1. Chapter 4 Periodontal Diseases

2. Introduction
Periodontal diseases are diseases induced by biofilm (dental plaque)
Early periodontal disease that is limited to the gingiva is referred to as gingivitis
Gingivitis is a common clinical finding that affects nearly everyone at some time during the life cycle
Gingivitis can be reversed by the use of primary preventive measures

3. FIGURE 4–1
Maxillary central incisors. Bone loss on radiographs. A. Slight interproximal bone loss. B. Greater bone loss is seen in advanced periodontal disease. (Courtesy of Dr. O. Langland, University of Texas Dental School at San Antonio.)

4. Introduction (Continued)
Periodontal disease that affects the tooth-supporting structures and alveolar bone is referred to as periodontitis
Damage caused by periodontitis usually is not reversible with primary preventive measures; however, these procedures aid in the control of periodontitis
Loss of attachment is the primary clinical and diagnostic difference between gingivitis and periodontitis

5. Introduction (Continued)
Examples of risk factors that affect the progress of periodontal disease are:
The close relationship between the severity of periodontal disease and the severity of type 2 diabetes mellitus
The strong relationship between periodontal disease and exposure to tobacco and tobacco products such as cigarettes and spit (chewing) tobacco, as well as the environmental exposure of nonsmokers to cigarette smoke

6. Introduction (Continued)
Risk factors continued:
The less-strong relationship between genetically influenced inflammatory mediators and periodontitis

7. Introduction (Continued)
Loss of attachment and bone loss are both rather uncommon in young individuals; however, incidence does increase in adolescents who are 12 to 17 years of age in comparison with children who are five to 11 years old
Studies have shown that the periodontal health of older adults is closely related to self-care and the cumulative effects of the disease process, rather than to age

8. Introduction (Continued)
Within the United States severe generalized periodontitis affects 5% to 15% of the overall population
There are three ways that systemic disease and periodontal diseases are related:
Systemic relationships might be suspected in individual situations in which periodontal disease appears to be disproportional to the local irritants

9. Introduction (Continued)
Periodontal disease systemic link continued:
Genetic (e.g., Down syndrome, Papillon-Lefevre syndrome, Cohen syndrome) or hematologic diseases (e.g., acute leukemia or acquired neutropenia) can cause periodontitis
A complex relationship also exists between periodontitis and systemic diseases such as cardiovascular diseases, diabetes mellitus, pregnancy outcomes, and osteoporosis

10. Introduction (Continued)
The prevalence of periodontal diseases in the United States may increase in the future because:
Longer life spans are increasing the time that teeth are at risk
People are taking better care of their teeth and maintaining their teeth longer, which, in turn increases the number of teeth at risk
Improved diagnosis and detection of periodontal diseases by oral health professionals could, perhaps, increase the prevalence of periodontal diseases

11. The Periodontium Four anatomical structures support the teeth:
Gingiva
Periodontal ligament
Cementum
Alveolar bone
Collectively these structures comprise the periodontium. The tissues of the periodontium attach the tooth to the alveolar process

12. Parts of the periodontium.
FIGURE 4–2
Parts of the periodontium.

13. The Gingiva
The gingiva consists of the free (or marginal) gingiva, interdental papillae, and attached gingiva
Marginal gingiva surrounds each tooth in a “cuff-like” fashion and is not attached to the tooth
Most apical portion is the free marginal groove, which defines the boundary between the attached and marginal gingiva)

14. FIGURE 4–3
Gingiva. Key: A. marginal gingiva, B. interdental papilla, C. attached gingiva,
D. mucogingival junction, E. alveolar mucosa, F. circular fibers, G. dentogingival fibers.
(Adapted from J. Lindhe and T. Karring. Wiley Publishers. Anatomy of the periodontium, in Clinical Periodontology and Implant Dentistry, ed. J. Lindhe. Copenhagen: Munksgaard, © 2003.)

15. Gingival Fibers
Gingival fibers aid the tissue in withstanding the forces of mastication, and connect the marginal gingiva with the cementum and the attached gingiva
Fibers that encircle the tooth within the marginal gingiva are called circular or circumferential fibers

16. FIGURE 4–4
Electron scanning microscopic view of collagen bundles in the periodontal ligament space. Note narrow bundle crossing thick bundle at right angle. (From Svejda J., & Skach M. (1973). The periodontium of the human teeth in the scanning electron microscope (stereoscan). J Periodont, 44:478–84.)

17. Gingival Fibers (Continued)
Gingivodental (or dentogingival) fibers, are inserted into the cementum, and extend into the crest (upper ridge) and the periosteum (connective tissue surrounding the alveolar bone) of the alveolar bone just beneath the epithelium at the base of the gingival sulcus
Dentoperiosteal fibers anchor the tooth to the bone
Alveologingival fibers extend from the alveolar crest to the marginal and attached gingiva

18. Gingival Fibers (Continued)
Transseptal fibers are located interproximally and extend from the cementum of one tooth, over the alveolar crest of interproximal bone, and into the cementum of the adjacent teeth

19. Principal fibers of the periodontal ligament.
FIGURE 4–5
Principal fibers of the periodontal ligament.

20. FIGURE 4–6
Cross-sectional view of interdental papillae showing A. transseptal fibers, B. alveolar crest, C. dental papilla, D. enamel space, and E. dentin.
(Courtesy of Dr. Don Willman, University of Texas Dental School at San Antonio.)

21. Interdental Gingival Composed of two papillae Connected by col
One is located on the facial side of the teeth
One is located on the lingual side of the teeth
Connected by col

22. FIGURE 4–7
Col area. Proximal view of tooth and gingiva. G, Interdental gingiva fills the gingival embrasure. (From P. F. Fedi, Jr., and A. R. Vernino. The Periodontic Syllabus. Copyright © 2000 by Lippincott Williams & Wilkins.)

23. PDL
The periodontal ligament is a network of collagen fibers. This structure surrounds the tooth root and connects it with the alveolar bone. Its collagen fibers embed into the cementum of the root on one side and into the alveolar bone on the other side
The five principal fibers of the periodontal ligament have different orientations and functions at various levels on the tooth root

24. FIGURE 4–8
Dentogingival junction: A. and B. The junction between the tooth and gingival soft tissues. C. This junction occurs where there are a few layers of junctional epithelial cells. D. The attachment mechanism for these cells consists of hemidesmosomes in each cell, and a basal lamina between the cell body and tooth.

25. PDL Fibers
Alveolar crest fibers extend obliquely from the cementum to the alveolar crest. They prevent lateral movement and extrusion of the tooth
Horizontal fibers are located at the cervical area and also resist lateral forces

26. PDL Fibers (Continued)
Oblique fibers extend in an oblique fashion from the alveolar bone to the cementum and bear the stress of chewing
Apical fibers form at the tooth apex and are generally parallel to the long axis of the tooth to help cushion the tooth from occlusal forces

27. PDL Fibers (Continued)
Interradicular fibers are found in the furcation area of a multi-rooted tooth and connect the cementum and tooth

28. Dentogingival Junction
The junctional epithelium and the gingival fibers are considered a functional unit called the dentogingival unit or dentogingival junction
The junctional epithelium is several layers thick when it initially forms, and the number of layers increases with age

29. Dentogingival Junction (Continued)
This biologic seal functions to anchor the sulcular epithelium to the tooth surface and to protect the underlying periodontal fibers from the hostile oral environment

30. Epithelial Cells
The junctional epithelial cells are joined to the tooth surface by hemidesmosomes, which consist of a few layers of epithelial cells that initially extend a short distance along the enamel surface at the cementoenamel junction

31. Epithelial Cells (Continued)
Inflammation, especially chronic inflammation such as in periodontitis, can result in apical migration of the cells, first over the cementoenamel junction, and then apically onto the cementum

32. Apical Migration
For each millimeter of apical migration of the attachment, there is also an accompanying loss of one mm of periodontal fibers attached between the cementum and bone
As the junctional epithelium migrates apically in more advanced disease, there is loss of alveolar bone and exposure of the cementum to which the fibers were originally attached

33. Apical Migration (Continued)
The migration also causes a deepening of the sulcus to form a periodontal pocket
This apical migration of the junctional epithelium and consequent loss of attachment (clinical attachment loss) is the hallmark sign for diagnosing periodontitis

34. Gingival Crevicular Fluid
In an inflamed disease state, fluid flows from the depths of the gingival sulcus. Gingival crevicular fluid (GCF) is a transudate, which contains a few cells and proteins as opposed to exudates which is inflammatory in nature
Gingival crevicular fluid is derived from blood vessels in the connective tissue adjacent to the sulcus

35. Gingival Crevicular Fluid (Continued)
An increase in GCF flow is one of the first detectable signs of impending gingivitis
After patients stop dental self-care, an increase of GCF can be observed as early as the ninth day

36. Gingival Crevicular Fluid (Continued)
GCF serves several protective functions:
It helps clear bacteria from the gingival sulcus
It is the vehicle for leukocytes, complement, antibodies, and assorted enzymes that help protect the enamel and the periodontium from bacterial attack

37. Periodontal Microflora: The Nonspecific Plaque Hypothesis
The nonspecific plaque hypothesis simply relates periodontal disease to the overall amount of plaque present. As the amount of plaque increases, inflammation and disease increase

38. Periodontal Microflora: The Nonspecific Plaque Hypothesis (Continued)
In the 1960s, Loe and others recognized a casual relationship between bacterial plaque and gingivitis. Gingivitis would result when plaque was not removed by self-care, and gingivitis would reverse when self-care was resumed. This landmark study seems to be the basis for the nonspecific plaque hypothesis

39. Periodontal Microflora: The Nonspecific Plaque Hypothesis (Continued)
Attributes the various demonstrations of signs or symptoms (manifestations) of the periodontal plaque-related diseases to “specific”, although not necessarily known, bacteria. Quality of bacterial plaque biofilm is more important than the quantity. In other words, specific types and complexes of bacteria and their pathogenic potential are more important than the amount of plaque biofilm present

40. Periodontal Microflora: The Nonspecific Plaque Hypothesis (Continued)
Also, not all plaque biofilm is associated with disease. Therefore, all individuals are not equally susceptible, gingivitis does not always progress to periodontitis, and treatment interventions vary depending on the type of disease

41. The Developing Gingival Lesion
There are four stages of inflammation in the periodontal lesion

43. FIGURE 4–9
A. A few plaque organisms (dark figures) from a relatively healthy sulcus as seen with a phase microscope. B. Great increase in number of organisms seen in moderate-to severe marginal gingivitis.

44. The Developing Gingival Lesion (Continued)
If self-care of a healthy mouth is stopped, gingivitis is observed clinically (i.e., changes in color, size, and/or texture) in only nine to 21 days. Presumably, inflammation might manifest itself sooner in some cases
With gingivitis, the extent of the gingival inflammation parallels the extent of plaque biofilm accumulation

45. The Developing Gingival Lesion (Continued)
Early gingival clinical changes include alterations in:
Color
Contour changes from knife-edge to rolled
Consistency change from firm to spongy
The free margin often bleeds on gentle manipulation such as from toothbrushing or probing

46. The Developing Gingival Lesion (Continued)
In the early stages, the developing inflammatory process can be completely reversed by professional oral health care interventions and patient self-care strategies

47. FIGURE 4–10
A. A severe gingivitis with calculus, food debris, and poor self-care. Note the rolled and edematous gingiva. B. After a few days of diligent use of a brush, floss, and irrigation.
(Courtesy of Dr. Donald Willmann, University of Texas Dental School at San Antonio.)

48. FIGURE 4–11
Healthy periodontium.
(Courtesy of Dr. Donald Willmann, University of Texas Dental School at San Antonio.)

49. The Developing Gingival Lesion (Continued)
Not all gingival pathology is caused solely by bacterial plaque biofilm
Systemic conditions such as pregnancy or other hormonal changes cause the tissues to react more readily to the bacterial insult
Inherited diseases such as hereditary fibromatosis and by drug therapy such as phenytoin used to control seizure disorders may cause changes

50. The Deepening Pocket
All periodontitis is preceded by gingivitis, but not all untreated gingivitis progresses to periodontitis
A diagnosis of gingivitis implies that the actual level of the junctional epithelial attachment has not migrated apically, but is still on the enamel or on the cementoenamel junction

51. The Deepening Pocket (Continued)
A diagnosis of periodontitis implies that the junctional epithelium has migrated apically two, three, or more millimeters from its original level at the cementoenamel junction

52. The Deepening Pocket (Continued)
As the pocket deepens, subgingival plaque acquires new characteristics that differentiate it from the supragingival plaque
In the supragingival plaque, the bacteria and the interbacterial matrix are well confined to the enamel

53. The Deepening Pocket (Continued)
In the subgingival plaque, a two-compartment subgingival plaque system begins to evolve, and that system is made up of:
Tooth-associated subgingival plaque, a biofilm on the cementum
A more fluid environment referred to as epithelium-associated plaque that bathes the cementum

54. The Deepening Pocket (Continued)
This fluid consists of:
Purulent fluids (pus)
Food debris
Body defense cells
Saliva confined under low-oxygen tension without circulation within the pocket

55. The Deepening Pocket (Continued)
The gram-negative organisms that extend deep into the pocket are believed to be the plaque biofilm responsible for the continued damage and migration of the epithelial attachment

56. The Deepening Pocket (Continued)
Change in the environment permits subgingival bacteria to colonize into bacterial plaque on the root, or in the sulcus
Aerobic bacteria become organized subgingivally in attached and unattached plaque. Toxins, enzymes, and metabolic byproducts then injure the periodontium, and cause an immune response that results in indirect toxicity

57. The Deepening Pocket (Continued)
As the host responds to the irritant, periodontal destruction occurs by immunopathologic reaction, that is, periodontal tissues are altered as a result of immune or allergic reactions to the irritant

58. The Deepening Pocket (Continued)
Elimination of supragingival plaque is critical in preventing periodontal diseases
Control of supragingival and subgingival plaque biofilm is critical to successful periodontal therapy
Professional subgingival mechanical instrumentation is mandatory to complement patient self-care to achieve and maintain periodontal health

59. Cellular Defense in the Periodontal Disease Process
The body has three key functions of immunologic defense:
To protect it from outside invaders (antigens)
To destroy or neutralize the antigens that do penetrate the epithelial defenses
To repair any damage caused by the antigen–antibody reactions

60. Cellular Defense in the Periodontal Disease Process (Continued)
The cells responsible for the cellular defense are:
Granular cells, which consist of granulocytes (basophils, eosinophils, and polymorphonuclear neutrophils [PMN, polys])
Monocytes (macrophages)
Those cells of lymphoid origin
T and B lymphocytes

61. Cellular Defense in the Periodontal Disease Process (Continued)
During the cellular response to a periodontal infection, there is first a chemotactic signal from an inflamed gingival site, which initiates the cellular immune response
The acute phase may last from a few days to a few weeks
If the inflammation continues, the number of PMN decreases and they are replaced by lymphocytes

62. Cellular Defense in the Periodontal Disease Process (Continued)
If healing does not occur, the lymphocytes are replaced largely by plasma cells, macrophages, and mast cells
The inflammation is now in the chronic stage
Cellular infiltrate is predominated by lymphocytes

63. Cellular Defense in the Periodontal Disease Process (Continued)
As the chronic inflammation continues, the epithelial attachment slowly migrates apically on the cementum
Alveolar bone and soft tissue continue to be lost, and the periodontal pocket becomes deeper, making the control of disease difficult
Eventually, this continuing loss of tooth support results in a loosening of the tooth or teeth

64. Cellular Defense in the Periodontal Disease Process
Interleukin-1
Has received attention as a marker that can help predict the risk for periodontal disease
A proinflammatory cytokine that is a key regulator of host responses to microbial infection
A major modulator of the catabolism (breakdown) of extracellular matrix and bone resorption

66. Classifications of Periodontal Disease
Seven categories of periodontitis
Chronic
Aggressive
Systemic periodontitis
Necrotizing disease
Abscesses
Endodontic lesions
Developmental or acquired deformities and conditions

67. Classifications of Periodontal Disease: Chronic Periodontitis
Most commonly diagnosed disease category
Occurs over a period of time
Usually treatable
Can be controlled

68. Classifications of Periodontal Disease: Chronic Periodontitis (Continued)
Generally, progresses slowly; however, some patients experience short periods of rapid progression
There are three stages of chronic periodontitis: slight (early), moderate, and advanced (severe)

69. Classifications of Periodontal Disease: Aggressive Periodontitis
Highly destructive
Occurs in otherwise healthy individuals and has a familial aggregation

70. Characteristics of aggressive periodontitis include
Classifications of Periodontal Disease: Aggressive Periodontitis (Continued)
Characteristics of aggressive periodontitis include
Microbial deposit accumulation that is inconsistent with the severity of the disease (i.e., not much deposit but significant destruction)
Advancement of loss of attachment and bone loss that can be self-arresting (stopped on its own without recent treatment)

71. Features of the localized form include:
Classifications of Periodontal Disease: Aggressive Periodontitis (Continued)
Features of the localized form include:
Onset around puberty
Destruction to permanent first molars and incisors
Association with the periodontal pathogen Actinobacillus actinomycetemcomitans
Abnormalities in neutrophil function

72. Classifications of Periodontal Disease: Aggressive Periodontitis (Continued)
Generalized aggressive periodontitis usually affects people under the age of 30 years
Generalized attachment loss is present, and affects at least three permanent teeth in addition to the first molars and incisors

73. Classifications of Periodontal Disease: Aggressive Periodontitis (Continued)
The loss of attachment occurs in major episodic periods of destruction, and it is also associated with Actinobacillus actinomycetemcomitans, and Porphyromonas gingivalis, as well as abnormalities in neutrophil function

74. Classifications of Periodontal Disease: Systemic Link
Periodontitis as a manifestation of systemic disease includes:
Diseases associated with hematologic disorders (e.g., leukemias)
Genetic disorders, such as cyclic neutropenia, Down syndrome, Papillon-Lefevre syndrome, Cohen syndrome, and hypophosphatasia, to name a few
These diseases actually cause periodontal destruction and loss of attachment

75. Classifications of Periodontal Disease: NUG
Necrotizing ulcerative gingivitis is a condition of sudden onset, and the patient might have a history of stress, change in living habits, inadequate rest, debilitating disease, and/or respiratory tract infection
In NUG, the lesions appear punched out and crater-like; the necrotic tissue separates from the healthy gingiva, forming a gray pseudomembrane (false membrane); and the gingiva shows pronounced linear erythema (redness)

76. Classifications of Periodontal Disease: NUP
When bone loss occurs NUG has become necrotizing ulcerative periodontitis

77. Classifications of Periodontal Disease: Periodontal Abcess
Periodontal abscess category relates to gingival, periodontal, or pericoronal lesions (gingival lesions close to the crown)
Periodontic–endodontic lesion classification recognizes the possible connection between periodontitis and endodontic lesions

78. Classifications of Periodontal Disease: Developmental or Aquired Deformities and Conditions
Refers to modifiers of the susceptibility to periodontal diseases and not to separate diseases
Modifiers: Recession, lack of keratinized gingiva, or decreased depth of the vestibule directly influence the outcomes of nonsurgical or surgical treatment

79. Risk Factors
Behavior, inherent characteristic, or environmental exposure associated with a disease
Associated with incidence, extent, and progression of periodontal diseases, and are usually identified through longitudinal studies

80. Risk Factors (Continued)
Specific examples of risk factors for periodontal diseases are age, gender, socioeconomic status, genetics, plaque biofilm, self-care, tobacco, stress, and diabetes
Not all risk factors are modifiable

81. Primary Prevention of Periodontal Disease
Requires daily mechanical plaque control (toothbrushing and interdental cleaning) often supplemented with chemical control measures for plaque biofilm as an additional component (adjunct) of the primary treatment
Fluoride mouth rinses can be used to aid in preventing root and coronal caries

82. Classifications of Periodontal Disease
A major challenge in primary preventative dentistry is to increase public awareness that patient self-care can maintain excellent oral health

83. Summary
Periodontitis is a disease involving pathology of one or more of the four components of the periodontium
Periodontal disease is an umbrella term for several clinically similar types of diseases