CHAPTER 22

The Role of Dental Calculus and Other Local Predisposing Factors

James E. Hinrichs
CHAPTER OUTLINE
CALCULUS Supragingival and Subgingival Calculus Prevalence Composition Attachment to the Tooth Surface Formation Etiologic Signicance Materia Alba, Food Debris, and Dental Stains OTHER PREDISPOSING FACTORS Iatrogenic Factors Malocclusion Periodontal Complications Associated with Orthodontic Therapy Extraction of Impacted Third Molars Habits and Self-Inicted Injuries Smokeless Tobacco Radiation Therapy

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he primary cause of gingival inflammation is bacterial plaque. Other predisposing factors inc lude calculus, faulty restorations, complications associated with or thodontic therapy, self-inflicted injuries, use of tobacco, and others. These will be discussed in turn.

CALCULUS
Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental pr ostheses.

Supragingival and Subgingival Calculus

Supragingival calculus is located coronal to the gingival margin and therefore is visible in the oral cavity. It is usuall y white or whitish yellow in color, hard with claylike consistency, and easily detached from the tooth sur face. Af ter removal, it may rapid ly recur, especially in the lingual ar ea of the mandibular incisors. The color is influenced by contact with such substances as tobacco and f ood pigments. It may localize on a single tooth or gr oup of teeth, or it may be generalized throughout the mouth. The two most common loc ations for supragingival c alculus to develop are the bucc al surf aces of the maxillar y molars ( Figure 22-1) and the lingual sur f aces of the mandibular anter ior teeth (Figure 22-2).32 Saliva from the parotid gland flows over the facial surfaces of upper molars via the parotid duct, whereas the subman-

dibular duct and lingual duct empt y onto the lingual sur f aces of the lower incisors f r om the submaxillar y 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 lac king functional antagonists. Subgingival calculus is loc ated below the cr est of the marginal gingiva and therefore is not visible on routine clinical examination. The location and extent of subgingival c alculus may be e valuated by careful tactile perception with a delicate dental instrument such as an explorer. Clerehugh et al29 used a World Health Organization #621 probe to detect and scor e subgingival calculus. Subsequently, these teeth were extracted and visuall y scored for subgingival c alculus. An agreement of 80% was found between these two scoring methods. Subgingival calculus is typically hard and dense and fr equently appears dark brown or greenish black in color (Figure 22-3) and 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 c alculus usually extend near ly to the base of periodontal pockets in chr onic periodontitis but do not r each the junctional epithelium. When the gingival tissues recede, subgingival calculus becomes exposed and is therefore reclassified as supragingival (Figure 22-4). Thus supragingival calculus can be composed of both supragingival calculus and previous subgingival calculus. A reduction in gingival

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Figure 22-1 Supragingival calculus is depicted on the bucc al surfaces of maxillary molars adjacent to or ifice for parotid duct. Figure 22-4 A 31-year-old white male is shown with extensive supragingival and subgingival c alculus deposits throughout his dentition.

Figure 22-2 Extensive supragingival c alculus is pr esent on the lingual surfaces of lower anterior teeth. Figure 22-5 The same patient shown in Figure 22-4, 1 year after receiving thorough scaling and root planing to remove supragingival and subgingival calculus deposits, followed by restorative care. Note the substantial reduction in gingival inflammation.

Figure 22-3 Dark pigmented deposits of subgingival c alculus are shown on the distal root of an extracted low er molar.

inflammation and probing depths with a gain in c linical attachment can be observed after the removal of subgingival plaque and calculus (Figure 22-5) (see Chapter 45).

Prevalence
Anerud and co-workers4 observed the periodontal status of a group of Sri Lankan tea laborers and a group of Norwegian academicians for a 15-year period. The Norwegian population had r eady access to preventive dental c are throughout their liv es, whereas the S ri Lankan tea laborers did not. The formation of supragingival calculus was observed early in life in the S ri Lankan individuals, probably shortly af ter the teeth erupted. The first areas to exhibit calculus deposits were the facial aspects of maxillary molars and the lingual surfaces of mandibular incisors. Deposition of supragingival calculus continued as individuals aged, reaching a maximal calculus score around 25 to 30 y ears of age. At this time, most of the teeth

were covered by calculus, although the facial sur faces had less c alculus than the lingual or palatal surf aces. Calculus accumulation appeared to be symmetric, and by age 45 only a few teeth, typically the premolars, were without calculus. Subgingival calculus appeared first either independently or on the inter proximal aspects of ar eas where supragingival calculus already existed.4 By age 30, all surfaces of all teeth had subgingival c alculus without any pattern of predilection. The Norwegian academicians received oral hygiene instructions and f requent preventive dental c are throughout their liv es. The Norwegians exhibited a marked reduction in the accumulation of calculus as compared with the Sri Lankan group. However, despite the fact that 80% of teenagers formed supragingival calculus on the facial surfaces of the upper molars and the lingual surfaces of lower incisors, no additional calculus formation occurred on other teeth, nor did it increase with age.4 Both supragingival calculus and subgingival calculus may be seen on radiographs (see Chapter 31). Highly calcified interproximal calculus deposits are readily detectable as radiopaque pr ojections that pr otrude into the inter dental spaces in Figure 22-6. However, the sensitivity level of detecting c alculus by radiographs is inconsistent.23 The location of c alculus does not indic ate the bottom of the per iodontal pocket because the most apic al plaque is not sufficiently calcified to be visible on radiographs.

Composition Inorganic Content. Supragingival calculus consists of inor-

ganic (70% to 90%50) and organic components.The major inorganic

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Figure 22-7 Calculus attached to pellic le on enamel sur face and cementum. An enamel void (E) has been created in the preparation of the specimen. CA, Calculus; P, pellicle; C, cementum.

Figure 22-6 A bitewing radiograph illustrating subgingival c deposits that are depicted as inter proximal spurs (arrows).

alculus

proportions of c alculus 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. 169 The percentage of inorganic constituents in c alculus is similar to that in other calcified tissues of the body. The principal inorganic components have been r eported as appr oximately 39% c alcium, 19% phosphorus, 2% carbon dioxide, and 1% magnesium and trace amounts of sodium, zinc, strontium, bromine, copper, manganese, tungsten, gold, aluminum, silicon, iron, and fluorine.107 At least two-thirds of the inorganic component is crystalline in structure.85 The f our main cr ystal f orms and their appr oximate percentages are as follows: hydroxyapatite 58%, magnesium whitlockite 21%, octacalcium phosphate 12%, and brushite 9%. Generally, two or more crystal f orms are typically f ound 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 anter ior region and magnesium whitlockite in the posterior areas. The incidence of the four crystal forms varies with the age of the deposit. 15

phosphate is higher subgingivally, and the sodium content increases with the depth of periodontal pockets.89 These altered compositions may be attr ibuted to the or igin of subgingival c alculus being plasma, whereas supragingival c alculus is par tially composed of saliva constituents. Salivary proteins present in supragingival c alculus are not f ound subgingivall y.10 Dental calculus, salivary duct calculus, and c alcified dental tissues ar e similar in inorganic composition.

Attachment to the Tooth Surface

Differences in the manner in which c alculus is attached to the tooth surf ace affect the r elative ease or difficulty encountered in its removal. Four modes of attachment have been described.81,138,145,173 Attachment by means of an organic pellic le on cementum is depicted in Figure 22-7, and attachment on enamel is shown in Figure 22-8. Mechanical locking into surface irregularities, such as caries lesions or r esorption lacunae, is illustrated in Figure 22-9. The fourth mode of attachment consists of close adaptation of the undersurface of c alculus to depressions or gentl y sloping mounds of the unaltered cementum sur f ace,154 as shown in Figure 22-10, and penetration of bacter ial calculus into cementum, as shown in Figures 22-11 and 22-12 .

Formation
Calculus is mineralized dental plaque. The sof t plaque is har dened by the precipitation of mineral salts, which usually starts between the first and fourteenth days of plaque formation. Calcification has been reported to occur in as little as 4 to 8 hours. 159 Calcif ying plaques may become 50% mineraliz ed in 2 day s and 60% to 90% mineralized in 12 day s.106,139,149 All plaque does not necessar ily undergo calcification. Early plaque contains a small amount of inorganic material, which incr eases as the plaque de velops into calculus. Plaque that does not de velop into c alculus reaches a plateau of maximal mineral content within 2 day s.140 Microorganisms are not always essential in calculus formation because calculus occurs readily in germ-free rodents.57 Saliva is the source of mineralization for supragingival calculus, whereas the ser um transudate c alled gingival crevicular fluid f urnishes the minerals f or subgingival c alculus.69,156 The calcium concentration/content in plaque is 2 to 20 times that f ound in saliva.15 Early plaque of heavy c alculus f ormers contains mor e calcium, three times more phosphorus, and less potassium than that

Organic Content. The organic component of calculus consists of a mixtur e of pr otein-polysaccharide complexes, desquamated epithelial cells, leukocytes, and various types of microorganisms.94
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The composition of subgingival c alculus 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.136,158 The ratio of calcium to

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E CA P D

Figure 22-10 Undersurface of subgingival calculus (C) previously attached to the cementum surf ace (S). Note impression of cementum mounds in calculus (arrows). (Courtesy Dr. John Sottosanti, La Jolla, CA.) CEJ

C Figure 22-8 Non-decalcified specimen with c alculus (CA) attached to enamel (E) surf ace just cor onal to cementoenamel junction (CEJ). Note plaque (P) on the surface of the calculus; dentin (D) and cementum (C) are identified. (Courtesy Dr. Michael Rohrer, Minneapolis.)

Figure 22-11 Subgingival calculus (C) embedded beneath the cementum surface (arrows) and penetrating to the dentin (D), making removal difficult. (Courtesy Dr. John Sottosanti, La Jolla, CA.)

cent to the tooth. Separate foci of c alcification increase in size and coalesce to form solid masses of c alculus (see Figure 22-12). Calcification may be accompanied by alterations in the bacter ial content and staining qualities of the plaque . As c alcification progresses, the number of filamentous bacteria increases and f oci of calcification change f rom basophilic to eosinophilic. There is a reduction in the staining intensit y of groups exhibiting a positiv e periodic acidSchiff reaction.
Figure 22-9 Calculus (CA) attached to a cemental r esorption area (CR) with cementum (C) adjacent to dentin (D). For more information on formation, please visit the companion website at www.expertconsult.com.

of noncalculus formers, suggesting that phosphorus may be more critical than c alcium in plaque mineraliz ation.94 Calcification entails the binding of c alcium ions to the c arbohydrate-protein complexes of the organic matrix and the precipitation of crystalline calcium phosphate salts.92 Crystals form initially in the intercellular matrix and on the bacter ial surf aces and finally within the bacteria.51,174 Calcification of supragingival plaque and in the attached component of subgingival plaque begins alo ng the inner sur face adja-

The initiation of calcification and the rate of calculus accumulation vary among individuals, between tooth var iety in the same dentition, and at different times in the same person. 107,161 On the basis of these differences, persons may be classified as heavy, moderate, or slight calculus formers or as noncalculus formers. The average daily increment in calculus formers is from 0.10% to 0.15% of dr y weight calculus.149,161 Calculus formations continue until it reaches a maximum, af ter which it may be r educed in amount. The time

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geneous nucleation. The seeding agents in calculus formation are not known, but it is suspected that the intercellular matrix of plaque plays an activ e role.95,106,174 The carbohydrate-protein complexes may initiate calcification by removing calcium from the saliva (chelation) and binding with it to f orm nuc lei that induce subsequent deposition of minerals. 92,164

Figure 22-12 Plaque and c alculus on tooth sur f ace. Note the spher ical areas of focal calcification (FC) and the perpendicular alignment of the filamentous (F) organisms along the inner sur face of plaque and cocci (C) on the outer surface.

larly around both gram-positive and gram-negative organisms but may also star t intracellularly.83 Filamentous organisms, diphtheroids, and Bacterionema and Veillonella species hav e the abilit y to form intracellular apatite cr ystals (see Figure 22-12). Mineralization spreads until the matr ix and bacteria are calcified.51,175 Bacterial plaque may activ ely participate in the mineraliz ation of calculus by forming phosphatases, which changes the pH of the plaque and induces mineralization,38,92 but the prevalent opinion is that these bacteria are only passively involved51,131,168 and are simply calcified with other plaque components. The occurrence of calculuslike deposits in germ-free animals supports this opinion.57 However, other experiments suggest that transmissible factors are involved in calculus formation and that penicillin in the diets of some of these animals reduces calculus formation.9

Role of Microorganisms in the Mineralization of Calculus. Mineralization of plaque gener ally starts extracellu-

Etiologic Signicance
Distinguishing between the effects of c alculus and plaque on the gingiva is difficult because calculus is always covered with a nonmineralized layer of plaque.140 A positive correlation between the presence of c alculus and the pr evalence of gingivitis exists, 126 but this correlation is not as great as that between plaque and gingivitis.53 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. 53,86
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required to reach the maximal level has been reported between 10 weeks30 and 6 months. 163
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The theoretical mechanisms by which plaque becomes mineralized can be stratified into two categories.108 1. Mineral precipitation results from a local rise in the degr ee of saturation of calcium and phosphate ions, which may be brought about in the following se veral ways: A rise in the pH of the saliva causes precipit ation of calcium phosphate salts by lowering the precipitation constant. The pH may be elevated by the loss of carbon dioxide and the formation of ammonia b y dental plaque bacter ia or b y protein degradation during stagnation.14,64 Colloidal proteins in saliva bind calcium and phosphate ions and maintain a supersaturated solution with respect to calcium phosphate salts. With stagnation of saliva, colloids settle out and the supersaturated state is no longer maintained, leading to precipitation of calcium phosphate salts. 124,142 Phosphatase liberated from dental plaque, desquamated epithelial cells, or bact eria precipitates calcium p hosphate by hydrolyzing organic phosphates in saliva, thus increasing the concentration of f ree phosphate ions.168 Esterase is another enz yme that is present in the cocci and filamentous organisms, leukocytes, macrophages, and desquamated epithelial cells of dental plaque.8 Esterase may initiate c alcification by hydrolyzing fatty esters into fr ee fatty acids. The fatty acids form soaps with calcium and magnesium that ar e later conv erted into the less-soluble calcium phosphate salts. 2. Seeding agents induce small f oci of c alcification that enlarge and coalesce to form a c alcified mass.109 This concept has been referred to as the epitactic concept or more appropriately, hetero-

Theories Regarding the Mineralization of Calculus.

Calculus does not contribute directly to gingival inflammation but provides a fixed nidus for the continued accumulation of plaque and its retention in close proximity of the gingiva ( Figure 22-13). Subgingival calculus is likely to be the product rather than the cause of periodontal pockets. Plaque initiates gingival inflammation, which leads to poc ket formation, and the poc ket in turn pr ovides 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 resulting in the f ormation of subgingival c alculus (Figure 22-14). Over a 6-year period, Albandar et al observed 156 teenagers with aggressive periodontitis.2 They noted that ar eas with detectable subgingival calculus at the initiation of the study w ere much more likely to experience loss of periodontal attachment than sites that did not initiall y exhibit subgingival c alculus. Although the bacterial plaque that coats the teeth is the main etiologic f actor in the de velopment of per iodontal disease, the removal of subgingival plaque and c alculus constitute the cornerstone of periodontal therapy. Calculus plays an important role in maintaining and accentuating per iodontal disease b y keeping plaque in close contact with the gingival tissue and cr eating areas where plaque r emoval is impossible . Theref ore the c linician must not only possess the clinical skill to remove the plaque and calculus but also must be very conscientious about per forming this task.

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Figure 22-15 Tobacco stains on the apic al third of the c linical crown caused by cigarette smoking.

Figure 22-13 Calculus (CA) penetrates the tooth surface and is embedded within the cementum (C). Note plaque (P) attached to the c alculus.

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 (Figure 22-15), coffee, tea, certain mouthrinses, and pigments in foods can contribute to stain formation. 90,155

OTHER PREDISPOSING FACTORS

Iatrogenic Factors
Deficiencies in the qualit y of dental r estorations or prostheses are contributing factors to gingival inflammation and per iodontal destruction. Inadequate dental pr ocedures that contr ibute to the deterioration of the periodontal tissues are referred to as iatrogenic factors. Iatrogenic endodontic complications that can adversely affect the per iodontium include root perf orations, vertical root f ractures, and endodontic f ailur es that may necessitate tooth extraction.172,173 Characteristics of dental r estorations and r emovable partial dentures that ar e important to the maintenance of per iodontal health include the location of the gingival margin for the r estoration, the space betw een the margin of the r estoration and the unprepared tooth, the contour of restorations, the occlusion, materials used in the restoration, the restorative procedure itself, and the design of the r emovable partial denture. These characteristics are described in this chapter as they relate to the etiology of periodontal disease. A more comprehensive review with special emphasis on the interrelationship between restorative procedures and the periodontal status is presented in Chapter 66.

Figure 22-14 Scanning electron microscope view of an extracted human tooth showing a cross-section of subgingival calculus (C) separated (arrows) from the cemental surface during processing of specimen. Note bacteria (B) attached to calculus and cemental surfaces. (Courtesy Dr. John Sottosanti, La Jolla, CA.)

Materia Alba, Food Debris, and Dental Stains

Materia alba is an accum ulation of microorganisms, desquamated epithelial cells, leukocytes, and a mixtur e of salivar y proteins and lipids, with few or no food particles, and it lacks the regular internal pattern observed in plaque.141 It is a y ellow or grayish-white, soft, sticky deposit and is somewhat less adherent than dental plaque. The irritating effect of mater ia alba on the gingiva is c aused by bacteria and their products. Most food debris is rapidly liquefied by bacterial enzymes and cleared f rom the oral c avity by salivary flow and the mechanic al action of the tongue , cheeks, and lips. The rate of c learance from the oral c avity varies with the t ype of f ood and the individual. Aqueous solutions are typically cleared within 15 minutes, whereas sticky foods may adher e for more than 1 hour.84,162 Dental plaque is not a der ivative of food debr is, nor is food debr is an important cause of gingivitis. 37,73

Margins of Restorations. Overhanging margins of dental restorations contribute to the de velopment of per iodontal disease by (1) changing the ecologic balance of the gingival sulcus to an area that f avors the growth of disease-associated organisms (pr edominately gram-negative anaerobic species) at the expense of the health-associated organisms (predominately gram-positive facultative species)84 and (2) inhibiting the patient s access to r emove accumulated plaque. The frequency of overhanging margins on proximal restorations varies in different studies f r om 16.5% to 75%. 17,49,68,115 A highl y significant statistical relationship has been reported between marginal defects and reduced bone height.17,58,68 Removal of overhangs permits more effective control of plaque, resulting in a reduction of gingival inflammation and a small increase in radiographic alveolar bone support52,61,152 (Figures 22-16 and 22-17 ). The location of the gingival margin of a r estoration is directly related to the health status of adjacent periodontal tissues.150

CHAPTER 22 The Role of Dental Calculus and Other Local Predisposing Factors
Numerous studies hav e shown a positiv e correlation between margins located apical to the marginal gingiva and the pr esence of gingival inflammation.49,65,72,129,152 Subgingival margins are associated with large amounts of plaque , more severe gingivitis, and deeper pockets. Even high-quality restorations, if placed subgingi-

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Figure 22-16 Radiograph of amalgam ov erhang on the distal sur face of maxillary second molar that is a source of plaque r etention and gingival irritation.

vally, will incr ease plaque accum ulation, gingival inflammation,* and the rate of gingival fluid flow.11,54 Margins placed at the le vel of the gingival crest induce less severe inflammation, whereas supragingival margins are associated with a degr ee of periodontal health similar to that seen with nonr estored interproximal surfaces.44,150 Roughness in the subgingival ar ea is considered to be a major contributing f actor to plaque buildup and subsequent gingival inflammation.150 The subgingival zone is composed of the margin of the restoration, the luting mater ial, and the prepared, as well as the unprepared tooth sur f ace. Sources of marginal r oughness include grooves and scratches in the surface of acrylic resin, porcelain, or gold restorations (Figure 22-18); separation of the restoration margin and luting mater ial f rom the cer vical finish line, thereby exposing the r ough surface of the pr epared tooth ( Figure 22-19); dissolution and disintegration of the luting mater ial between the preparation and the restoration, leaving a space (Figure 22-20); and inadequate marginal fit of the r estoration.150 Subgingival margins t ypically have a gap of 20 to 40 m between the margin of the r estoration and the unpr epared tooth.148 Colonization of this gap b y bacterial plaque undoubted ly contributes to the detr imental effect of margins placed in a subgingival environment.

Contours/Open Contacts. Overcontoured crowns and restorations tend to accumulate plaque and possibly prevent the selfcleaning mechanisms of the adjacent cheek,lips, and tongue6,79,104,171 (Figures 22-21 and 22-22 ). Restorations that f ail to r eestablish adequate interproximal embrasure spaces are associated with papillary inflammation. Undercontoured crowns that lac k a pr otective height of contour do not r etain as much plaque as ov ercontoured crowns and therefore may not be as detrimental during mastication as once thought. 171 The contour of the occ lusal surface as established b y the marginal ridges and related developmental grooves normally serves to deflect f ood away f r om the inter proximal spaces. The optimal cervico-occlusal location f or a poster ior contact is at the longest mesiodistal diameter of the tooth, which is generally just apical to the crest of the marginal r idge. The integrity and location of the proximal contacts along with the contour of the marginal r idges and developmental grooves typically prevent interproximal f ood
*References 82, 84, 105, 111, 130, and 151.

Figure 22-17 Radiograph of the same patient shown in after the excessive amalgam has been r emoved.

Figure 22-16

Figure 22-18 A, Polished gold alloy crown demonstrates surface scratches. B, Gold alloy crown that had been in the mouth for several years has scratches filled with deposits. (From Silness J: Dent Clin North Am 24:317, 1980.)

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Figure 22-21 Inflamed marginal and papillar y gingiva adjacent to an overcontoured porcelainfused-to-metal crown on the maxillary left central.

Figure 22-19 After cementation, luting material prevents approximation of the cr own margin and the finishing line, leaving par t of the pr epared tooth uncovered (area between arrowheads). (From Silness J: Dent Clin North Am 24:317, 1980.)

Figure 22-22 Radiograph of ill-fitting porcelain f used to metal cr own shown in Figure 22-21.

R
Figure 22-20 Craters have formed after dissolution and disintegration of the luting mater ial. Spherical bodies ar e not identified. Crown (C); root (R). (From Silness J: Dent Clin North Am 24:317, 1980.)

impaction. Food impaction is the forceful wedging of food into the periodontium by occlusal f orces. As the teeth wear down, their originally convex proximal surf aces become flattened and the wedging effect of the opposing cusp is exaggerated. Cusps that tend to forcibly wedge food into interproximal embrasures are known as plunger cusps. The interproximal plunger cusp effect may also be observed when missing teeth are not replaced and the relationship between proximal contacts of a djacent teeth is alter ed. An intact proximal contact precludes the f orcef ul wedging of f ood into the interproximal embrasure space, whereas a light or open contact is conducive to impaction. The classic analysis of the factors leading to food impaction was made by Hirschfeld,63 who recognized the following factors: uneven occlusal wear, opening of the contact point as a r esult of loss of proximal support or from extrusion, congenital morphologic abnormalities, and improperly constructed restorations. The presence of the pr eviously mentioned abnormalities does not necessarily lead to food impaction and periodontal disease. A study of interproximal contacts and marginal r idge relationships84 in three groups of periodontally healthy males revealed that 0.7%

Figure 22-23 Inflamed palatal gingiva associated with a maxillar y provisional acrylic partial denture. Note the substantial difference in color of the inflamed gingiva adjacent to the pr emolars and first molar compared with the gingiva adjacent to the second molar .

to 76% of the proximal contacts were defective and 33.5% of adjacent marginal r idges were uneven.114 However, greater probing depth and loss of c linical attachment have been reported for sites that exhibited both an open contact and food impaction as compared with contralateral control sites without open contacts or food impaction.70 Excessive anterior overbite is a common cause of food impaction on the lingual sur f aces of the maxillar y anterior teeth and the f acial sur f aces of the opposing mandibular teeth. These areas may be exemplified by attachment loss with gingival recession. injurious to the per iodontal tissues.6,75 One exception to this may be self-curing acrylics166 (Figure 22-23).

Materials. In general, restorative materials are not in themselves

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Figure 22-24 Lower incisor showing a pr ominent root with gingival recession and lack of attached gingiva.

Figure 22-25 The same patient as shown in Figure 22-24 after placement of a sof t tissue graf t to gain attached gingiva and tr eat the gingival recession.

Plaque that f orms at the margins of r estorations 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.109 Although surface textures of r estorative materials differ in their capacity to retain plaque,170 all c an be adequatel y cleaned if they ar e polished and accessible to methods of oral h ygiene.110,137 The undersurf ace of pontics in fixed bridges should barely touch the mucosa. Access for oral hygiene is inhibited with excessiv e pontic to tissue contact, thereby contributing to plaque accumulation that will cause gingival inflammation and possibly formation of pseudopoc kets.43,150

Design of Removable Partial Dentures. Several investigations have shown that af ter the inser tion of par tial dentures, the mobility of the abutment teeth, gingival inflammation, and periodontal pocket f ormation all incr ease.16,25,144 This is because partial dentures f avor the accum ulation of plaque , particularly if they cover the gingival tissue. Partial dentures that are worn during both night and day induce mor e plaque f ormation than those worn only during the day time.16 These observations emphasize the need f or c aref ul and personaliz ed oral h ygiene instruction to avoid harmful effects of par tial dentures on the r emaining teeth and periodontium.11 The presence of r emovable partial dentures induces not onl y quantitative changes in dental plaque 47 but also qualitative changes, promoting the emergence of spir ochetal microorganisms.48 Restorative Dentistry Procedures. The use of r ubber dam clamps, matrix bands, and burs in such a manner as to lacerate the gingiva r esults in var ying degrees of mechanic al trauma and inflammation. Although such transient injur ies generally undergo repair, they are needless sources of discomfort to the patient. Forceful packing of a gingival r etraction cord into the sulcus to pr epare subgingival margins on a tooth or for the pur pose of obtaining an impression may mechanic ally injure the per iodontium and leave behind impacted debris capable of c ausing a f or eign body reaction.

Figure 22-26 Anterior open bite with flared incisors as observed in association with a habit of tongue thr usting.

high f renal attachment and small quantities of attached gingiva frequently exhibit recession.1,101
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Malocclusion
Irregular alignment of teeth as f ound in c ases of malocc lusion may make plaque control more difficult. Several authors have found a positive correlation between crowding and per iodontal disease,24,117,157 whereas other investigators did not find any correlation.46 Uneven marginal ridges of contiguous poster ior teeth have been f ound to hav e a low corr elation with poc ket depth, loss of attachment, plaque, calculus, and gingival inflammation.77 Roots of teeth that ar e prominent in the ar ch (Figures 22-24 and 22-25 ), such as in a bucc al or lingual version, or that are associated with a

Tongue thrusting exerts excessive lateral pressure on the anterior teeth, which may result in spreading and tilting of the anterior teeth (Figures 22-26 and 22-27). Tongue thrusting is an important contributing f actor in tooth migration and the de velopment of an anterior open bite.26 Mouth breathing may be observed in association with a habit of tongue thr usting and an anter ior open bite . Marginal and papillar y gingivitis is fr equently encountered in the maxillary anterior sextant in c ases involving an anterior open bite with mouth breathing. However, the role of mouth breathing as a local etiologic f actor is unclear because conflicting evidence has been reported.3,66,67,157 Restorations that do not conform to the occ lusal pattern of the mouth result in occlusal disharmonies that may cause injury to the supporting periodontal tissues. Teeth with deeper initial pr obing depths, worse prognoses, and greater mobility have been observed f or teeth with occlusal discrepancies than teeth without initial occlusal discrepancies. 60,112 Histologic features of the periodontium f or a tooth subjected to traumatic occ lusion include a widened subcrestal periodontal ligament space , a r eduction in collagen content of the oblique and horizontal fibers, an increase in vascularity and leukoc yte infiltration, and an incr ease in the number of osteoclasts on bordering alveolar bone.13 However, these obser vations are generally apical and separate fr om the bacterial-induced inflammation that occurs at the base of the sulcus. On the basis of current human trials, it is still impossible to definitively answer the question, Does occlusal trauma modif y the pr ogression o f periodontal attachment loss associated with per iodontal

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PART 4 Etiology of Periodontal Diseases

Figure 22-27 Radiographs of patient shown in Figure 22-26 with anterior open bite. Note severe periodontal destruction (arrows) in molar regions.

Figure 22-28 Gingival inflammation and enlargement associated with orthodontic appliance and poor oral h ygiene.

placed beyond the level of attachment because this will detach the gingiva f rom the tooth and result in apical prolif eration of the junctional epithelium with an incr eased incidence of gingival recession.118 The mean al veolar bone loss per patient f or adolescents who underwent 2 years of orthodontic care during a 5-year observation period ranged between 0.1 and 0.5 mm.19 This small magnitude of alveolar bone loss was also noted in the control group and therefore considered to be of little c linical significance. However, the degree of bone loss during adult orthodontic care may be higher than that observed in adolescents,91 especially if the periodontal condition is not treated bef ore initiating or thodontic therapy. Theref ore orthodontic treatment should not b e commenced in the presence of uncontrolled periodontal disease.

inflammation?147 (See Chapter 49 for a more detailed explanation of periodontal trauma from occlusion and the periodontal response to external forces.)

Periodontal Complications Associated with Orthodontic Therapy

Orthodontic therapy may affect the per iodontium by f avoring plaque retention, by directly injuring the gingiva as a r esult of overextended bands, and by creating excessive f orces, unf avorable forces, or both on the tooth and suppor ting structures.

Plaque Retention and Composition. Orthodontic appliances not only tend to retain bacterial plaque and food debris, resulting in gingivitis (Figure 22-28), but also are capable of modif ying the gingival ecosy stem. An incr ease in Prevotella melaninogenica, Prevotella intermedia, and Actinomyces odontolyticus and a decrease in the pr oportion of f acultativ e microorganisms was detected in the gingival sulcus af ter the placement of or thodontic bands.35 More recently, Aggregatibacter actinomycetemcomitans was found in at least one site in 85% of childr en wearing orthodontic appliances.116 In contrast, only 15% of unbanded contr ol subjects were positive for A. actinomycetemcomitans. Gingival Trauma and Alveolar Bone Height. Orthodontic treatment is of ten started soon af ter eruption of the permanent teeth, when the junctional epithelium is still adher ent to the enamel sur f ace. Orthodontic bands should not be f or cef ully

Tissue Response to Orthodontic Forces. Orthodontic tooth movement is possible because the periodontal tissues are responsive to externall y applied f or ces.128,143 Alveolar bone is remodeled by osteoclasts inducing bone resorption in areas of pressure and osteoblasts f orming bone in ar eas of tension. Although moderate orthodontic forces ordinarily result in bone r emodeling and repair, excessive force may produce necrosis of the periodontal ligament and adjacent al veolar bone.121-123 Excessive orthodontic forces also increase the risk of apical root resorption.21,22 The prevalence of severe root resorption, as indicated by resorption of more than one third of the root length, during orthodontic therapy in adolescents has been r eported at 3%. 71 The incidence of moderate to severe root resorption for incisors among adults ranging in age f rom 20 to 45 years has been reported as 2% pretreatment and 24.5% posttreatment.91 Risk factors associated with root resorption during orthodontic treatment include duration of treatment, magnitude of the for ce applied, direction of the tooth mov ement, and continuous versus intermittent applic ation of f or ces120 (Figures 22-29 to 22-31 ). It is imp ortant to avoid excessive f orce and/or t oo rapid of tooth movement in orthodontic treatment. The use of elastics to c lose a diastema may r esult in se vere attachment loss with possible tooth loss as the elastics migrate apically along the r oot (Figures 22-32 and 22-33 ). Surgical exposure of impacted teeth and orthodontic-assisted eruption has the potential to compr omise the per iodontal attachment on adjacent teeth (Figures 22-34 and 22-35). However, the majority of impacted teeth that ar e surgically exposed and aided in their er uption by

CHAPTER 22 The Role of Dental Calculus and Other Local Predisposing Factors

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Figure 22-29 Panoramic radiograph illustrating a limited degr ee of pretreatment root resorption (arrows) existed bef or e orthodontic care was initiated.

Figure 22-32 Maxillary central incisors in which an elastic ligatur e was used to close a midline diastema. Note inflamed gingiva and deep probing depths.

Figure 22-33 The same patient as shown in Figure 22-32 with a f ullthickness mucoperiosteal flap reflected to expose the elastic ligatur e and angular intrabony defects around the central incisors. Figure 22-30 Panoramic radiograph of the same patient as shown in Figure 22-29 after 4 years of intermittent orthodontic treatment. Note that several roots have undergone severe resorption (arrows) during orthodontic care.

Figure 22-31 Panoramic radiograph of the same patient as depicted in Figure 22-30. Note the teeth that had de veloped extensive root resorption with accompanying hypermobility have been extracted and r eplaced by implant supported crowns. Figure 22-34 Radiograph of an impacted maxillar y canine that required surgical exposure and orthodontic assistance to er upt.

orthodontic treatment subsequently exhibited >90% of their attachment intact.62 It has been r eported that the dentoal veolar gingival fibers that are located within the marginal and attached gingiva are stretched when teeth are rotated during orthodontic therapy.36 Surgical severing or removal of these gingival fibers in combination with a brief period of retention may reduce the incidence of relapse after orthodontic treatment intended to realign rotated teeth.20,102

Extraction of Impacted Third Molars

Numerous clinical studies hav e reported that the extraction of impacted third molars of ten results in the cr eation of v ertical defects distal to the seco nd molars.7 This iatrogenic effect is unrelated to flap design28 and appears to occur mor e often when third molars are extracted in individuals older than 25 y ears.7,80,99 Other

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Figure 22-35 Same patient shown in Figure 22-34 with palatal flap reflected to reveal bony dehiscence on the maxillary lateral incisor af ter orthodontic therapy.

Figure 22-37 Gingival recession on a maxillar y canine caused by self inflicted trauma from the patient s fingernail.

Figure 22-36 Panoramic radiograph illustrating a mesial impacted low er left third molar with a widened follic le and no apparent bone on the distal interproximal surf ace of the second molar . Alternatively, the low er right third molar is vertically impacted and exhibits inter proximal bone distal to the second molar and mesial to the thir d molar.

Figure 22-38 Tongue pierced with oral je welry.

factors that appear to play a r ole in the de velopment of lesions on the distal surface of second molars, particularly in those older than 25 years, include the presence of visible plaque, bleeding on probing, root resorption in the contact ar ea between second and thir d molars, presence of a pathologically widened follicle, inclination of the third molar, and c lose proximity of the thir d molar to the second molar ( Figure 22-36).80 Other potential iatrogenic adverse consequences of removal of third molars include permanent paresthesia (numbness of the lip , tongue, and cheek), which occurs at a f requency of appr oximately 1 in 100,000 among wisdom teeth removed in the United S tates.45

Habits and Self-Inicted Injuries

Patients might not be awar e of their self-inflicted injurious habits that may be impor tant to the initiation and pr ogression of their periodontal disease. Mechanical f orms of trauma c an stem f r om improper use of a toothbr ush, wedging of toothpicks between the teeth, application of fingernail pressure against the gingiva, pizza burns, and others 18 (Figure 22-37). Sources of chemic al irritation include topical applications of caustic medications such as aspir in or cocaine, allergic reactions to toothpaste and che wing gum, use of chewing tobacco, and concentrated mouthr inses.146 Accidental and iatrogenic gingival injur ies may be c aused by a var iety of chemical, physical, and thermal sources, yet they are generally selflimiting. Iatrogenic injuries are often acute, whereas factitious injuries tend to be mor e chronic in nature.127

Figure 22-39 Probing depth of 8 mm with 10 mm clinical attachment loss on lingual sur f ace of lower central incisor adjacent to oral je welry in pierced tongue. Central incisor was found to be vital. (Courtesy Dr. Leonidas Batas, Minneapolis.)

recently among teenagers and young adults (Figure 22-38). Whittle and Lamden170 surveyed 62 dentists and found that 97% had seen patients with either lip- or tongue-pier cing jewelry within the previous 12 months. The incidence of lingual recession with pocket formation (Figure 22-39) and radiographic e vidence of bone loss (Figure 22-40) was 50% among subjects with a mean age of 22 years who w ore lingual barbells f or 2 or mor e years.34 Chipped lower anterior teeth were noted in 47% of the patients who w ore tongue-piercing jewelry f or 4 y ears or mor e. Patients need to be informed of the risks of wearing oral jewelry and cautioned against such practices.

Trauma Associated with Oral Jewelry. The use of piercing jewelry in the lip or tongue has become mor e common

Toothbrush Trauma. Abrasions of the gingiva, as w ell as

alterations in tooth str ucture, may result from aggressive brushing

CHAPTER 22 The Role of Dental Calculus and Other Local Predisposing Factors

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Figure 22-42 Chemical burn caused by aspirin that depicts sloughing gingival tissue and resultant recession.

Figure 22-40 Radiograph of lower incisor shown in Figure 22-39 depicting bone loss associated with tongue pier ced by oral jewelry.

Figure 22-43 Biopsy of aspirin-induced chemical burn. Note intraepithelial vesicles (V) and an inflammatory infiltrate (I) within the under lying connective tissue.

Figure 22-41 Overzealous use of a toothbr ush resulted in denudation of the gingival epithelial sur f ace and exposur e of the under lying connective tissue as a painful ulcer.

brush abrasion.153 Improper use of dental floss may result in lacerations of the interdental papilla.

Chemical Irritation. Acute gingival inflammation may be

in a hor izontal or r otary f ashion. The deleterious effect of excessively forceful brushing is accentuated when highly abrasive dentif rices are used. The gingival changes attr ibutable to toothbr ush trauma may be acute or chr onic. The acute changes var y in their appearance and duration fr om scuffing of the epithelial sur face to denudation of the underlying connective tissue with the formation of a painf ul gingival ulcer ( Figure 22-41). Diffuse erythema and denudation of the attached gingiva throughout the mouth may be a striking result of ov erzealous brushing. Signs of acute gingival abrasion are f requently noted when the patient first uses a ne w brush. Puncture lesions may be pr oduced when heavy pr essure is applied to firm bristles that are aligned perpendicular to the surface of the gingiva. A f or cibly embedded toothbr ush bristle may be retained in the gingiva and c ause an acute gingival abscess. Chronic toothbrush trauma r esults in gingival r ecession with denudation of the r oot surf ace. Interproximal attachment loss is generally a consequence of bacteria-induced periodontitis, whereas buccal and lingual attachment loss is frequently the result of tooth-

caused by chemical irritation resulting f rom either sensitivit y or nonspecific tissue injury. In allergic inflammatory states, the gingival changes range fr om simple erythema to painful v esicle formation and ulceration. Severe reactions to or dinarily innocuous mouthwashes, dentif rices, or dentur e materials are of ten explainable on this basis. Acute inflammation with ulceration may be pr oduced by the nonspecific injurious effect of chemicals on the gingival tissues. The indiscriminate use of str ong mouthwashes, topical application of corrosive drugs such as aspir in (Figure 22-42) or coc aine, and accidental contact with dr ugs such as phenol or sil ver nitrate are common examples of chemicals that cause irritation of the gingiva. A histologic view of an aspirin-induced chemical burn shows vacuoles with serous exudates and an inflammatory infiltrate in the connective tissue ( Figure 22-43).

Smokeless Tobacco
Snuff and che wing tobacco constitute the tw o main f orms of smokeless tobacco. Snuff is a fine cut form of tobacco available as loosely packed or in small sachets. Chewing tobacco is a mor e coarse-cut available in the f orm of loose leaves, a solid block, or

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effect of smokeless tobacco on the periodontium and found double the incidence of se vere periodontitis (odds ratio 2.1; 95% CI 1.2 to 3.7) among 12,932 adults who used smokeless tobacco but never smoked cigarettes.41 However, Bergstrom et al found similar incidences of severe periodontitis among both smokeless tobacco users and nonusers.12 It c an be conc luded that the use of smokeless tobacco is associated with at least localized gingival recession, clinical attachment loss, leukoplakia, and possibly enhanced susceptibility to severe periodontitis.

plug and as a twist of dr ied leaves. Chewing tobacco is t ypically placed in the mandibular buccal vestibule for several hours, during which time saliva and dilute tobacco is periodically expectorated.167 The nicotine uptake of smokeless tobacco is similar to smoking cigarettes in that consumption of a 34-g container of smokeless tobacco is approximately equal to 1.5 pac ks of cigarettes.55 Many professional baseball players use che wing tobacco. Perceived benefits of chewing tobacco are those derived from nicotine, including improved mental aler tness and diminished r eaction time, muscle relaxation, and reduced anxiety and appetite.56,132 A 1990 survey of 1109 prof essional baseball play ers in the United S tates reported 39% of the play ers used smokeless tobacco with 46% of the users exhibiting leukoplakia within the gingiva and/or m ucosa (Figure 22-44).40 Histologic f eatur es of oral leukoplakia associated with smokeless tobacco include (1) chevronlike pattern of hyperkeratosis with focal areas of inflammation and (2) h yperplasia in the basal cell layer (Figure 22-45). Increased incidence of gingival recession, cervical root abrasion, and r oot caries have been r eported with smokeless tobacco (Figure 22-46).113,133,134,160 The incidence of gingival recession among adolescents who use smokeless tobacco has been reported as 42% compared to 17% among nonusers.31,100,101,103 The NHANES III epidemiologic study inv estigated the adv erse

Radiation Therapy
Radiation therapy has c ytotoxic effects on both normal cells and malignant cells. A typical total dose of radiation for head and neck tumors is in the range of 5000 to 8000 cGy (cGy = 1 rad) or equivalent to 50 to 80 S ieverts (Sv).119 The total dose of radiation is generally given in par tial incremental doses referred to as fractionation. Fractionation helps minimize the adverse effects of the radiation while maximizing the death rate f or the tumor cells. 42 Fractionated doses are typically administered in the range of 100 to 1000 cGy, or 1 to 10 Sv, per week. Radiation treatment induces an obliterativ e endarteritis that results in sof t tissue ischemia and fibrosis while irradiated bone

Figure 22-44 Oral leukoplakia in vestibule associated with use of smokeless tobacco.

Figure 22-46 Oral leukoplakia, recession, and c linical attachment loss associated with use of smokeless tobacco .

Figure 22-45 Histologic features of oral leukoplakia associated with smokeless tobacco. A, Chevronlike pattern of hyperkeratosis with focal areas of inflammation, B, Hyperplasia in basal cell lay er.

CHAPTER 22 The Role of Dental Calculus and Other Local Predisposing Factors
becomes hypovascular and hypoxic.97 Adverse affects of head and neck radiation therap y include dermatitis and m ucositis of the irradiated area, as well as muscle fibrosis and tr ismus, which may restrict access to the oral cavity.135 The mucositis typically develops 5 to 7 day s after radiation therapy is initiated. The severity of the mucositis can be reduced by asking the patient to avoid secondary sources of irritation, such as smoking , alcohol, and spicy foods, to the mucous membrane. Use of a chlorhexidine digluconate mouthrinse may help r educe the mucositis.125 However, most chlorhexidine mouthrinses currently available in the U.S. have a high alcohol content that may act as an astr ingent, which dehydrates the mucosa, thereby intensif ying the pain. Saliva production is permanentl y impaired when salivary glands that are located within the portal of radiation receive 6000 cGy or 60 Sv.98 Xerostomia results in greater plaque accum ulation and a r educed buffering capacity by saliva. The use of effective oral hygiene, professional dental prophylaxis cleanings, fluoride applications, and frequent dental examinations are essential to control caries and periodontal disease. The use of customized trays appears to be a more effective method of fluoride application as compared with the toothbr ush.76 Periodontal attachment loss and tooth loss has been r eported to be greater in c ancer patients who w ere treated with high-dose unilateral radiation as compared with the nonradiated control side of the dentition.39 Patients diagnosed with oral cancer that require radiation therapy should ideall y be assessed f or dental needs (mucositis, xerostomia, faulty restorations, periapical lesion, coronal and cervical decay, and periodontal status) before initiating radiation treatment.59 Treatment and prevention of trismus, oral fungal inf ections, odontogenic inf ections, osteoradionecrosis, decay, and periodontal disease is critical to minimize oral morbidity for these

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patients. Dental and periodontal infections have the potential to be a severe risk for a patient who has been treated with head and neck radiation. The risk of osteoradionecrosis for oncology patients can be minimized by evaluating their oral status, providing dental care, and allowing time f or tissue r epair bef ore the commencement of radiotherapy.78 Oral conditions that increased the risk of osteoradionecrosis for patients about to undergo radiation therap y for oral malignancies include >5 mm periodontal probing depths, >40% dental plaque score, and >60% alveolar bone loss.74 Nonrestorable teeth and/or teeth with significant periodontal problems should be extracted bef ore radiation therap y to r educe the r isk of postradiotherap y osteoradionecrosis.78 (See Chapter 37 for more detail on the periodontal management of medically compromised patients.) The risk of osteoradionecr osis must be evaluated bef ore performing atraumatic extractions or limited periodontal surgical procedures in pr eviously irradiated sites. Theref ore the dentist may choose to consult with the patient s oncologist bef or e initiating therapy. A r ecent randomized multicenter clinical trial questions the merit of using hyperbaric oxygen (HBO) therapy to treat osteoradionecrosis, since at 1-y ear af ter treatment only 19% of test subjects responded to H BO versus 32% of placebo subjects. 5 Administration of the combination of pento xifylline with vitamin E as antioxidants currently shows the gr eatest promise f or revascularization and treatment of osteoradionecrosis sites.33

References can be found on the companion website at www.expertconsult.com.

SCIENCE TRANSFER
Calculus plays a significant role in per iodontal inflammation primarily because it provides an ideal surface for bacterial plaque accumulation. One of the univ ersal goals for treatment of gingivitis and per iodontitis is the complete removal of all c alculus, particularly subgingival calculus. The presence of residual subgingival calculus after treatment predisposes the patient to ongoing periodontal destruction. The removal of calculus embedded into cementum with root planing is one of the most difficult procedures in periodontal therapy and requires special skills that clinicians are only able to develop with repeated procedures over time. Exposing subgingival calculus with surgical approaches increases the possibility of calculus removed compared to nonsurgical root planing. Theref ore the cornerstone of all per iodontal flap techniques is commitment to r oot planing, even though the patient may have previously had nonsurgical or initial therapy. Other predisposing f actors f or per iodontitis, such as r estorative inadequacies and poor ly designed r emovable partial dentures, are significant primarily because they increase the accumulation of bacterial dental plaque. Loss of even one tooth can lead to a plethora of positional changes of adjacent and opposing teeth with an increasing risk of periodontal breakdown caused by open contacts, plunger cusps, and occlusal instability. Thus it is good clinical procedure to replace missing teeth with implants or fixed bridges to maintain periodontal health of the remaining dentition.