Aggressive Periodontitis Finals Lesson 1-5 PDF

Group 7 : Aggressive Periodontitis  Epidemiology of Gingival and Periodontal Diseases CHAPTER 5 91 attachment loss remains controversial. Although Although aggressive periodontitis is char...

Group 7 : Aggressive Periodontitis  Epidemiology of Gingival and Periodontal Diseases CHAPTER 5 91 attachment loss remains controversial. Although Although aggressive periodontitis is characterized by some reports claim that the presence of these species age at onset and pattern of periodontal destruction, is a good predictor, others observed an association case definitions for early onset disease or its subtypes with disease progression but found that the presence have varied across epidemiologic studies. In a national of putative pathogenic species was unreliable as a pre- survey of the oral health of U.S. school children, three dictor for future clinical attachment loss in individual case definitions were used for aggressive periodontitis, as follows:48 patients and at specific sites. Subject prediction usu- ally is more accurate than site prediction. The absence of any of the group of five to seven putative periodon- Localized aggressive periodontitis: At least one first tal pathogens is a reliable indicator for the absence of molar and at least one incisor or second molar and future clinical attachment loss for most patients. two or fewer canines or premolars had >3 mm of at- Bleeding on probing: Longitudinal data are available. tachment loss. Multivariate analyses implicate bleeding on probing Generalized aggressive periodontitis: Criteria for local- in combination with increasing pocket depth. At ized disease were not met, four or more teeth had present, bleeding on probing is widely used as an in- >3 mm of attachment loss, and at least 2 affected dication for needed treatment. However, bleeding on teeth were second molars, canines, or premolars. probing alone is not a predictor of elevated risk for fu- Incidental loss of periodontal attachment: Criteria for ture loss of clinical attachment. On the other hand, a localized or generalized were not met, and one or lack of bleeding on probing, especially on two or more teeth had >3 mm of attachment loss. more occasions, is an excellent indicator of periodon- tal health, with a predictive value of 0.972. Other studies have based case definitions on various Previous periodontal disease: Longitudinal data are combinations of disease patterns and the extent and available. Multivariate analyses implicate past disease. severity of pocket depth, attachment loss, and bone loss. The risk for future periodontal deterioration in a A thorough review of studies that have investigated ag- given individual is strongly associated with the pres- gressive forms of periodontitis in childhood and adoles- ence and severity of existing periodontitis. In other cence can be found in an article by Papapanou. 62 As our words, individuals with the most advanced existing understanding of aggressive periodontitis changes, the periodontitis are at greatest risk for future clinical at- nomenclature for the disease and case definitions will tachment loss. Individuals who are currently free of likely continue to evolve. periodontitis are less likely to experience future clini- cal attachment loss than those with periodontitis. However, past disease is only a good clinical predictor. How Much Aggressive Periodontitis Is Present? It is not likely to be causal, and it is unclear whether Most studies from the U.S. and other countries that have past disease is predictive of both incidental attach- examined localized aggressive periodontitis in adolescents ment loss and progression of current disease. have reported prevalence estimates below 1%.62 In the Genetic factors: Longitudinal data are available. Mul- U.S., the prevalence of localized and generalized aggres- tivariate analyses implicate genetic factors. Genetic sive periodontitis were estimated to be 0.53% and 0.13%, factors are strongly associated with the aggressive respectively.48 Another 1.61% of the adolescents had inci- forms and, to a lesser extent, with the chronic form. dental attachment loss-attachment loss that did not fit Stress: Most studies involve necrotizing ulcerative gin- the study's case definitions for localized or generalized dis- givitis (NUG). Case control and a few short-term lon- ease. 73 Although these prevalence estimates are small, to- gitudinal studies indicate associations. Multivariate gether they represented almost 300,000 U.S. adolescents and intervention studies are needed. Biologic mecha- at the time of the study (1986-87). 48 nisms are known. How Much New Aggressive Periodontitis AGGRESSIVE PERIODONTITIS I s Present? Aggressive periodontitis (formerly known as early onset Very few longitudinal studies of aggressive periodontitis periodontitis) isperiodontal destruction that becomes clin- have been conducted. One longitudinal study conducted ically significant around adolescence or early adulthood. in the United Kingdom followed 167 subjects from ages The disease has been classified into two types-localized 14 to 19. 25 Periodontal attachment loss was measured and generalized. 68 Other terms found in the literature on the mesiofacial surfaces of the first molars, first pre- that have been used to describe aggressive forms of peri- molars, and central incisors. During the 5 years of odontitis include juvenile, localized juvenile, generalized follow-up, the percentage of subjects with attachment j uvenile, rapidly progressive, severe, and prepubertal peri- loss on one or more of the examined teeth increased dra- odontitis (see Table 4-3). 68 The distinction between the matically-from 3% to 77% for attachment loss of >1 localized and generalized forms is based on the distribu- mm and from 0% to 14% for attachment loss of >2 mm. tion of the periodontal destruction in the mouth. Local- By age 19, 31% of the sites examined had attachment ized aggressive periodontitis is characterized by bone loss loss of >1 mm, and 3.1% had attachment loss of >2 around the first molars and incisors. As the name implies, mm. The teeth most commonly affected were the maxil- generalized aggressive periodontitis is characterized by a lary first molars and the mandibular central incisors. In more widespread pattern of periodontal destruction. the 19-year-old subjects, 9% of the maxillary molars had 92 PA RT 2 Classification and Epidemiology of Periodontal Diseases Why Do Patients Have Aggressive Periodontitis, attachment loss of >2 mm. The presence of subgingival and What Puts Them at Risk? calculus and plaque at baseline were significant predic- tors of loss of attachment at 5 years. Although this study The bacterium A. actinomycetemcomitans is found in provides useful information on the change in prevalence high numbers in localized aggressive periodontal lesions of aggressive periodontitis, its authors pointed out that and is the primary pathogen associated with the dis- the cohort was not a randomly selected group of 14- ease.79 Elimination of the pathogen is associated with year-olds, and therefore the results cannot be generalized clinical improvement.79 The bacterium produces a strong to the population at large. leukotoxin that kills neutrophils, which provide an im- Another study that followed a cohort of 14-year-old portant defense against periodontal infections. Different subjects was conducted among Norwegians.' Of the strains of A. actinomycetemcomitans produce different lev- 2767 subjects examined at baseline (14 years old) in els of leukotoxin. Highly toxic strains produce 10 to 20 1984, 215 were reexamined in 1992 (they were also ex- times the levels of leukotoxin as do minimally toxic amined in 1986 and 1988). At each examination, the strains." Patients with localized aggressive periodontitis prevalence of radiographic alveolar bone loss was as- are more likely to harbor the highly leukotoxic strains sessed on sets of bite-wing radiographs. Bone loss was than periodontally healthy persons or persons with measured on the mesial and distal of fully erupted teeth chronic periodontitis.81 In a study of 21 families with (distal of the canines to the mesial of the second molars) at least one family member with localized disease, chil- and was defined as the distance from the cemento- dren infected with the highly leukotoxic strains of A. enamel junction to the alveolar crest. The distance had actinomycetemcomitans were more likely to develop local- to exceed 2 mm for bone loss to be present. At baseline, ized aggressive periodontitis.17 Persons with African the prevalence of subjects with one or more lesions was backgrounds have been found more likely to be infected approximately 3.5%. By 1992 the prevalence of subjects with the more virulent strains of A. actinomycetemcomi- with bone loss had doubled. The percentage of subjects tans, which may explain the elevated risk of localized with 3 or more sites with bone loss also increased during juvenile periodontitis among African-Americans." Al- that time from 2.5% to 33.3%. though infection with A. actinomycetemcomitans is A review of the available longitudinal studies of peri- strongly associated with cases of localized disease, not odontitis in childhood and adolescence concluded that all individuals infected with A. actinomycetemcomitans subjects with signs of periodontal disease at a young age develop localized aggressive periodontitis, and not all in- are likely to have further periodontal deterioration. Pro- dividuals with localized disease have detectable levels of gression is more extensive at initially infected sites and A. actinomycetemcomitans. among subjects of low socioeconomic status. 62 Another factor believed to be involved in the patho- genesis of aggressive periodontitis is defective neutrophil function. Depressed neutrophil chemotaxis is a consis- Does My Patient with Aggressive Periodontitis Fit tent finding among patients with localized or general- the Typical Profile? ized forms of the disease.77 Studies have shown that 70% The prevalence of aggressive periodontitis is higher in to 75% of patients with localized disease have depressed African-Americans than in whites. In a study of aggres- neutrophil chemotaxis.77 Localized aggressive periodonti- sive periodontitis among adolescents in the U.S., it was tis tends to occur in families, and this neutrophil chemo- estimated that 2.05% of African-Americans had localized taxic abnormality is genetic in origin and may predis- periodontitis, compared with 0.14% of whites.48 For gen- pose individuals to localized disease." However, not all eralized disease, the prevalence was 0.59% for African- individuals with localized disease have depressed neu- Americans and 0.03% for whites. The prevalence of inci- trophil chemotaxis, and not all individuals with de- dental attachment loss was much higher among pressed neutrophil chemotaxis develop localized disease. African-Americans than whites-4.63% versus 0.91%. Other, currently unidentified host factors are likely in- Whether or not the prevalence of aggressive peri- volved in the pathogenesis of the disease. odontitis differs by gender is unclear. Early case reports and small studies often found the condition to be more REFERENCES prevalent among women; however, findings from larger studies have suggested the distribution of the disease is 1. Aass AM, Tollefsen T, Giermo P: A cohort study of radi- fairly equal between the genders." The 1986-87 survey ographic alveolar bone loss during adolescence. J Clin Peri- odontol 1994; 21:133. of U.S. schoolchildren indicated that males had slightly 2. Abdellatif HM, Burt BA: An epidemiological investigation higher but statistically insignificant prevalence of local- into the relative importance of age and oral hygiene status ized and generalized aggressive periodontitis and inci- as determinants of periodontitis. J Dent Res 1987; 66:13. dental attachment loss. 48 However, when the distribu- 3. Addy M, Hunter ML, Kingdon A, et al: An 8-year study of tion of the disease by gender was examined among race changes in oral hygiene and periodontal health during ado- groups, differences by gender became much more evi- lescence. Int J Paediatr Dent 1994; 4:75. dent. Among African-Americans, males were 2.9 times 4. Albandar JM: A 6-year study on the pattern of periodontal more likely than females to have localized disease. disease progression. J Clin Periodontol 1990; 17:467. Among whites, the association was reversed. White fe- 5. Albandar JM, Brunelle JA, Kingman A: Destructive peri- males were 2.5 times more likely than white males to odontal disease in adults 30 years of age and older in the have localized disease. United States, 1988-1994. J Periodontol 1999; 70:13.  Aggressive Periodontitis Richard J. Nagy and Karen F. Novak CHAPTER CHAPTER OUTLINE LOCALIZED AGGRESSIVE PERIODONTITIS Radiographic Findings Historical Background Prevalence and Distribution by Age and Sex Clinical Characteristics RISK FACTORS FOR AGGRESSIVE PERIODONTITIS Radiographic Findings Microbiologic Factors Prevalence and Distribution by Age and Sex I mmunologic Factors GENERALIZED AGGRESSIVE PERIODONTITIS Genetic Factors Clinical Characteristics Environmental Factors ggressive periodontitis generally affects systemi- by a loss of collagen fibers in the periodontal ligament cally healthy individuals less than 30 years old, and their replacement by loose connective tissue and ex- although patients may be older. Aggressive peri- tensive bone resorption, resulting in a widened peri- odontitis may be universally distinguished from odontal ligament space. The gingiva apparently was not chronic periodontitis by the age of onset, the rapid rate involved. In 1928, Gottlieb" attributed this condition to of disease progression, the nature and composition of the inhibition of continuous cementum formation, the associated subgingival microflora, alterations in the which he considered essential for maintenance of the host's immune response, and a familial aggregation of periodontal ligament fibers. He then termed the disease diseased individuals.18 In addition, a strong racial influ- deep cementopathia. Gottlieb hypothesized that deep ence is observed in the United States; the disease is more cementopathia was a "disease of eruption" and that ce- prevalent among African-Americans." Aggressive peri- mentum initiated a foreign body response. As a result, odontitis describes three of the diseases formerly classi- it was postulated that the host attempted to exfoliate fied as early onset periodontitis. Localized aggressive pe- the tooth, resulting in the observed bone resorption and riodontitis was formerly classified as localized juvenile pocket formation. 14 periodontitis (LJP). Generalized aggressive periodontitis In 1938, Wannenmacher49 described incisor-first mo- encompasses the diseases previously classified as general- lar involvement and called the disease parodontitis mar- ized juvenile periodontitis (GJP) and rapidly progressive ginalis progressiva. Several explanations evolved for the periodontitis (RPP) (see Chapter 4). etiology and pathogenesis of this type of disease. Many individuals considered this to be a degenerative, nonin- flammatory disease process 12,34,45 and therefore gave it LOCALIZED AGGRESSIVE PERIODONTITIS the name periodontosis. Other investigators denied the existence of a degenerative type of periodontal disease Historical Background and attributed the changes observed to trauma from oc- In 1923, Gottlieb" reported a patient with a fatal case of clusion.6 Ultimately, in 1966 the World Workshop in Pe- epidemic influenza and a disease that he called diffuse at- riodontics38 concluded that the concept of periodontosis rophy o f the alveolar bone. This disease was characterized as a degenerative entity was unsubstantiated and that 409 41 0 PART 4 Periodontal Pathology the term should be eliminated from periodontal nomen- odontitis have been found to have hypoplastic or clature. The committee did recognize that a clinical en- aplastic cementum. This was true not only of root sur- tity different from adult periodontitis might occur faces exposed to periodontal pockets but also of roots among adolescents and young adults. still surrounded by their periodontium. The term juvenile periodontitis was introduced by Cha- put and colleagues in 1967 and by Butler' in 1969. In A striking feature of localized aggressive periodontitis 1971, Baer' defined it as "a disease of the periodontium is the lack of clinical inflammation despite the presence occurring in an otherwise healthy adolescent which is of deep periodontal pockets (see Color Fig. 28-1, E and characterized by a rapid loss of alveolar bone about more F). Furthermore, in many cases the amount of plaque on than one tooth of the permanent dentition. The amount the affected teeth is minimal, which seems inconsistent of destruction manifested is not commensurate with the with the amount of periodontal destruction present. 22 amount of local irritants." In 1989 the World Workshop The plaque that is present forms a thin biofilm on the in Clinical Periodontics8 categorized this disease as local- teeth and rarely mineralizes to form calculus." Although ized juvenile periodontitis (LJP), a subset of the broad clas- the quantity of plaque may be limited, it often contains sification of early onset periodontitis (EOP). Under this elevated levels of A. actinomycetemcomitans, and in some classification system, age of onset and distribution of le- patients, Porphyromonas gingivalis. The potential signifi- sions were of primary importance when making a diagno- cance of the qualitative composition of the microbial sis of LJP Most recently, disease with the characteristics of flora in localized aggressive periodontitis is discussed LJP has been renamed localized aggressive periodontitis. later in this chapter (Risk Factors for Aggressive Peri- odontitis: Microbiologic Factors). As the name suggests, localized aggressive periodonti- Clinical Characteristics tis progresses rapidly. Evidence suggests that the rate of Localized aggressive periodontitis usually has an age of bone loss is about three to four times faster than in onset around puberty.22 Clinically, it is characterized as chronic periodontitis. 2 Other clinical features of localized having "localized first molar/incisor presentation with aggressive periodontitis may include distolabial migra- interproximal attachment loss on at least two permanent tion of the maxillary incisors with concomitant diastema teeth, one of which is a first molar, and involving no formation (see Color Fig. 28-1, B), increasing mobility of more than two teeth other than first molars and in- the first molars, sensitivity of denuded root surfaces to cisors" (Color Fig. 28-1, A-D). The localized distribution thermal and tactile stimuli, and deep, dull, radiating pain of lesions in localized aggressive periodontitis is charac- during mastication, probably because of irritation of the teristic but as yet unexplained. The following possible supporting structures by mobile teeth and impacted food. reasons for the limitation of periodontal destruction to Periodontal abscesses may form at this stage, and re- certain teeth have been suggested: gional lymph node enlargement may occur.30 It should be noted that not all cases of localized ag- 1. After initial colonization of the first permanent teeth gressive periodontitis progress to the degree described to erupt (the first molars and incisors), A ctinobacillus previously. In some patients, the progression of attach- actinomycetemcomitans evades the host defenses by dif- ment loss and bone loss may be self-arresting.22 ferent mechanisms, including production of polymor- phonuclear leukocyte chemotaxis-inhibiting factors, Radiographic Findings endotoxin, collagenases, leukotoxin, and other factors that allow the bacteria to colonize the pocket and ini- Vertical loss of alveolar bone around the first molars and tiate the destruction of the periodontal tissues. After incisors, beginning around puberty in otherwise healthy this initial attack, adequate immune defenses are stim- teenagers, is a classic diagnostic sign of localized aggres- ulated to produce opsonic antibodies to enhance the sive periodontitis. Radiographic findings may include an clearance and phagocytosis of invading bacteria and "arc-shaped loss of alveolar bone extending from the dis- neutralize leukotoxic activity. In this manner, colo- tal surface of the second premolar to the mesial surface nization of other sites may be prevented.51 A strong of the second molar"" (see Color Fig. 28-1, D). antibody response to infecting agents is one character- istic of localized aggressive periodontitis. 22 Prevalence and Distribution by Age and Sex 2. Bacteria antagonistic to A. actinomycetemcomitans may colonize the periodontal tissues and inhibit A. actino- The prevalence of localized aggressive periodontitis in mycetemcomitans from further colonization of periodon- geographically diverse adolescent populations is esti- tal sites in the mouth. This would localize A. actino- mated to be below 1%. Most reports suggest a low preva- mycetemcomitans infection and tissue destruction." lence, about 0.2%. 27 Two independent radiographic stud- 3. A. actinomycetemcomitans may lose its leukotoxin- ies of 16-year-old adolescents, one in Finland" and the producing ability for unknown reasons." If this hap- other in Switzerland ,21 followed the strict diagnostic cri- pens, the progression of the disease may become ar- teria delineated by Baer 2 and reported a prevalence rate rested or retarded and colonization of new periodon- of 0.1%. A clinical and radiographic study of 7266 tal sites averted. English adolescents 15 to 19 years old also showed a 4. The possibility that a defect in cementum formation prevalence rate of 0.1%.'0 In the U.S., a national survey may be responsible for the localization of the lesions of adolescents age 14 to 17 reported that 0.53% had has been suggested. 25,35 Root surfaces of teeth ex- localized aggressive periodontitis. 27 Blacks were at much tracted from patients with localized aggressive peri- higher risk for localized aggressive periodontitis, and  A ggressive Periodontitis CHAPTER 28 41 1 black males were 2.9 times more likely to have the dis- eralized aggressive periodontitis must have their medical ease than black females. In contrast, white females were histories updated and reviewed. These patients should more likely to have localized aggressive periodontitis receive medical evaluations to rule out possible systemic than white males. Several other studies have found the involvement. As seen with localized aggressive periodon- highest prevalence of localized aggressive periodontitis titis, cases of generalized aggressive periodontitis may be among black males, 5,32,40 followed in descending order arrested spontaneously or after therapy, whereas others by black females, white females, and white males.32 may continue to progress inexorably to tooth loss de- Localized aggressive periodontitis affects both males spite intervention with conventional treatment. and females and is seen most frequently in the period between puberty and 20 years of age. Some studies have suggested a predilection for female patients, particularly Radiographic Findings in the youngest age groups,20 whereas others report no The radiographic picture in generalized aggressive peri- male-female differences in incidence when studies are odontitis can range from severe bone loss associated designed to correct for ascertainment bias." (For addi- with the minimal number of teeth, as described previ- tional epidemiologic data on localized aggressive peri- ously, to advanced bone loss affecting the majority of odontitis, see Chapter 5.) teeth in the dentition (see Fig. 28-1, B). A comparison of radiographs taken at different times illustrates the ag- gressive nature of this disease (see Fig. 28-2, B and C). GENERALIZED AGGRESSIVE PERIODONTITIS Page and co-workers36 described sites in generalized ag- gressive periodontitis (formerly RPP) patients that Clinical Characteristics demonstrated osseous destruction of 25% to 60% during Generalized aggressive periodontitis usually affects indi- a 9-week period. Despite this extreme loss, other sites in viduals under the age of 30, but older patients also may the same patient showed no bone loss. be affected.22 In contrast to localized aggressive peri- odontitis, evidence suggests that individuals affected with generalized aggressive periodontitis produce a poor antibody response to the pathogens present. Clinically, generalized aggressive periodontitis is characterized by "generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors" (Figs. 28-1, A and B, and 28-2, A and B). The de- struction appears to occur episodically with periods of advanced destruction followed by stages of quiescence of variable length (weeks to months or years). Radiographs often show bone loss that has progressed since the previ- ous evaluation (see Fig. 28-2, B and C). As seen in localized aggressive periodontitis, patients with generalized aggressive periodontitis often have small amounts of bacterial plaque associated with the af- fected teeth. 22 Quantitatively, the amount of plaque seems inconsistent with the amount of periodontal de- struction. Qualitatively, P. gingivalis, A. actinomycetem- comitans, and Bacteriodes forsythus frequently are detected in the plaque that is present. 46 Two gingival tissue responses can be found in cases of generalized aggressive periodontitis. One is a severe, acutely inflamed tissue, often proliferating, ulcerated, and fiery red (see Fig. 28-1, A). Bleeding may occur spon- taneously or with slight stimulation. Suppuration may be an important feature. This tissue response is consid- ered to occur in the destructive stage, in which attach- ment and bone are actively lost. In other cases, the gin- gival tissues may appear pink, free of inflammation, and occasionally with some degree of stippling, although the last feature may be absent (see Fig. 28-2, A). However, de- spite the apparently mild clinical appearance, deep pock- ets can be demonstrated by probing. This tissue response has been considered by Page and Schroeder" to coincide with periods of quiescence in which the bone level re- Fig. 28-1 A, Generalized aggressive periodontitis in a 30-year-old mains stationary. Some patients with generalized aggres- white patient. Note the generalized discoloration and smooth sive periodontitis may have systemic manifestations surface of the gingival tissues. B, Radiographs of this same patient, such as weight loss, mental depression, and general showing advanced generalized bone loss. (Courtesy Dr. Philip malaise. 36 Patients with a presumptive diagnosis of gen- Melnick, Los Angeles, Calif.) 412 PA RT 4 Periodontal Pathology Fig. 28-2 A, Generalized aggressive periodontitis in a 32- year-old white female. Note the apparently normal color and surface texture of the gingival tissues. B, Radiographs of this patient taken in 1988, showing advanced general- ized bone loss. Despite repeated aggressive treatment, the patient's condition continued to deteriorate. C, Radio- graphs taken in 1992, showing progressive bone loss. Clinical pictures were taken at the later date. (Courtesy Dr. Philip Melnick, Los Angeles, Calif.) Prevalence and Distribution by Age and Sex mary pathogen associated with this disease. As summa- In a study of untreated periodontal disease conducted in rized by Tonetti and Mombelli, 46 this link is based on the Sri Lanka by Loe and colleagues,36 8% of the population following evidence: (1) A. actinomycetemcomitans is found had rapid progression of periodontal disease character- in high frequency (approximately 90%) in lesions charac- ized by a yearly loss of attachment of 0.1 to 1.0 mm. In teristic of localized aggressive periodontitis, (2) sites with the U.S., a national survey of adolescents aged 14 to 17 evidence of disease progression often show elevated levels reported that 0.13% had generalized aggressive peri- of A. actinomycetemcomitans, (3) many patients with the odontitis.27 In addition, blacks were at much higher risk clinical manifestations of localized aggressive periodonti- than whites for all forms of aggressive periodontitis and tis have significantly elevated serum antibody titers to males were more likely to have generalized aggressive pe- A. actinomycetemcomitans, (4) clinical studies show a cor- riodontitis than females. (For additional epidemiologic relation between reduction in the subgingival load of data on aggressive periodontitis, see Chapter 5.) A. actinomycetemcomitans during treatment and a suc- cessful clinical response, and (5) A. actinomycetemcomi- tans produces a number of virulence factors that may RISK FACTORS FOR AGGRESSIVE contribute to the disease process (see also Chapter 6). PERIODONTITIS It should be noted that not all reports support the asso- ciation of A. actinomycetemcomitans and localized aggres- Microbiologic Factors sive periodontitis. In some studies, A. actinomycetemcomi- Although several specific microorganisms frequently are tans either could not be detected in patients with this detected in patients with localized aggressive periodontitis form of disease or could not be detected at the previously (A. actinomycetemcomitans, Capnocytophaga sp., Eikenella reported frequencies. Another study found elevated levels corrodens, Prevotella intertnedia, and Campylobacter rectus), of P. gingivalis, P. intennedia, Fusobacterium nucleatum, A. actinomycetemcomitans has been implicated as the pri- C. rectus, and Treponema denticola in patients with either  A ggressive Periodontitis CHAPTER 28 41 3 localized or generalized aggressive disease, but no signifi- odontitis.46 Specifically, several authors have described a cant association was found between the presence of ag- familial pattern of alveolar bone loss and have impli- gressive disease and A. actinomycetemcomitans. In addi- cated genetic factors in aggressive periodontitis. 4,28,29,31 tion, A. actinomycetemcomitans often can be detected Currently, specific genes have not been identified that in periodontally healthy subjects, suggesting that this are responsible for these diseases. However, segregational microorganism may be part of the normal flora in many analyses and linkage analyses of families with a genetic individuals. predisposition for localized aggressive periodontitis sug- Electron microscopic studies of localized aggressive gest that a major gene plays a role in this disease, which periodontitis have revealed bacterial invasion of connec- is transmitted through an autosomal dominant mode of tive tissue 9,11 that reaches the bone surface.' The invad- inheritance in U.S. populations31 (see Chapter 10). It ing flora has been described as morphologically mixed should be noted that most of the segregational studies but composed mainly of gram-negative bacteria, includ- were conducted in African-American populations and ing cocci, rods, filaments, and spirochetes.11 Using differ- therefore other modes of inheritance may exist in differ- ent methods, including immunocytochemistry and elec- ent populations. tromicroscopy, several tissue-invading microorganisms Evidence suggests that some immunologic defects as- have been identified as A. actinomycetemcomitans, Capno- sociated with aggressive periodontitis may be inherited. cytophaga sputigena, Mycoplasma spp., and spirochetes. 39 For example, Van Dyke et a1 4 ' reported a familial cluster- ing of the neutrophil abnormalities seen in localized ag- gressive periodontitis. This clustering suggests that the I mmunologic Factors defect(s) may be inherited.46 Studies also have demon- Some immune defects have been implicated in the strated that the antibody response to periodontal patho- pathogenesis of aggressive periodontitis. The human gens, particularly A. actinomycetemcomitans, is under ge- leukocyte antigens (HLA), which regulate immune re- netic control and that the ability to mount high titers sponses, have been evaluated as candidate markers for of specific, protective antibody (primarily IgG2) against aggressive periodontitis. Although the findings with A. actinomycetemcomitans may be race dependent.15 many HLA antigens have been inconsistent, HLA-A9 and In summary, data support the idea that a gene of ma- B15 antigens are consistently associated with aggressive j or effect exists for aggressive periodontitis. Data also periodontitis (see Chapter 10). support a genetic basis for some of the immunologic de- Several investigators 10,23,24 have shown that patients fects seen in patients with aggressive periodontitis. How- with aggressive periodontitis display functional defects of ever, it is unlikely that all patients affected with aggres- polymorphonuclear leukocytes (PMNs), monocytes, or sive periodontitis have the same genetic defect. As both. These defects can impair either the chemotactic at- summarized by Tonetti and Mombelli,46 "It seems that traction of PMN to the site of infection or their ability to specific genes may be different in various populations phagocytose and kill microorganisms. Current studies and/or ethnic groups and therefore true heterogeneity in have also demonstrated a hyperresponsiveness of mono- disease susceptibility may be present. The role of specific cytes from localized aggressive periodontitis patients with genes remains to be elucidated." (For additional informa- respect to their production of PGE 2 in response to tion on genetic factors, see Chapter 10.) lipopolysaccharide (LPS). 43 This hyperresponsive pheno- type could lead to increased connective tissue or bone loss Environmental Factors due to excessive production of these catabolic factors. Ad- ditionally, poorly functional inherited forms of monocyte The amount and duration of smoking are important FcyRII, the receptor for human IgG2 antibodies, have been variables that can influence the extent of destruction shown to be disproportionately present in patients with seen in young adults. 46 Patients with generalized aggres- localized aggressive periodontitis.50 These PMN and mono- sive periodontitis who smoke have more affected teeth cyte defects may be induced by the bacterial infection or and more loss of clinical attachment than nonsmoking may be genetic in origin. Further studies are needed to patients with generalized aggressive periodontitis. 16 characterize the origin of these cellular alterations. However, smoking may not have the same impact on at- Autoimmunity has been considered to have a role in tachment levels in younger patients with localized ag- generalized aggressive periodontitis according to Anusak- gressive periodontitis. 42 (For additional information on sathien and Dolby,' who found host antibodies to colla- smoking and periodontal disease, see Chapter 14.) gen, DNA, and immunoglobulin G (IgG). Possible im- mune mechanisms include an increase in the expression REFERENCES of type II major histocompatibility complex (MHC) mol- ecules, HLA DR4 3 , altered helper or suppressor T-cell 1. Anusaksathien O, Dolby AE: Autoimmunity in periodontal function, polyclonal activation of B cells by microbial disease. J Oral Pathol Med 1991; 20:101. plaque, and genetic predisposition. (For additional infor- 2. Baer PN: The case for periodontosis as a clinical entity. J Pe- riodontol 1971; 42:516. mation on the immunology of aggressive periodontitis, 3. Bonfil JJ, Dillier FL, Mercier P: A "case control" study on the see Part Three.) role of HLA DR4 in severe periodontitis and rapidly progres- sive periodontitis. Identification of types and subtypes us- Genetic Factors ing molecular biology. J Clin Periodontol 1999; 26:77. 4. Butler JH: A familial pattern of juvenile periodontitis (peri- Results from several studies support the concept that all odontosis). J Periodontol 1969; 40:115. individuals are not equally susceptible to aggressive peri- 41 4 PART 4 Periodontal Pathology 5. Burmeister JA, Best AM, Palcanis KG, et al: Localized juve- 28. Long JC, Nance WE, Waring P, et al: Early onset periodonti- nile periodontitis and generalized severe periodontitis: Clin- tis: A comparison and evaluation of two modes of inheri- ical findings. J Clin Periodontol 1984; 11:181. tance. Genet Epidemiol 1987; 4:13. 6. Carranza FA Sr, Carranza FA Jr: A suggested classification of 29. Lopez NJ: Clinical, laboratory and immunological studies of common periodontal disease. J Periodontol 1959; 30:140. a family with a high prevalence of generalized prepubertal 7. Carranza FA Jr, Saglie R, Newman MG: Scanning and trans- and juvenile periodontitis. J Periodontol 1992; 63:457. mission electron microscopy study of tissue invading mi- 30. Manson JD, Lehner T: Clinical features of juvenile peri- croorganisms in localized juvenile periodontitis. J Periodon- odontitis (periodontosis). J Periodontol 1974; 45:636. tol 1983; 54:598. 31. Marazita ML, Burmeister JA, Gunsolley JC, et al: Evidence 8. Caton J. Consensus Report: Periodontal diagnosis and diag- for autosomal dominant inheritance and race-specific het- nostic aids. In: Proceedings of the World Workshop in Clin- erogeneity in early-onset periodontitis. J Periodontol 1994; ical Periodontics. The American Academy of Periodontol- 65:623. ogy. Chicago. 1989. 32. Melvin WL, Sandifer JB, Gray JL: The prevalence and sex ra- 9. Christersson LA, Albini B, Zambon J, et al: Demonstration tio of juvenile periodontitis in a young racially mixed popu- of Actinobacillus actinomycetemcomitans in gingiva in local- lation. J Periodontol 1991; 62:330. ized juvenile periodontitis in humans. Abstract. J Dent Res 33. Miller SC: Precocious advanced alveolar atrophy. J Peri- 1983;62:255. odontol 1948; 19:146. 10. Clark RA, Page RC, Wilde G: Defective neutrophil chemo- 34. Orban B, Weinmann JP: Diffuse atrophy of alveolar bone. taxis in juvenile periodontitis. Infect Immun 1977; 18:694. J Periodontol 1942; 13:31. 11. Gillett R, Johnson NW: Bacterial invasion of the periodon- 35. Page RC, Baab DA: A new look at the etiology and patho- tium in a case of juvenile periodontitis. J Clin Periodontol genesis of early-onset periodontitis. Cementopathia revis- 1982; 9:93. ited. J Periodontol 1985; 56:748. 12. Goldman HM: Similar condition to periodontosis in two 36. Page RC, Altman LC, Ebersole JL, et al: Rapidly progressive spider monkeys. Am J Orthod 1947; 33:749. periodontitis. A distinct clinical condition. J Periodontol 13. Gottlieb B: Die diffuse Atrophy des Alveolarknochens. Z 1983; 54:197. Stomatol 1923; 21:195. 37. Page RC, Schroeder HE: Periodontitis in Man and Other An- 14. Gottlieb B: The formation of the pocket: Diffuse atrophy of i mals. A Comparative Review. Basel, Karger, 1982. alveolar bone. J Am Dent Assoc 1928; 15:462. 38. Ramfjord SP, Ash MM, Kerr DA (eds): World Workshop in 15. Gunsolley JC, Tew JG, Gooss CM, et al: Effects of race, Periodontics. Ann Arbor, University of Michigan, 1966. smoking and immunoglobulin allotypes on IgG subclass 39. Saglie FR, Carranza FA Jr, Newman MG, et al: Identification concentrations. J Periodont Res 1997: 32:381. of tissue invading bacteria in juvenile periodontitis. J Peri- 16. Haber J, Wattles J, Crowley M, et al: Evidence for cigarette odont Res 1982; 17:452. smoking as a major risk factor for periodontitis. J Periodon- 40. Saxby MS: Juvenile periodontitis: An epidemiologic study in tol 1993; 64:16. the West Midlands of the United Kingdom. J Clin Periodon- 17. Hart TC, Marazita ML, Schenkein HA, et al: No female pre- tol 1987; 14:594. ponderance in juvenile periodontitis after correction of as- 41. Saxen L: Prevalence of juvenile periodontitis in Finland. certainment bias. J Periodontol 1991; 62:745. J Clin Periodontol 1980; 7:177 18. Hart TC: Genetic risk factors for early-onset periodontitis. 42. Schenkein JA, Gunsolley JC, Koertge TE, et al: Smoking and J Periodontol 1996; 67:355. its effects on early-onset periodontitis. J Am Dent Assoc 19. Hillman JD, Socransky SS: Bacterial interference in the oral 1995; 126:1107. ecology of Actinobacillus actinomycetemcomitans and its rela- 43. Shapira L, Soskolone WA, Van Dyke TE, et al: Prostaglandin tionship to human periodontosis. Arch Oral Biol 1982; E2 secretion, cell maturation, and CD 14 expression by 27:75. monocyte-derived macrophages from localized juvenile pe- 20. Hormand J, Frandsen A: Juvenile periodontitis. Localization riodontitis patients. J Periodontol 1996; 67:224. of bone loss in relation to age, sex, and teeth. J Clin Peri- 44. Slots J, Zambon JJ, Rosling BC, et al: Actinobacillus actino- odontol 1979; 6:407. mycetemcomitans in human periodontal disease. Association, 21. Kronauer E, Borsa G, Lang NP: Prevalence of incipient juve- serology, leukotoxicity, and treatment. J Periodont Res nile periodontitis at age 16 years in Switzerland. J Clin Peri- 1982; 17:447. odontol 1986; 13:103. 45. Thoma KH, Goldman HM: Wandering and elongation of 22. Lang N, Bartold PM, Cullinan M, et al: Consensus Report: the teeth and pocket formation in paradontosis. J Am Dent Aggressive periodontitis. Ann Periodontol 1999; 4:53. Assoc 1940; 27:335. 23. Lavine WS, Maderazo EG, Stolman J, et al: Impaired neu- 46. Tonetti MS, Mombelli A: Early-onset periodontitis. Ann Pe- trophil chemotaxis in patients with juvenile and rapidly riodontol 1999: 4:39. progressing periodontitis. J Periodont Res 1979; 14:10. 47. Van Dyke TE, Schweinebraten M, Cinaciola LJ, et al: Neu- 24. Leino L, Hurttia H: A potential role of an intracellular sig- trophil chemotaxis in families with localized juvenile peri- naling defect in neutrophil functional abnormalities and odontitis. J Periodont Res 1985: 20:503. promotion of tissue damage in patients with localized juve- 48. Waerhaug J: Subgingival plaque and loss of attachment in nile periodontitis. Clin Chem Lab Med 1999; 37:215. periodontosis as well as observed in autopsy material. J Peri- 25. Lindskog S, Blomlof L: Cementum hypoplasia in teeth af- odontol 1976; 47:636. fected by juvenile periodontitis. J Clin Periodontol 1983; 49. Wannenmacher E: Ursachen auf dem Gebiet der Paraden- 10:443. topathien. Zbl Gesant Zahn Mund Kieferheilk 1938; 3:81. 26. Loe H, Anerud A, Boysen H, et al: Natural history of peri- 50. Wilson ME, Kalmar JR: FcyRIIa (CD32): A potential marker odontal disease in man. Rapid, moderate and no loss of at- defining susceptibility to localized juvenile periodontitis. tachment in Sri Lankan laborers 14 to 46 years of age. J Clin J Periodontol 1996; 67:323. Periodontol 1986; 13:431. 51. Zambon JJ, Christersson LA, Slots J: Actinobacillus actino- 27. Loe H, Brown LJ: Early-onset periodontitis in the United mycetemcomitans in human periodontal disease. Prevalence States of America. J. Periodontol 1991; 62:608. in patient groups and distribution of biotypes and serotypes within families. J Periodontol 1983; 54:707. Color Fig. 27-1 A-C, Necrotizing ulcerative periodontitis in a 45-year-old, HIV-negative, white male. Note the deep craters asso- ciated with bone loss. Color Fig. 28-1 Localized aggressive periodontitis. A-C, Clinical views of a case of localized aggressive periodontitis in a 19-year-old female. Note the migration of the maxillary anterior teeth, lack of calculus, and scant clinical inflammation. D, Radiographs of the same case, showing typical mo- lar-incisor lesions. E, Lingual view of the left mandibular molar area in a patient with localized aggressive periodontitis. Note the apparently normal gingival tissue and the presence of a deep pocket, as denoted by the probe. F, The same area after the elevation of a mucoperiosteal flap. Note the advanced bone loss localized to the first molar. (D, Courtesy Dr. Philip Melnick, Los Angeles, Calif.; F, courtesy Dr. Terry Fiori, Palo Alto, Calif.) Color Fig. 29-1 AIDS and the periodontium. A, Hairy leukoplakia on the lateral margin of the tongue, causing a corrugated appearance. B, Painless ANUG-like lesion of several months' duration. The patient had a second ANUG-like lesion that was painful. C-E, ANUG-like lesion and candidiasis of the palate and tongue in a 29-year-old woman. F, Kaposi's sarcoma involving the anterior hard palate and right and left palatal mucosa. Candidiasis is also noted on the hard palate. G, Same patient as in F, with Kaposi's sarcoma of the labial gingiva presenting as a small purple nodule next to a parulis. H, Kaposi's sarcoma involving the anterior facial gingiva and producing a gingival enlargement. (Courtesy Dr. Frank Lucatorto.) Chapter 16 Aggressive Periodontitis Section 1 Aggressive Periodontitis—Highly Destructive Form 270 General Characteristics of Aggressive Periodontitis Localized and Generalized Aggressive Periodontitis Treatment Considerations for Aggressive Periodontitis Section 2 Focus on Patients 276 Learning Objectives Compare and contrast the clinical and radiographic features of chronic periodontitis and aggressive periodontitis. Discuss the differences between ideal and reasonable treatment goals for aggressive periodontitis. Given the clinical and radiographic features for a patient with a history of aggressive periodontitis, determine if the disease is localized or generalized aggressive periodontitis. Key Terms Aggressive periodontitis (AgP) Episodic disease progression Localized aggressive periodontitis (LAP) Generalized aggressive periodontitis (GAP)  A B C  A B C CEJ to Alveolar crest Group 2 : NUP A B A B A B  A B A B A B C Group 3 : Abscess  The Periodontal Pocket CHAPTER 22 349 Fig. 22-21 Intrabony pocket on the mesial surface of the mandibular canine. A, Rolled gingival margin and space be- tween gingiva and canine suggest the presence of a peri- odontal pocket. B, Flap reflected to show calculus on the root and a three-wall bone defect. When loss of attachment and bone occur as a result of suprabony pockets, the alveolar crest and the peri- odontal ligament gradually attain a more apical position in relation to the tooth but retain their general morphol- ogy and architecture. This is usually associated with a horizontal pattern of bone loss. In intrabony pockets, the morphology of the alveolar crest changes completely with the formation of angular bony defects as a result of vertical bone loss. This may affect the function of the area. 14 The distinguishing features of suprabony and intra- bony pockets are summarized in Table 22-2. The mor- phologic features of the intrabony pocket are important because they necessitate modification in treatment tech- niques (see Chapters 62 and 63). The classification of in- trabony pockets is discussed in Chapter 23. PERIODONTAL ABSCESS A periodontal abscess is a localized purulent inflamma- tion in the periodontal tissues (Fig. 22-23). It is also known as a lateral or parietal abscess. Abscesses localized Fig. 22-22 Two suprabony pockets in an interdental space be- in the gingiva, caused by injury to the outer surface of tween the maxillary cuspid and the lateral incisor. Note the normal the gingiva, and not involving the supporting structures horizontal arrangement of the transseptal fibers. are called gingival abscesses. They may occur in the pres- ence or absence of a periodontal pocket (see Chapter 18). Periodontal abscess formation may occur in the fol- lowing ways: shrinks, occluding the pocket orifice, and a periodon- tal abscess occurs in the sealed-off portion of the 1. Extension of infection from a periodontal pocket pocket. deeply into the supporting periodontal tissues and lo- 5. A periodontal abscess may occur in the absence of calization of the suppurative inflammatory process periodontal disease after trauma to the tooth or perfo- along the lateral aspect of the root. ration of the lateral wall of the root in endodontic 2. Lateral extension of inflammation from the inner sur- therapy. face of a periodontal pocket into the connective tissue of the pocket wall. Localization of the abscess results Periodontal abscesses are classified according to loca- when drainage into the pocket space is impaired (Fig. tion as follows: 22-24). 3. In a pocket that describes a tortuous course around 1. A bscess in the supporting periodontal tissues along the the root, a periodontal abscess may form in the cul- lateral aspect of the root. In this condition, a sinus de-sac, the deep end of which is shut off from the sur- generally occurs in the bone that extends laterally face. from the abscess to the external surface. 4. Incomplete removal of calculus during treatment of a 2. A bscess in the soft tissue wall of a deep periodontal periodontal pocket. In this instance, the gingival wall pocket. 35 0 PART 4 Periodontal Pathology Distinguishing Features of the Suprabony and Intrabony Pockets Suprabony Pocket I ntrabony Pocket 1. The base of the pocket is coronal to the level of the The base of the pocket is apical to the crest of the alveo- alveolar bone. l ar bone so that the bone is adjacent to the soft tissue wall (see Fig. 22-2). 2. The pattern of destruction of the underlying bone is 2. The bone destructive pattern is vertical (angular) (see horizontal. Figs. 22-20 and 22-21). 3. I nterproximally, the transseptal fibers that are restored 3. I nterproximally, the transseptal fibers are oblique rather during progressive periodontal disease are arranged than horizontal. They extend from the cementum be- horizontally in the space between the base of the pocket neath the base of the pocket along the bone and over and the alveolar bone (see Fig. 22-22). the crest to the cementum of the adjacent tooth (see Fig. 22-20). 4. On the facial and lingual surfaces, the periodontal 4. On the facial and lingual surfaces, the periodontal liga- li gament fibers beneath the pocket follow their normal ment fibers follow the angular pattern of the adjacent horizontal-oblique course between the tooth and the bone. They extend from the cementum beneath the base bone. of the pocket along the bone and over the crest to join with the outer periosteum. 3. Primordial cyst of supernumerary tooth germ. 4. Stimulation of epithelial rests of the periodontal liga- ment by infection from a periodontal abscess or the pulp through an accessory root canal. A periodontal cyst is usually asymptomatic and with- out grossly detectable changes, but it may present as a localized tender swelling. Radiographically, an interprox- imal periodontal cyst appears on the side of the root as a radiolucent area bordered by a radiopaque line. Its radi- ographic appearance cannot be differentiated from that of a periodontal abscess. Bacterial invasion of tissues has been reported in ab- scesses; the invading organisms were identified as gram- negative cocci, diplococci, fusiforms, and spirochetes.23 Invasive fungi were also found and were interpreted as being opportunistic invaders.23 Microorganisms that col- onize the periodontal abscess have been reported to be primarily gram-negative anaerobic rods.55 PERIODONTAL CYST The periodontal cyst is an uncommon lesion that pro- duces localized destruction of the periodontal tissues along a lateral root surface, most often in the mandibu- lar canine-premolar area. 25,11 The following possible etiologies have been suggested: 1. Odontogenic cyst caused by proliferation of the ep- ithelial rests of Malassez; the stimulus initiating the cellular activity is not known. 2. Lateral dentigerous cyst retained in the jaw after tooth eruption. Fig. 22-23 Periodontal abscess on an upper central incisor. 30 6 PA RT 4 Periodontal Pathology reported ,3° it does not ordinarily recur unless immunity 4. Brown RH: Necrotizing ulcerative gingivitis in mongoloid is destroyed by debilitating systemic disease. Secondary and nonmongoloid retarded individuals. J Periodont Res herpetic infection of the skin, such as herpes labialis, 1973; 8:290. does recur.bb 5. Cahn LR: The penetration of the tissue by Vincent's organ- isms. A report of a case. J Dent Res 1929; 9:695. 6. Cawson RA: Infections of the oral mucous membrane. In PERICORONITIS Cohen B, Kramer IRH (eds): Scientific Foundations of Den- tistry. Chicago, Year-Book Medical Publishers, 1976. The term pericoronitis refers to inflammation of the gin- 7. Chapman OD, Harris AE: Oral lesions associated with di- giva in relation to the crown of an incompletely erupted etary deficiencies in monkeys. J Infect Dis 1941; 69:7. tooth (Fig. 19-10). It occurs most often in the mandibu- 8. Chilton NW: Herpetic stomatitis. Am J Orthod Oral Surg lar third molar area. Pericoronitis may be acute, sub- 1944; 30:335. acute, or chronic. 9. Chung CP, Nisengard RJ, Slots J, et al: Bacterial IgG and IgM antibody titers in acute necrotizing ulcerative gingivitis. J Periodontol 1983; 54:557. Clinical Features 10. Cogen RB, Stevens AW Jr, Cohen-Cole SA, et al: Leukocyte The partially erupted or impacted mandibular third mo- function in the etiology of acute necrotizing ulcerative gin- lar is the most common site of pericoronitis. The space givitis. J Periodontol, 54:402, 1983. 11. Cohen-Cole SA, et al: Psychiatric, psychosocial and endocrine between the crown of the tooth and the overlying gingi- correlates of acute necrotizing ulcerative gingivitis (trench val flap is an ideal area for the accumulation of food mouth): a preliminary report. Psychiatr Med 1:215, 1983. debris and bacterial growth. Even in patients with no 12. Curtois GJ III, Cobb CM, Killoy WJ: Acute necrotizing ulcer- clinical signs or symptoms, the gingival flap is often ative gingivitis. A transmission electron microscope study. chronically inflamed and infected and has varying de- J Periodontol 1983; 54:671. grees of ulceration along its inner surface. Acute inflam- 13. Daley FH: Studies of Vincent's infection at the clinic of Tufts matory involvement is a constant possibility. College Dental School from October 1926 to February 1928. Acute pericoronitis is identified by varying degrees of J Dent Res 1928; 8:408. inflammatory involvement of the pericoronal flap and 14. Dean HT, Singleton JE Jr: Vincent's infection-a wartime adjacent structures as well as systemic complications. disease. Am J Pub Health 1945; 35:433. 15. Dodd, K, Johnston LM, Budding GJ: Herpetic stomatitis. The inflammatory fluid and cellular exudate increase the J Pediatr 1938; 12:95. bulk of the flap, which then may interfere with complete 16. Duckworth R, Waterhouse JP, Britton DG, et al: Acute ulcer- closure of the jaws, and can be traumatized by contact ative gingivitis. A double blind controlled clinical trial with with the opposing jaw, aggravating the inflammatory metronidazole. Br Dent J 1966; 120:599. involvement. 17. Ellerman V: Vincent's organisms in tissue. Z Hyg Infect Pr The resultant clinical picture is that of a markedly red, 1907; 56:453. swollen, suppurating lesion that is exquisitely tender, 18. Emslie RD: Cancrum oris. Dent Pract, 13:481, 1963. with radiating pains to the ear, throat, and floor of the 19. Enwonwu CO: Epidemiological and biochemical studies of mouth. The patient is extremely uncomfortable because necrotizing ulcerative gingivitis and noma (cancrum oris) in of a foul taste and an inability to close the jaws, in addi- Nigerian children. Arch Oral Biol 1972; 17:1357, 1972. 20. Enwonwu CO: Cellular and molecular effects of malnutri- tion to the pain. Swelling of the cheek in the region of tion and their relevance to periodontal diseases. J Clin Peri- the angle of the jaw and lymphadenitis are common odontol 1994; 21:643. findings. The patient may also have toxic systemic com- 21. Eversole LR: Diseases of the oral mucous membranes. Re- plications such as fever, leukocytosis, and malaise. view of the literature. In Millard HD, Mason DK (eds): World Workshop on Oral Medicine. Chicago, Year-Book Complications Medical Publishers, 1989. 22. Falkler WA Jr, Martin SA, Vincent JW, et al: A clinical, demo- The involvement may become localized in the form of a peri- graphic and microbiologic study of NUG patients in an ur- coronal abscess. It may spread posteriorly into the oro- ban dental school. J Clin Periodontol 1987; 14:307. pharyngeal area and medially to the base of the tongue, 23. Formicola AJ, Witte ET, Curran PM: A study of personality making it difficult for the patient to swallow. Depending traits and acute necrotizing ulcerative gingivitis. J Periodon- tol 1970; 41:36. on the severity and extent of the infection, there is in- 24. Gardner PS, McQuillin J, Black MM, et al: Rapid diagnosis of volvement of the submaxillary, posterior cervical, deep herpesvirus hominis infections in superficial lesions by im- cervical, and retropharyngeal lymph nodes.34,51 Peritonsil- munofluorescent antibody techniques. Br Med J 1968; 4:89. lar abscess formation, cellulitis, and Ludwig's angina are 25. Giddon DB: Psychophysiology of the oral cavity. J Dent Res infrequent but potential sequelae of acute pericoronitis. (Suppl 6) 1966; 45:1627. 26. Giddon DB, Zackin SJ, Goldhaber P: Acute necrotizing gin- REFERENCES givitis in college students. J Am Dent Assoc 1964; 68:381. 27. Goldhaber P, Giddon DB: Present concepts concerning the l. Barnes GP, Bowles WF III, Carter HG: Acute necrotizing ul- etiology and treatment of acute necrotizing ulcerative gin- cerative gingivitis. A survey of 218 cases. J Periodontol givitis. Int Dent J 1964; 14:468. 1973; 44:35. 28. Greenberg MS, Brightman VJ, Ship II: Clinical and labora- 2. Berke JD: Experimental study of acute ulcerative stomatitis. tory differentiation of recurrent intraoral herpes simplex J Am Dent Assoc 1961; 63:86. virus infections following fever. J Dent Res 1969; 48:385. 3. Box HK: Necrotic Gingivitis. Toronto, University of Toronto 29. Greenspan D, Pindborg JJ, Greenspan JS, et al: AIDS and the Press, 1930. Dental Team. Copenhagen, Munksgaard, 1986.  Clinical Diagnosis CHAPTER 30 449 Fig. 30-27 Acute periodontal abscess between the lower central Fig. 30-29 Acute periodontal abscess in the wall of a deep i ncisors. pocket. mittent exudation. The orifice of the sinus may appear as a difficult-to-detect pinpoint opening, which, when probed, reveals a sinus tract deep in the periodontium (Fig. 30-30). The sinus may be covered by a small, pink, beadlike mass of granulation tissue (Fig. 30-31). The chronic periodontal abscess is usually asymptomatic. However, the patient may report episodes of dull, gnaw- ing pain; slight elevation of the tooth; and a desire to bite down on and grind the tooth. The chronic peri- odontal abscess often undergoes acute exacerbations, with all the associated symptoms. Diagnosis of the periodontal abscess requires correla- tion of the history and clinical and radiographic findings. The suspected area should be probed carefully along the gingival margin in relation to each tooth surface to detect a channel from the marginal area to the deeper periodon- tal tissues. Continuity of the lesion with the gingival mar- gin is clinical evidence that the abscess is periodontal. The abscess is not necessarily located on the same sur- Fig. 30-28 Acute periodontal abscess associated with a deep peri- face of the root as the pocket from which it is formed. A odontal pocket facial and mesial of upper central incisor. pocket at the facial surface may give rise to a periodontal abscess interproximally. It is common for a periodontal abscess to be located at a root surface other than that along which the pocket originated, because drainage is more likely to be impaired when a pocket follows a tor- relatively firm, or pointed and soft. In most cases, pus tuous course. may be expressed from the gingival margin with gentle In children a sinus orifice along the lateral aspect of digital pressure. a root is usually the result of periapical infection of a The acute periodontal abscess is accompanied by deciduous tooth. In the permanent dentition such an symptoms such as throbbing, radiating pain; exquisite orifice may be caused by a periodontal abscess, as well as tenderness of the gingiva to palpation; sensitivity of the by apical involvement. The orifice may be patent and tooth to palpation; tooth mobility; lymphadenitis; and, draining, or it may be closed and appear as a red, nodu- less frequently, systemic effects such as fever, leukocyto- lar mass (Fig. 30-32). Exploration of such masses with a sis, and malaise. Occasionally, the patient may have probe usually reveals a pinpoint orifice that communi- symptoms of an acute periodontal abscess without any cates with an underlying sinus. notable clinical lesion or radiographic changes. The chronic periodontal abscess usually presents a sinus Periodontal Abscess and Gingival Abscess. that opens onto the gingival mucosa somewhere along The principal differences between the periodontal abscess the length of the root. There may be a history of inter- and the gingival abscess are the location and history 450 PA RT 5 Treatment of Periodontal Disease Fig. 30-30 Suppuration from a chronic periodontal abscess. A, Suppurative draining sinus between the ca- nine and first premolar. B, Radiograph showing extensive bone destruction in the area of the draining sinus. Fig. 30-31 Pinpoint orifice of a sinus from a palatal periodontal abscess. A, Pinpoint orifice on the palate i ndicative of a sinus from a periodontal abscess. B, Probe extends into the abscess deep in the periodon- tium. (see Chapters 18 and 65). The gingival abscess is con- An apical abscess may spread along the lateral aspect fined to the marginal gingiva, and it often occurs in pre- of the root to the gingival margin. However, when the viously disease-free areas (Fig. 30-33). It is usually an apex and lateral surface of a root are involved by a single acute inflammatory response to forcing of foreign mater- lesion that can be probed directly from the gingival mar- ial into the gingiva. The periodontal abscess involves the gin, the lesion is more likely to have originated in a peri- supporting periodontal structures and generally occurs odontal abscess. in the course of chronic destructive periodontitis. Radiographic findings are sometimes helpful in differ- entiating between a periodontal and a periapical lesion Periodontal Abscess and Periapical Abscess. (see Chapter 31). Early acute periodontal and periapical Several characteristics can be used as guidelines in differ- abscesses present no radiographic changes. Ordinarily, a entiating a periodontal abscess from a periapical abscess. radiolucent area along the lateral surface of the root sug- If the tooth is nonvital, the lesion is most likely periapi- gests the presence of a periodontal abscess, whereas apical cal. However, a previously nonvital tooth can have a rarefaction suggests a periapical abscess. However, acute deep periodontal pocket that can abscess. Moreover, a periodontal abscesses that show no radiographic changes deep periodontal pocket can extend to the apex and often cause symptoms in teeth with long-standing, radi- cause pulpal involvement and necrosis. ographically detectable periapical lesions that are not con-  Treatment of the Periodontal Abscess Henry H. Takei CHAPTER CHAPTER OUTLINE THE ACUTE PERIODONTAL ABSCESS THE GINGIVAL ABSCESS Treatment THE CHRONIC PERIODONTAL ABSCESS I eriodontal abscesses are commonly encountered Drainage through the Pocket. The area is anes- in patients with deep pockets. They are an acute thetized topically and, if necessary, local anesthesia is in- exacerbation of a preexisting pocket resulting j ected around the periphery of the abscess. Care is taken from exudates and purulent material being entrapped in not to inject into the swelling itself. A flat instrument or the pocket with no pathway for drainage. Abscesses may a probe is carefully introduced into the pocket in an at- be acute or chronic. Acute abscesses are painful, edema- tempt to distend the pocket wall for drainage. A curette tous, red, shiny ovoid elevations of the gingival margin, can then be gently inserted into the pocket to further the attached gingiva, or both. After their purulent con- drain and gently curette the mass of tissue internally. tent is partially exuded, they become chronic. Chronic abscesses may produce a dull pain and may at times be- Drainage through an External Incision. The come acute (see Chapter 30). abscess is isolated and dried with gauze sponges. After the application of topical anesthesia, local anesthesia is injected around the periphery of the abscess. THE ACUTE PERIODONTAL ABSCESS A #15 blade is used to make a vertical incision To undertake the proper course of therapy, it is essential through the most fluctuant part of the swelling, extend- to establish the differential diagnosis between a peri- ing to an area just apical to the abscess (Fig. 46-1). A odontal and a pulpal abscess. Box 46-1 compares the curette or periosteal elevator is used to gently elevate the symptoms associated with the two lesions. tissue to create drainage and curette the granulomatous tissue in the internal aspect of the abscess. The external aspect of the abscess is gently pushed to drain the re- Treatment maining purulent material and approximate the wound The purpose of treatment of an acute abscess is to alleviate edges. Sutures are usually not required. the pain, control the spread of infection, and establish After the drainage stops, the area is dried and painted drainage! The patient's general systemic response should with an antiseptic. Patients without systemic complica- be evaluated. Rise in temperature, feverish appearance, tions are instructed to rinse often with a solution of 1 tsp and a feeling of malaise should be noted and a proper salt in a glass of warm water and to return for follow-up antibiotic regimen started if necessary. evaluation the next day. In addition to the rinses, peni- Drainage can be established through the pocket or by cillin or other antibiotics are prescribed for patients with means of an incision from the outer surface. The former elevated temperatures. The patient is also instructed to is preferable. avoid exertion and is placed on a copious fluid diet. 629 630 PA RT 5 Treatment o f Periodontal Disease Differences between Periodontal and Pulpal Abscesses Fig. 46-1 Incision of an acute periodontal abscess. A, Fluctuant acute periodontal abscess. B, Abscess in- cised. C, After acute signs subside. If necessary, bed rest is recommended. Analgesics are gauze pad. After bleeding stops, the patient is dismissed prescribed for pain. for 24 hours and instructed to rinse every 2 hours with a The next day, the swelling is generally markedly re- glassful of warm water. duced or absent and the symptoms should have sub- When the patient returns, the lesion is generally re- sided. If acute symptoms persist, the patient is instructed duced in size and free of symptoms. A topical anesthetic to continue the regimen prescribed the previous day and is applied, and the area is scaled. If the residual size of to return in 24 hours. The symptoms invariably disap- the lesion is too great, it is removed surgically. pear by this time, and the lesion is ready for the usual treatment of a chronic periodontal abscess. THE CHRONIC PERIODONTAL ABSCESS After adequate drainage, antibiotic treatment, or both, THE GINGIVAL ABSCESS the acute abscess becomes chronic. Some cases have In contrast to the periodontal abscess, which involves drained spontaneously and the patient is then diagnosed the supporting tissues, the gingival abscess is a lesion of as having a chronic abscess. Further treatment is similar the marginal or interdental gingiva, usually produced by to that of a periodontal pocket. an impacted foreign object. It is treated as follows: Under topical and local infiltrative anesthesia, the REFERENCE fluctuant area of the lesion is incised with a #15 blade, and the incision is gently widened to permit drainage. 1. Manson JD: Periodontics, ed 3. Philadelphia, Lea & Febiger, The area is cleansed with warm water and covered with a 1975. Group P : Perio-endo  The Periodontic-Endodontic Continuum William F. Ammons, Jr. and Gerald W. Harrington CHAPTER CHAPTER OUTLINE ETIOLOGIC FACTORS OF PULPAL DISEASE THERAPEUTIC MANAGEMENT OF PULPAL AND CLASSIFICATION OF PULPAL DISEASE PERIODONTAL DISEASE EFFECTS OF PULPAL DISEASE ON THE ENDODONTIC LESION PRIMARY PERIODONTIUM I NDEPENDENT PERIODONTAL AND EFFECT OF PERIODONTITIS ON THE DENTAL PULP ENDODONTIC LESIONS DIFFERENTIATION OF PERIODONTAL AND COMBINED LESIONS (PERIO-ENDO) PULPAL LESIONS PROGNOSIS OF COMBINED LESIONS The Signs and Symptoms of Periodontitis POTENTIAL COMPLICATIONS TO The Signs and Symptoms of Pulpal Disease ENDODONTIC THERAPY DIFFERENTIATION BETWEEN PULPAL AND RESTORATIVE IMPLICATIONS OF PERIODONTAL ABSCESSES ENDODONTIC THERAPY he simultaneous existence of pulpal problems and minish in the deepest layers of the dentin, the ability inflammatory periodontal disease can complicate of microorganisms and their by-products to penetrate diagnosis and treatment planning and affect the through the dentinal tubules and to provoke pulpal in- sequence of care to be performed. This is particularly flammation is well documented. Direct exposure of the true for the patient with advanced periodontitis, tooth pulp by caries21 or sealing infected pulps may alter the loss and pulpal disease. process of infection if the pulp is unable to eliminate the bacteria. 6.20 The dynamics of the pulpal reaction is dic- ETIOLOGIC FACTORS OF PULPAL DISEASE tated by the virulence of the bacteria, the host response, the effectiveness of pulpal circulation, and the degree of The major causes of pulpal inflammation are 1) instru- vascular and lymphatic drainage. 42 mentation during periodontal, restorative or prosthetic Pulpal infection is a polymicrobial process. Although dentistry; 2) the progression of dental caries; and 3) di- a correlation between causation and any species of bacte- rect, local trauma such as tooth fracture. The extent of ria is not currently possible , 2 studies based on culturing inflammation of the pulp and the signs and symptoms suggest that a mean of five bacterial strains may be cul- that result vary with the severity of the insult and the tured from infected root canals.2 The organisms cultured ability of the host to ameliorate the inflammation that are predominately gram-negative anaerobes.2.3.10.13.38 A s results. the infective process proceeds the proportion of strict Of these, dental caries is the most common cause of anaerobic-to-facultative organisms and the total number pulpal disease. Bacteria are present in carious enamel of bacteria increases. The most common organisms asso- and dentin. Although the numbers of bacteria may di- ciated with pulpitis are listed in Table 65-1. 840  The Periodontic-Endodontic Continuum CHAPTER 65 841 the deposition of reparative dentin if odontoblasts are destroyed. The reversibility of inflammation and symp- Bacteria Associated with Pulpitis toms, without permanent pulpal damage, has led to a classification of this condition as reversible pulpitis. Number of If the pulp is so affected that the inflammatory lesion Bacteria Strains Gram Stain cannot be resolved, even though the source of the trauma is eliminated, a progressive degeneration of the Eubacterium ssp. 59 Gram-positive, pulp results. This progression has been described as be- nonmotile ing an irreversible pulpitis. Irreversible pulpitis may be Peptostreptococcus ssp. 54 Gram-positive, void of symptoms or it may be associated with intermit- nonmotile tent or continuous episodes of spontaneous pain. The Fusobacterium ssp. 50 Gram-negative, application of heat to a tooth with irreversible pulpitis nonmotile can lead to an immediate painful response that can per- Prophyromonas ssp. 32 Gram-negative, sist for a prolonged period. Cold may also provoke such nonmotile a response, although occasionally, the application of Prevotella spp. 45 Gram-negative, cold may provide relief from the pain. A reduced respon- nonmotile siveness of teeth with irreversible pulpitis to thermal Streptococcus spp. 28 Gram-positive, stimuli has been claimed, but Mumford found similar nonmotile pain thresholds in both inflamed and noninflamed Lactobacillus spp. 24 Gram-positive, pulps. nonmotile Irreversible pulpitis ultimately leads to loss of pulpal Wolinella spp. 18 Gram-negative, vitality (necrosis). Necrosis usually results from the same motile factors that induced the irreversible pulpitis and may lead Actinomyces spp. 14 Gram-positive rod, to an alteration in the patient's symptoms. Not all nonvi- nonmotile tal teeth display signs and symptoms of pulpal disease and necrotic pulps are commonly asymptomatic. When Modified from Sundqvist G, Johansson E, Sjogren U: Prevalence symptoms do occur, they may be manifested as episodes of black-pigmented bacteroides species in root canal infections. of spontaneous pain. Testing the pulp with heat may be J Endodon 1989; 15(1):13; and Baumgartner JC, Falkler WA: inconclusive, and a response to cold stimuli is rare. Bacteria in the apical 5 mm of infected root canals. J Endodon 1 991; 17(8):380. EFFECTS OF PULPAL DISEASE ON THE PERIODONTIUM Pulpal tissue may be significantly inflamed and yet exert CLASSIFICATION OF PULPAL DISEASE little or no effect on the periodontium. As long as the The correlation between the histology of pulpal disease pulp remains vital it is unlikely that significant changes and the patient's symptoms is poor. Therefore pulpal dis- will occur in the periodontium. Necrosis of the pulp, ease is generally classified based on clinical signs and however, can result in bone resorption and the produc- symptoms rather than on histologic changes. Such a tion of radiolucency at the apex of the tooth, in the fur- classification is illustrated in Box 65-1. cation or at points along the root2 5.34,41,43 (Fig. 65-1). Minor injury such as periodontal root planing or the Dental radiographs usually document the presence of conservative preparation of a tooth for a restoration may apical or lateral lesions. lead to pulpal symptoms. A transient hypersensitivity to The lesion that results may be an acute apical lesion thermal stimuli is the most common symptom noted. or abscess, a more chronic periradicular lesion (cyst or The application of a thermal stimulus results in a brief, granuloma); or a lesion associated with a lateral or acces- painful response that varies in intensity from mild to se- sory canal. The lesion may remain small, or it can ex- vere. The response rapidly disappears after removal of pand sufficiently to destroy a substantial amount of the the stimulus. Although permanent pulpal damage may attachment of the tooth and/or to communicate with a not occur, a transient inflammatory response can lead to lesion of periodontitis. A classification of periradicular le- sions is found in Box 65-2. The histopathologic structure of the periapical inflam- matory lesion is usually a highly vascularized granula- tion tissue infiltrated to varying degrees by inflammatory cells. Neutrophils may be present near the apical fora- Classification of Pulpal Disease men, whereas plasma cells, macrophages, lymphocytes and fibroblasts are increased in the periphery of the lesion.5,28,39,44 This cellular infiltrate may vary with the nature and intensity of the irritants to the tissues. Similar lesions may develop adjacent to accessory or lateral canals. These canals form when the epithelial root sheath breaks down before root formation or anasto- 842 PART 5 Treatment o f Periodontal Disease cidence is unknown.9,12,43 The majority of these canals occur in the apical portion of the root, with decreased numbers in the furcation area. They are more common in posterior teeth and in the apical portion of the root. 9,22,33 The prevalence of lateral canals in the middle and cervi- cal areas of the root and the prevalence of endodontic- derived lesions in the marginal periodontium via lateral or accessory canals are low. The clinical significance of ac- cessory or lateral canals in spreading infection from the necrotic pulp to the periodontium is therefore unclear. Necrotic pulps apparently exert no effect through the dentinal tubules on the cementum.' EFFECT OF PERIODONTITIS ON THE DENTAL PULP Although the effects of pulpal disease on the periodon- tium are well documented, a clear-cut relationship be- tween periodontitis and pulpal involvement is less evi- dent. One may postulate that bacterial and the inflammatory products of periodontitis could gain access to the pulp via accessory canals, apical foramina, or dentinal tubules. This process, the reverse of the effects of a necrotic pulp on the periodontal ligament, has been Fig. 65-1 Diagrammatic representation of different types of en- referred to as retrograde pulpitis. 31,35 doperiodontal problems. A, An originally endodontic problem with However, although inflammatory changes have been fistulization from the apex and along the root to the gingiva. Pulpal reported adjacent to accessory canals exposed by infection can also spread through accessory canals to the gingiva or periodontitis, periodontitis rarely produces significant to the furcatioh. B, A long-standing periapical lesion draining changes in the dental pulp. Neither irreversible pulpitis through the periodontal ligament can become secondarily compli- or pulpal necrosis has been consistently found in histo- cated, leading to a retrograde periodontitis. C, A periodontal pocket logic studies of teeth extracted because of severe peri- can deepen to the apex and secondarily involve the pulp. D, A peri- odontal disease. 8,20,40 It has been suggested that the pres- odontal pocket can infect the pulp through a lateral canal, and this, ence of an intact layer of cementum may protect the i n turn, can result in a periapical lesion. E, Two independent le- pulp from injurious elements produced by plaque micro- sions, periapical and marginal, can coexist and eventually