the edge of the tongue, separated by deep folds; and the vallate papillae, 1 mm in height and 2 to 3 mm in diameter. These innumerable depressions in the tongue surface are ideal niches for bacterial adhesion and growth, sheltered from cleaning actions. Moreover, desquamated cells and food remnants also remain trapped in these retention sites and consequently can be putrefied by the bacteria.5 A fissurated tongue (deep fissures on dorsum, also called scrotal tongue or lingua plicata) and a hairy tongue (lingua villosa) have an even rougher surface. Periodontal Infections. A relationship between periodontitis and oral malodor has been shown. However, not all patients with gingivitis and/or periodontitis complain about bad breath, and there is some disagreement in the literature as to what extent oral malodor and periodontal disease are related. Bacteria associated with gingivitis and periodontitis are indeed able to produce VSCs.Several studies have shown that the VSC levels in the mouth correlate positively with the depth of periodontal pockets (the deeper the pocket, the more bacteria, particularly anaerobic species) and that the amount of VSCs in breath increases with the number, depth, and bleeding tendency of the periodontal pockets. It is important to realize that VSCs aggravate the periodontitis process by, for example, increasing the permeability of the pocket and mucosal epithelium and therefore exposing the underlying connective tissues of the periodontium to bacterial metabolites. Moreover, methylmercaptan enhances interstitial collagenase production, interleukin-1 (IL-1) production by mononuclear cells, and cathepsin B production, thus further mediating connective tissue breakdown. It was also shown that human gingival fibroblasts developed an affected cytoskeleton when exposed to methylmercaptan. The same gas alters cell proliferation and migration. VSCs are also known to impede wound healing. Thus, when periodontal surgery is planned, especially the insertion of implants, clinicians should recognize this pathologic role of VSCs. Dental Pathologies. Possible causes within the dentition are deep carious lesions with food impaction and putrefaction, extraction wounds filled with a blood clot, and purulent discharge leading to important putrefaction. The same applies to interdental food impaction in large interdental areas and crowding of teeth favor food entrapment and accumulation of debris. Acrylic dentures, especially when kept continuously in the mouth at night or not regularly cleaned, can also produce a typical smell. The denture surface facing the gingiva is porous and retentive for bacteria, yeasts, and debris, which are compounds needed for putrefaction. Dry Mouth. Saliva has an important cleaning function in the oral cavity. Patients with xerostomia often present with large amounts of plaque on teeth and an extensive tongue coating. The increased microbial load and the escape of VSCs when saliva is drying up explain the strong breath malodor. Several studies link stress with VSC levels, but it is not clear whether this can simply be explained by a reduction of salivary flow. Fundamentals of Malodor Detection The breath of a person contains up to 150 different molecules. The characteristics of the expired molecules determine whether we can smell them or not. Some gases can cause a striking odor at very low concentrations, whereas others need to be present in much higher quantities. The perception of the molecules depends on the following factors: 1. The odor itself (olfactory response) can be pleasant, unpleasant, or even repulsive. 2. Each particular molecule has its specific concentration before it can be detected (threshold concentration). 3. The odor power is the extent of concentration that is necessary to increase the odor score with one unit. 4. The volatility of the compound: Malodorous molecules only express themselves when they become volatile. 5. The substantivity: The capacity of the molecule to stay present and thus to remain the cause of smell. Extraoral Causes Ear-Nose-Throat. During chronic or purulent tonsillitis, the deep crypts of the tonsils accumulate debris and bacteria, especially periopathogens, resulting in putrefaction. In the crypts, even calculus (e.g., subgingivally) can be formed (tonsilloliths or tonsil stones). Other examples include acute pharyngitis (viral or bacterial) and postnasal drip. The latter is a rather common condition, which is perceived by patients as a liquid flow in the throat, originating from the nasal cavity. It is often associated with chronic sinusitis or regurgitation esophagitis, in which the acidic content of the stomach reaches the nasopharynx and causes mucositis. Ozena (caused by Klebsiella ozaenae) is a rare atrophic condition of the nasal mucosa, with the appearance of crusts that causes a very strong breath malodor. Finally, a foreign body in a nasal or sinus cavity can cause local irritation, ulceration, and subsequent putrefaction (e.g., children and mentally handicapped persons tend to put objects such as peas or wet paper in the nose). Bronchi and Lungs. Pulmonary causes include chronic bronchitis, bronchiectasis (infection of standing mucus secretion in cystic dilations through walls of bronchioles), pneumonia, pulmonary abscesses, bronchial carcinoma, and carcinoma of the lung. The relevance of an early diagnosis is evident. Gastrointestinal Tract. In contrast to the common public opinion, even among medical physicians, gastrointestinal pathologies are rarely responsible for bad breath.Liver. Patients with various degrees of hepatocellular failure and/or portosystemic shunting of blood may acquire a sweet, musty, or even slightly fecal aroma of the breath, termed fetor hepaticus, which has been mainly attributed to the accumulation of dimethyl sulfide.Kidney. Kidney insufficiency, primarily caused by chronic glomerulonephritis, will lead to an increase of the amines dimethylamine and trimethylamine, which causes a typical fishy odor of the breath. Systemic Metabolic Disorders. Uncontrolled diabetes mellitus results in the accumulation of ketones, which have a sweet smell, like the odor of rotten apples. Insulin resistance leads to an increase of triglycerides and free fatty acids and ketones (such as acetone, acetoacetate, and hydroxybutyrate) are formed during lipolysis. Trimethylaminuria. Trimethylaminuria is a hereditary metabolic disorder that leads to a typical fishy odor of the breath, urine, sweat, and other bodily secretions. Trimethylaminuria is an enzymatic defect that prevents the transformation of trimethylamine to trimethylaminoxide, resulting in abnormal amounts of this molecule. The prevalence is unknown but approaches 1% in the United Kingdom. Hormonal Causes. At certain moments during the menstrual cycle, a typical breath odor can develop; partners are often well aware of this odor. Evidence also indicates that VSC levels in the expired air are increased twofold to fourfold around the day of ovulation and in the perimenstrual period. Increases in VSCs are smaller in midfollicular phases. Diagnosis of Malodor Anamnesis Each consultation should start with a thorough questioning about the breath malodor, eating habits, and medical and dental history. This can be done with a questionnaire that the patient fills out in the waiting room and/or orally at the beginning of the consultation, depending on the preferences of the examiner and the practical possibilities. To start with, the patient should be asked about the frequency of the halitosis (e.g. constantly, every day), the time of appearance during the day (e.g. after meals can indicate a stomach hernia), when the problem first appeared and whether others have identified the problem (to exclude imaginary breath odor). Also the medical history has to be recorded, with an emphasis on medication, and systemic diseases of the lungs, liver, kidneys, stomach, and pancreas. Concerning the ENT history, attention should be paid to the presence of nasal obstruction, mouth breathing, postnasal drip, allergy, tonsillitis, dysphagia, and previous ENT encounters. The dental history includes questions assessing the frequency of dental visits, the use of mouth rinses, the presence and maintenance of a dental prosthesis, and the frequency and the instruments used for tooth brushing, interdental cleaning, and tongue brushing and scraping. Finally, the patient is asked about his smoking, drinking, and dietary habits. Clinical and Laboratory Examination Self-Examination. Smelling one’s own breath by expiring in the hands kept in front of the mouth is not relevant because the nose gets used to the odor and the smell of the skin and soaps used for handwashing may interfere. Moreover, studies have shown that self-assessment of oral malodor is notoriously unreliable and one should be careful with the information obtained from the patient. The following self-testing can be used: • Smelling a metallic or nonodorous plastic spoon after scraping the back of the tongue • Smelling a toothpick after introducing it in an interdental area • Smelling saliva spit in a small cup or spoon (especially when allowed to dry for a few seconds so that putrefaction odors can escape from the liquid) • Licking the wrist and allowing it to dry (reflects the saliva contribution to malodor) Oropharyngeal Examination. The oropharyngeal examination includes inspection of deep carious lesions, interdental food impaction, wounds, bleeding of the gums, periodontal pockets, tongue coating, dry mouth, and the tonsils and pharynx (for tonsillitis and pharyngitis). The tongue coating can be scored with regard to the thickness and surface. Several methods have been proposed for the thickness, Gross and coworkers (1975) proposed an index, ranging from 0 (= no coating) to 3 (= severe coating). Miyazaki72 assessed the tongue-coating status according to the area: score 0 = none visible, score 1 = less than one-third of the tongue dorsum covered, score 2 = less than two-thirds, and score 3 = more than two-thirds.Organoleptic Rating. Even though devices are available, the organoleptic assessment by a judge is still the gold standard in the examination of breath malodor. It is the easiest and most often used method because it gives a reflection of the everyday situation when halitosis is noticed. follows: 1. Breath odor: The subject expires through the mouth while the judge smells both at the beginning (rather oral) and at the end (rather extraoral) of the expiration. The first part of the breath is derived from the mouth and dead-space air of the upper airways and nasopharynx, whereas the last part is alveolar air from the lungs. 2. Nasal breath odor: The subject expires through the nose, keeping the mouth closed. When the nasal expiration is malodorous, yet the air expired through the mouth is not, a nasal/ paranasal cause can be suspected. 3. Oral cavity odor: The subject opens the mouth and refrains from breathing while the judge places his or her nose close to the mouth opening (smelling the air while the patient counts from 1 to 20 reveals the same but favors oral malodor because drying of the palatal and tongue mucosa will occur, which promotes the expression of VSCs thus far soluble in the salivary coating). 4. Saliva: The patient is asked to lick his or her wrist. After drying, the judge gives a score. 5. Tongue coating: The judge smells a tongue scraping. This is also presented to the patient or the confidant to evaluate whether this smell is similar to the experienced malodor. Although the organoleptic assessment is still the gold standard for diagnosis of halitosis, the method also has some important drawbacks. The assessment can, for example, be influenced by several aspects such as the position of the head, hunger, and the experience of the judge. Odor judges are also supposed to rest their noses for several minutes between the tests to avoid habituation. The most important disadvantage of the method, however, is that it clearly has a degree of subjectivity. Researchers are trying to improve the reliability and reproducibility of the organoleptic method. When using a panel of odor judges instead of one judge, the reliability is already considered to increase. Furthermore, the agreement among judges may be improved by standardization of the sense of smell using an odor solution kit for measuring the olfactory response.163 Training is also considered to reduce the odor judges’ errors. Portable Volatile Sulfur Monitor. The portable volatilesulfur monitor (Halimeter, Interscan, Chatsworth, CA) is an electronic device that detects the presence of volatile sulfur compounds such as hydrogen sulfide and methylmercaptan in breath. The instrument cannot discriminate among the different sulfur compounds. The sensitivity for methylmercaptan is five times lower than for hydrogen sulfide, and the device is almost insensitive to dimethyl sulfide. Moreover, ethanol and other compounds can disturb the measurements. Gas Chromatography. A gas chromatograph can analyze air, saliva, or crevicular fluid. About 100 compounds have been isolated from the headspace of saliva and tongue coating, from ketones to alkanes, and sulfur-containing compounds to Dark-Field or Phase-Contrast Microscopy. Oral malodor is typically associated with a higher incidence of motile organisms and spirochetes, so shifts in these proportions allow monitoring of therapeutic progress. Another advantage of direct microscopy is that the patient becomes aware of bacteria being present in plaque, tongue coating, and saliva. Too often, patients confuse plaque with food remnants. Saliva Incubation Test. The analysis of the headspace above incubated saliva by gas chromatography reveals VSCs and other compounds such as indole, skatole, lactic acid, methylamine, diphenylamine, cadaverine, putrescine, urea, ammonia, dodecanol, and tetradecanol. By adding some proteins, such as lysine or cysteine, the production of respectively cadaverine or hydrogen sulfide is dramatically increased. Organoleptic evaluation (or assessment of the VSCs) of the saliva headspace offers promising perspectives for monitoring treatment results. Electronic Nose. Electronic noses identify the specific components of an odor and analyze its chemical makeup. They consist of a mechanism for chemical detection, such as an array of electronic sensors, and a mechanism for pattern recognition. They are smaller, less expensive, and easier to use than, for example, gas chromatography, but can only be developed for specific applications if the important metabolites are already known. An artificial nose that has the same capacities as the human nose would be ideal. Currently, although significant improvements still need to be made, the first trials thus far have been promising.Chair-Side Test. A salivary chair-side test may be an alternative tool for the general practitioner for diagnosing halitosis. Currently, several tests based on the detection of bacteria or metabolites involved in the process of oral malodor, are commercially available. All these tests have reported acceptable correlation with the organoleptic ratings and some of them even with the VSC level. The BANA test is based on the ability of some bacterial species to hydrolyze a synthetic trypsin substrate (N-benzoyl-DL-arginine-2-naphthylamine). In this way the test can detect three specific bacteria: P. gingivalis, Bacteroides forsythus, and Treponema denticola related to periodontal disease. As already mentioned, periodontitis is not the most common cause of oral malodor,111 as not all patients with periodontitis suffer from bad breath. Treatment of Oral Malodor The treatment of oral malodor (thus with an intraoral origin) should preferably be cause-related. Because oral malodor is caused by the metabolic degradation of available proteins to malodorous gases by certain oral microorganisms, the following general treatment strategies can be applied: • Masking the malodor • Mechanical reduction of intraoral nutrients (substrates) and microorganisms • Chemical reduction of oral microbial load • Rendering malodorous gases nonvolatile Treatment should be centered on reducing the bacterial load and micronutrients by effective mechanical oral hygiene procedures, including tongue scraping. Periodontal disease should be treated and controlled, and as an auxiliary aid, oral rinses containing chlorhexidine (CHX) and other ingredients may further reduce the oral malodor. If breath malodor persists after these approaches, other sources of the malodor, such as the tonsils, lung disease, Masking the Malodor Treatments with rinses, mouth sprays, and lozenges containing volatiles with a pleasant odor have only a short-term effect. Typical examples are the mint-containing lozenges and the aroma present in rinses without antibacterial components.19 Another pathway is to increase the solubility of malodorous compounds in the saliva by increasing the secretion of saliva; a larger volume allows the retention of larger volumes of soluble VSCs. The latter can also be achieved by ensuring a proper liquid intake or by using a chewing gum; chewing triggers the periodontalparotid reflex, at least when the lower (pre)molars are still present. Mechanical Reduction of Intraoral Nutrientsand Microorganisms Because of the extensive accumulation of bacteria on the dorsum of the tongue, tongue cleaning should be emphasized. Previous investigations demonstrated that tongue cleaning reduces both the amount of coating (and thus bacterial nutrients), as well as the number of bacteria and thereby improves oral malodor effectively. Other reports indicated that the reduction of the microbial load on the tongue after cleaning is negligible and that the malodor reduction probably results from the reduction of the bacterial nutrients Chemical Reduction of Oral Microbial Load Together with toothbrushing, mouth rinsing has become a common oral hygiene practice. Formulations have been modified to carry antimicrobial and oxidizing agents with impact in the process of oral malodor formation. The active ingredients usually include antimicrobial agents such as chlorhexidine, cetylpyridinium chloride (CPC), essential oils, chlorine dioxide, triclosan (TCN), amine fluoride and stannous fluoride, hydrogen peroxide, and baking soda. Some of these agents have only a temporary effect on the total number of microorganisms in the oral cavity. Chlorhexidine. Chlorhexidine is considered the most effective antiplaque and antigingivitis agent.1-4, Its antibacterial action can be explained by disruption of the bacterial cell membrane by the chlorhexidine molecules, increasing its permeability and resulting in cell lysis and death. Because of its strong antibacterial effects and superior substantivity in the oral cavity, chlorhexidine rinsing provides significant reduction in VSC levels and organoleptic ratings Unfortunately, as mentioned in some trials, chlorhexidine at a concentration of 0.2% or greater also has some disadvantages, such as the increased tooth and tongue staining, bad taste, and some temporary reduction in taste sensation. Essential Oils. Previous studies evaluated the short-term effect (3 hours) of a Listerine rinse (which contains essential oils) compared with a placebo rinse. Listerine was found to be only moderately effective against oral malodor (±25% reduction vs. 10% for placebo of VSCs after 30 minutes) and caused a sustained reduction in the levels of odorigenic bacteria. Similar VSC reductions were found after rinsing for 4 days.9 Chlorine Dioxide. Chlorine dioxide (ClO2) is a powerful oxidizing agent that can eliminate bad breath by oxidation of hydrogen sulfide, methylmercaptan, and the amino acids, methionine, and cysteine. Studies demonstrated that a single use of a ClO2-containing oral rinse slightly reduces mouth odor. Two-Phase Oil-Water Rinse. Rosenberg et al designed a two-phase oil-water rinse containing CPC. The efficacy of oilwater- CPC formulations is thought to result from the adhesion of a high proportion of oral microorganisms to the oil droplets, which is further enhanced by the CPC. A twice-daily rinse with this product (before bedtime and in the morning) showed reductions in both VSC levels and organoleptic ratings. These reductions were superior to Listerine and significantly superior to a placebo Aminefluoride/Stannous Fluoride. The association of aminefluoride with stannous fluoride (AmF/SnF2) resulted in encouraging reductions of morning breath odor, even when oral hygiene was insufficient. Recently, new evidence supporting the use of this AmF/SnF2 rinse became available. The formulation showed not only short-term but also long-term effect on malodor indicators in patients with obvious malodor. Hydrogen Peroxide. Suarez et al reported that rinsing with 3% hydrogen peroxide (H2O2) produced impressive reductions (±90%) in sulfur gases that persisted for 8 hours. Oxidizing Lozenges. Greenstein et al42 reported that sucking a lozenge with oxidizing properties reduces tongue dorsum malodor for 3 hours. This antimalodor effect may be caused by the activity of dehydroascorbic acid, which is generated by peroxide-mediated oxidation of ascorbate present in the lozenges. Baking Soda. Baking soda dentifrices have been shown to confer a significant odor-reducing benefit for time periods up to 3 hours. The mechanisms by which baking soda produces its inhibition of oral malodor is related to its bactericidal effect. 1-Newman M, Takei H, Klokkevold P, Carranza F. Newman and Carranza (2019); Clinical Periodontology, 13th Ed., Elsevier.