“Periodontology” is the study of the tooth-supporting tissues, the “periodontium.” The periodontium is made up of those tissues that surround each tooth and which anchor each tooth into the alveolar process (Latin: para = adjacent to; Greek: odus = tooth).
The following soft and hard tissues constitute the structure of the periodontium:
• Periodontal Ligament
• Root Cementum
• Alveolar Bone
The structure and function of these periodontal tissues have been extensively researched (Schroeder 1992). Knowledge of the interplay between and among the cellular and molecular components of the periodontium leads to optimum therapy, and also helps to establish the goals for future intensive research.
Gingivitis – Periodontitis
There are numerous diseases that affect the periodontium. By far the most important of these are plaque-associated gingivitis (gingival inflammation without attachment loss) and periodontitis (inflammation-associated loss of periodontal supporting tissues).
• Gingivitis is limited to the marginal, supracrestal soft tissues. It is manifested clinically by bleeding upon probing of the gingival sulcus, and in more severe cases by erythema and swelling, especially of the interdental papillae (Fig. 3).
• Periodontitis can develop from a pre-existing gingivitis in patients with compromised immune status, the presence of risk factors and pro-inflammatory mediators, as well as the presence of a predominately periodontopathic microbial flora. The inflammation of the gingiva may then extend into the deeper structures of the tooth-supporting apparatus. The consequences include destruction of collagen and loss of alveolar bone (attachment loss). The junctional epithelium degenerates into a “pocket” epithelium, which proliferates apically and laterally. A true periodontal pocket forms. Such a pocket is a predilection site and a reservoir for opportunistic, pathogenic bacteria; these bacteria sustain periodontitis and enhance the progression of the disease processes (Fig. 4).
Gingival recession is not actually a “disease,” but rather an anatomic alteration that is elicited by morphology, improper oral hygiene (aggressive scrubbing), and possibly functional overloading.
• Teeth are not lost due to classical gingival recession, but patients may experience cervical hypersensitivity and esthetic complications. If gingival recession extends to the mobile oral mucosa, adequate oral hygiene is often no longer possible. Secondary inflammation is the consequence.
In addition to classical gingival recession, apical migration of the gingiva is often observed in patients with longstanding, untreated periodontitis, and it may be a consequence of periodontitis therapy in elderly patients (“involution”; Fig. 2).
These three periodontal disorders – gingivitis, periodontitis, gingival recession – are observed world-wide; they affect almost the entire population of the earth to greater or lesser degree. In addition to these common forms of oral pathology, there are many less frequently encountered diseases and defects of the periodontal tissues. All of these diseases were comprehensively classified at an international World Workshop in 1999 (see Appendix, p. 519).
Periodontitis is usually a very slowly progressing disease (Locker & Leake 1993; Albandar et al. 1997), which in severe cases—particularly when untreated—can lead to tooth loss. Enormous variation in the speed of progression of periodontitis is observed when one differentiates between individual patients. In addition to the quantity and composition of the bacterial plaque, individually varying influences also play important roles: the systemic health of the patient, the patient’s genetic constitution, psychically influenced immune response status, ethnic and social factors, as well as risk factors such as smoking and stress (p. 22, Fig. 41). All of these circumstances can influence the onset and the speed at which the disease process accelerates in different patient age groups.
Not all teeth or individual surfaces of teeth are equally susceptible (Manser & Rateitschak 1996):
• Molars are the most endangered
• Premolars and anterior teeth are less susceptible
• Canines are the most resistant.
Phase of quiescence
The primary goal is prevention of periodontal diseases, and the secondary goal is to enhance the healing of existent periodontitis, as far as possible toward complete Restitutio ad integrum. Clinical and basic research is targeted today toward realization of these goals in the near future.
At the present time, proven therapeutic concepts are available for the elimination of inflammation and the cessation of the progression of disease. In addition, to a certain degree, it is possible today to regenerate lost periodontal attachment (GTR, p. 338). The following treatment modalities are available to the periodontal therapist:
1 Closed or open root planing (“causal therapy,” the “gold standard”)
2 Regenerative surgical therapies
3 Resective surgical therapies
4 Alternatives: extraction or dental implants?
1 Root planing is the Conditio sine qua non in all periodontal therapy. This is pure causal therapy, during which the causative “biofilm” (plaque) and subgingival calculus are removed. If the pockets are shallow and the morphological relationships simple (single-rooted teeth), treatment can be performed closed, but in advanced cases, open treatment with direct visual access following reflection of a tissue flap is often preferable (e. g., modified Widman procedure). The result of such treatment is usually healing in the sense of “repair” (p. 206). A long junctional epithelium forms.
2 Regenerative therapeutic methods (“guided tissue regeneration” [GTR]; autogenous, alloplastic implants) have taken on increased significance in recent years. These procedures are constantly being further developed, and in the future they may be enhanced by the use of growth and differentiation factors.
Regenerative therapy can lead to the actual re-formation of significant periodontal tissues.
3 Radical surgery for the elimination of periodontal pockets has lost some its popularity in recent years, although the results are generally more predictable and the tendency toward recurrence is low.
4 In cases of complex, severely advanced periodontitis, e. g., with severe furcation involvement in the molar region, the dentist may consider tooth extraction and replacement with a root-form implant instead of resective or regenerative periodontal surgery. Even in such cases, periodontal treatment of the remaining dentition must be performed, as well as optimum plaque control by the patient and the creation of an adequate amount of bone for the implant.
“Structural biology” is a general term referring to the classical macromorphology and histology of tissues, as well as their function, including the biochemistry of the cells and the intercellular substances.
Basic knowledge of the normal structural biology of periodontal tissues and their dynamics (mediator-guided homeostasis, “turnover”) is a prerequisite for full understanding of pathobiological changes in the periodontium, which can involve adaptations of the normal structures or an imbalance of otherwise normal functions (Schroeder 1992).
The term “periodontium” encompasses four different soft and hard tissues: gingiva, root cementum, alveolar bone, and the periodontal ligament, which attaches root cementum to bone. Each of these four tissues can be further differentiated in terms of structure, function and localization.
C Radiating collagen fibers
D Cementoblast (fibroblast-like) building acellular exogenous fiber cement
The gingiva is one portion of the oral mucosa. It is also the most peripheral component of the periodontium. Gingiva begins at the mucogingival line, and covers the coronal aspect of the alveolar process. On the palatal aspect, the mucogingival line is absent; here, the gingiva is a part of the keratinized, non-mobile palatal mucosa.
The gingiva ends at the cervix of each tooth, surrounds it, and forms there the epithelial attachment by means of a ring of specialized epithelial tissue (junctional epithelium; p. 10). Thus the gingiva provides for the continuity of the epithelial lining of the oral cavity.
The gingiva is demarcated clinically into the free marginal gingiva, ca. 1.5 mm wide; the attached gingiva, which may be of varying width; and the interdental gingiva.
Healthy gingiva is described as “salmon” pink in color; in Blacks (seldom also in Caucasians) the gingiva may exhibit varying degrees of brownish pigmentation. Gingiva exhibits varying consistency and is not mobile upon the underlying bone. The gingival surface is keratinized and may be firm, thick and deeply stippled (“thick phenotype”), or thin and scarcely stippled (“thin phenotype”; Müller & Eger 1996, Müller et al. 2000).
The attached gingiva becomes wider as a patient ages (Ainamo et al. 1981). The width varies between individuals and among various groups of teeth in the same person. Although it was once believed that a minimum width of attached gingiva (ca. 2 mm) is necessary to maintain the health of the periodontium (Lang & Löe 1972), this concept is not accepted today. However, a wide band of attached gingiva does offer certain advantages in the case of periodontal surgery, both therapeutically and esthetically.
Apical to the contact area between two teeth, the interdental gingiva assumes a concave form when viewed in labiolingual section. The concavity, the “col,” is thus located between the lingual and facial interdental papillae and is not visible clinically. Depending on the expanse of the contacting tooth surfaces, the col will be of varying depth and breadth. The epithelium covering the col consists of the marginal epithelia of the adjacent teeth (Cohen 1959, 1962; Schroeder 1992). The col is not keratinized. In the absence of contact between adjacent teeth, the keratinized gingiva courses uninterrupted from the facial to the oral aspect.
Junctional Epithelium—Epithelial Attachment—Gingival Sulcus
The marginal gingiva attaches to the tooth surface by means of the junctional epithelium, an attachment that is continuously being renewed throughout life (Schroeder 1992).
The junctional epithelium (JE) is approximately 1–2 mm in coronoapical dimension, and surrounds the neck of each tooth. At its apical extent, it consists of only a few cell layers; more coronally, it consists of 15–30 cell layers. Subjacent to the sulcus bottom, the JE is about 0.15 mm wide.
The junctional epithelium consists of two layers, the basal (mytotically active) and the suprabasal layer (daughter cells). It remains undifferentiated and does not keratinize. The basal cell layer interfaces with the connective tissue via hemidesmosomes and an external basal lamina. Healthy JE exhibits no rete ridges where it contacts the connective tissue. JE turnover rate is very high (4–6 days) compared to oral epithelium (6–12 days, Skougaard 1965; or up to 40 days, Williams et al. 1997).
The epithelial attachment to the tooth is formed by the JE, and consists of an internal basal lamina (IBL) and hemidesmosomes. It provides the epithelial attachment between gingiva and tooth surface. This can be upon enamel, cementum or dentin in the same manner. The basal lamina and the hemidesmosomes of the epithelial attachment are structural analogs of their counterparts comprising the interface between epithelium and connective tissues.
All cells of the JE are in continual coronal migration, even those cells in immediate contact with the tooth surface. Such cells must continually dissolve and reestablish their hemidesmosomal attachments. Between the basal lamina and the tooth surface, a 0.5–1 μm thick “dental cuticle” is observed; this is possibly a serum precipitate or a secretion product of the junctional epithelial cells.
The sulcus is a narrow groove surrounding the tooth, about 0.5 mm deep. The bottom of the sulcus is made up of the most coronal cells of the junctional epithelium, which are sloughed (exfoliated) in rapid succession. One lateral wall of the sulcus is made up of the tooth structure, the other wall is the oral sulcular epithelium (OSE; Schroeder 1992).
Gingival and Periodontal Fiber Apparatus
The fibrous connective tissue structures provide the attachment between teeth (via cementum) and their osseous alveoli, between teeth and gingiva, as well as between each tooth and its neighbor. These structures include:
• Gingival fiber groups
• Periodontal fiber groups (periodontal ligament)
Gingival Fiber Groups
In the supra-alveolar area, collagen fiber bundles course in various directions. These fibers give the gingiva its resiliency and resistance, and attach it onto the tooth surface subjacent to the epithelial attachment. The fibers also provide resistance to forces and stabilize the individual teeth into a closed segment (Fig. 22). The periosteogingival fibers are also a component of the gingival fiber complex. These connect the attached gingiva to the alveolar process.
Periodontal Fiber Groups, Periodontal Ligament
The periodontal ligament (PDL) occupies the space between the root surface and the alveolar bone surface. The PDL consists of connective tissue fibers, cells, vasculature, nerves and ground substance. An average of 28,000 fiber bundles insert into each square millimeter of root cementum!
The building block of a fiber bundle is the 40–70 nm thick collagen fibril. Many such fibrils in parallel arrangement make up a collagen fiber. Numerous fibers combine to form collagen fiber bundles. These collagen fiber bundles (Sharpey’s fibers) insert into the alveolar bone on one end and into cementum at the other (Feneis 1952). The most ubiquitous cells are fibroblasts, which appear as spindle-shaped cells with oval nuclei and numerous cytoplasmic processes of varying lengths. These cells are responsible for the synthesis and break-down of collagen (“turnover”). Cells responsible for the hard tissues are the cementoblasts and osteoblasts. Osteoclastic cells are only observed during phases of active bone resorption. Near the cementum layer, within the PDL space, one often observes string-like arrangements of epithelial rest cells of Malassez.
Types of Cementum
From a purely anatomic standpoint, root cementum is part of the tooth, but also part of the periodontium. Four types of cementum have been identified (Bosshardt & Schroeder 1991, 1992; Bosshardt & Selvig 1997):
|1 Acellular, afibrillar cementum||(AAC)|
|2 Acellular, extrinsic-fiber cementum||(AEC)|
|3 Cellular intrinsic-fiber cementum||(CIC)|
|4 Cellular mixed fiber cementum||(CMC)|
AEC and CMC are the most important types of cementum.
Fibroblasts and cementoblasts collaborate in the formation of cementum. Periodontal ligament fibroblasts secrete acellular extrinsic cementum. Cementoblasts secrete cellular intrinsic cementum, and a portion of the cellular mixed fiber cementum, and probably also acellular afibrillar cementum. Cementocytes evolve from the cementoblasts, which become entrapped in cementum during cementogenesis. As a result, cementocytes are observed within cellular mixed fiber cementum and frequently in cellular intrinsic cementum (see also Cementum Formation and Healing, p. 206).
1 Acellular, Afibrillar Cementum (AAC; red) AAC is formed at the most cervical enamel border following completion of pre-eruptive enamel maturation, and sometimes also during tooth eruption. It is probably secreted by cementoblasts.
2 Acellular, Extrinsic-fiber Cementum (AEC; green) AEC forms both pre- and post-eruptively. It is secreted by fibroblasts. On the apical portions of the root, it comprises a portion of the mixed-fiber cementum.
3 Cellular, Intrinsic-fiber Cementum (CIC; blue) CIC is formed both pre- and post-eruptively. It is synthesized by cementoblasts, but does not contain extrinsic Sharpey’s fibers.
4 Cellular, Mixed-fiber Cementum (CMC; orange/green) CMC is formed by both cementoblasts and fibroblasts; it is a combination of cellular intrinsic-fiber cementum and acellular extrinsic-fiber cementum.
Acellular Extrinsic Cementum (AEC)
The AEC is primarily responsible for the anchorage of the tooth in the alveolus. It is found in the cervical third of all deciduous and permanent teeth. The AEC consists of tightly packed and splaying fiber bundles (Sharpey’s fibers), which are embedded in the calcified cementum.
The collagenous structures of cementum and dentin intertwine with each other during root formation and before calcification. This phenomenon explains the tight connection between these two hard tissues.
AEC is the type of cementum that is desired following regenerative periodontal surgical procedures.
Cellular Mixed-fiber Cementum (CMC)
The CMC is also of importance for the anchorage of the tooth in its alveolus. But it is only the acellular extrinsic-fiber cementum portion (AEC) within the mixed cementum, into which the Sharpey’s fibers secreted by fibroblasts insert and therefore affix the tooth. CMC is layered vertically but also horizontally to the root surface. The portions secreted by cementoblasts contains high numbers of cementocytes (Fig. 30, left). The CMC is also tightly affixed to the dentin because of the intertwining of the collagen fiber bundles during tooth formation. The CMC “grows” faster than AEC.
Alveolar Process—Alveolar Bone
The alveolar processes of the maxilla and the mandible are tooth-dependent structures. They develop with the formation of and during the eruption of the teeth, and they atrophy for the most part after tooth loss. Three structures of the alveolar process may be discriminated:
• Alveolar bone proper
• Trabecular bone
• Compact bone
Compact bone covers and contains the alveolar processes. At the entrance to the alveoli, the alveolar crest, it blends into the cribriform plate, the alveolar bone proper, which forms the alveolar wall and is approximately 0.1–0.4 mm thick. It is perforated with numerous small canals (Volkmann canals) through which vessels as well as nerve fibers enter into and exit the periodontal ligament space. The trabecular bone occupies the space between compact bone and alveolar bone proper. The distance between the marginal gingiva and the alveolar crest is referred to as the “biologic width” of 2–3 mm (Gargiulo et al. 1961, see p. 490).
All periodontal tissues, but especially the periodontal ligament, have a copious blood supply even in the healthy state. This is due not only to the high metabolism of this cell- and fiber-rich tissue, but also to the peculiar mechanical/functional demands on the periodontium. Occlusal forces are resisted not only by the periodontal ligament and the alveolar process, but also by means of the tissue fluid and its transfer within the periodontal ligament space (hydraulic pressure distribution, dampening).
The most important afferent vessels for the alveolar process and the periodontium are:
• In the maxilla, the anterior and posterior alveolar arteries, the infraorbital artery and the palatine artery
• In the mandible, the mandibular artery, the sublingual artery, the mental artery, and the buccal and facial arteries.
Lymph vessels follow for the most part the blood vascular tree.
The sensory innervation of the maxilla occurs via the second branch of the trigeminal nerve, and that of the mandible via the third branch. The following description of the neural distribution within the periodontal structures is based upon investigations by Byers (1985), Linden et al. (1994) and Byers & Takeyasu (1997).
The periodontium, especially the gingiva and periodontal ligament, contains “Ruffini-like” mechanoreceptors and nociceptive nerve fibers, in addition to the ubiquitous branches of the sympathetic nervous system.
The functions of these innervations are coordinated with those of the dental pulp and the dentin. The stimulus threshold of the mechanoreceptors, which react to tactile (pressure) stimulus, as well as to the stretching of the periodontal ligament fibers, is very low. In contrast, the pain-sensing nociceptive nerve endings have a relatively high threshold. It is via these two separate afferent systems that “information” about jaw position, tooth movements, speech, tooth contact during swallowing and chewing, minor positional alterations (physiologic tooth mobility), pain during unphysiologic loading, as well as injuries are transmitted. In this way, various mechanoreceptors transmit “conscious reactions” via trigeminal ganglia to the sensory nucleus of the trigeminal in the central nervous system, while unconscious reflexes transmit to mesencephalic sensory neurons. These various receptors are localized in varying regions of the periodontal structures: At the level of the middle of the root, one finds more receptors for up-take of “conscious reactions,” whereas in the apical region there are more receptors for the unconscious reflexes whose signals transmit to the mesencephalic sensory neurons.
|A||Mesencephalic sensory neurons of the trigeminal nerve|
|B||Motor nucleus of the trigeminal|
|C||Sensory nucleus of the trigeminal|
|D||Spinal sensory trigeminal nucleus|
|E||Fibers of the masticatory musculature|
|TG||Trigeminal ganglion (Gasserian ganglion) with its three branches:
|CNS||Central Nervous System|
The junctional epithelium as well as the epithelia of the free and attached gingiva, neither of which are vascularized, are served by a dense network of nociceptive and tactile nerve endings. The same is true for the subepithelial, supracrestal gingival connective tissue.
Somatosensory perception in certain gingival diseases (e. g., ulcerative gingivoperiodontitis), as well as pressure and pain sensation during probing of the healthy gingival sulcus or periodontal pockets are the clinical manifestations of the innervation of gingival tissues.
Within the healthy periodontium, there is a constant turnover of all tissues, except cementum. The term tissue homeostasis was coined to characterize the process by which the composition of the various structures, i. e., the balance of their volumes, their integrity vis-à-vis each other, and their mutually interwoven functions (Williams et al. 1997). The apposition and/or resorption of the various tissues can vary even in the healthy condition, depending upon several factors; for example, the periodontal tissues undergo a process known as adaptation, or in cases of reduced occlusal loading (afunction, hypofunction) or increased loading (hyperfunction, parafunction). This concept is not limited only to an adaption to masticatory forces, but is broader in the sense of all “insults” that the periodontal tissues may encounter, including the always present—although in very differing degrees—infection.
Host defense against all “attacks” refers primarily to the immune system (p. 41), but also to the healthy tissue. Disease (periodontitis) will ensue if the demands upon the tissues are larger than their capability to reactively adapt.
The adaptability of the tissues, i. e., their ability to vary the rate of turnover in response to various mediators (e. g., cytokines) also plays an important role in healing, for example following injury or after mechanical periodontal therapy (scaling and root planing—S/RP).
Primary Functions of the Periodontal Tissues
The epithelium of the attached gingiva (OE, oral epithelium) is referred to as masticatory mucosa. Like the palatal mucosa, it is keratinized. Keratinization is a mechanism for protection against all mechanical challenges, but also against thermal, chemical and infectious attack.
The turnover rate of the gingival epithelium has been variously reported between 6 (Schroeder 1992) and 40 days (Williams et al. 1997). Probably it is influenced by “chalones” (substances which inhibit mitosis) on the one hand and by cytokines (Fig. 95), e. g., epidermal growth factor (EGF) and transforming growth factor (TGF-b) on the other.
The junctional epithelium exhibits a faster turnover rate than gingival epithelium. Cell division occurs in the basal cell layer. All of the daughter cells migrate in the direction of the gingival sulcus, where they are rapidly sloughed.
Through this constant flow of junctional epithelial cells, sulcus fluid, and active migration of granulocytes (PMN), the sulcus is effectively cleared of invading bacteria and their metabolic products. In addition to immunocompetent cells, it is also primarily the dynamics of the resident tissue cells and the coronally streaming flow of tissue fluid that is responsible for the prevention of infection and therefore also for the maintenance of health of the marginal periodontal structures.
Gingival Connective Tissue
The circumstance for the periodontal connective tissue is similar to that of the epithelial structures. It has a turnover rate of only a few days, orchestrated by cytokines and growth factors (platelet-derived growth factor/PDGF; fibroblast growth factor/FGF, among others). In this matrix, it is the fibroblasts that are responsible for the synthesis and breakdown of collagen matrix. The matrix metalloproteinases (Fig. 102) that are responsible for the breakdown of collagen depend upon divalent cations (e. g., Zn+2). The balance between synthesis and breakdown can be “shifted” to a certain degree toward synthesis in the presence of pathogenic influences. However, if the pathogenic insult is too great, the process of increased resorption (or reduced synthesis?) can occur and lead ultimately to tissue destruction.
Bone synthesis and resorption, especially the bone loss characteristic of periodontitis, is covered in detail in the chapter “Etiology and Pathogenesis” (pp. 60–61).
In contrast to epithelium, connective tissue and bone, cementum is not subject to continuous turnover. Throughout life, cementum tends to increase in thickness due to apposition. Local resorption observed as resorption lacunae may result from trauma, orthodontic forces, or they may be idiopathic. Such defects are often “repaired” by synthesis of cellular intrinsic-fiber cementum.
The healthy periodontal structures have the capacity to mount a certain defense potential even before the actual immune response is mounted; the latter, of course, also introduces certain destructive elements into the milieu.
The most common diseases of the tooth-supporting apparatus are plaque-induced, usually chronic, inflammatory alterations in the gingiva and the subjacent periodontal structures. Gingivitis may persist for many years without progressing to periodontitis. With good oral hygiene and effective professional removal of plaque and calculus, gingivitis is completely reversible. Periodontitis usually develops out of a more or less pronounced gingivitis. Periodontitis is only partially reversible (see periodontal healing, p. 205; regenerative therapies, p. 323).
The reasons why gingivitis develops into periodontitis (or does not) are still incompletely understood. As with all infections, it appears that the proliferation of pathogenic microorganisms, their toxic potency, their capacities to invade tissues, and above all the individual host response to such infection are the determining factors (p. 55; Kornman et al. 1997, Page & Kornman 1997, Salvi et al. 1997).
An absolutely plaque-free condition in the oral cavity, with prevention of any biofilm formation on tooth surfaces is unachievable, and illusion, and probably even unphysiologic. Nevertheless, gingival and periodontal health can be maintained if the accumulation of plaque is small and if the biofilm contains only weakly virulent organisms (gram-positive, facultative anaerobes), and if an effective host response is mounted.
If the bacterial flora takes on periodontally pathogenic characteristics (e. g., certain gram-negative microorganisms), the result will be inflammation and specific immunologic responses; these responses may represent not only defense mechanisms, but—especially in long-term chronic infection—also destructive potential (cytotoxic, immunopathologic; p. 34).
Inflammation-inducing products of bacteria include enzymes, antigens, toxins, and “signal” substances that activate macrophages and T-cells (Birkedal-Hansen 1998). It is likely that bacterial enzymes, other metabolic products and toxins can directly elicit injury to the periodontal tissues even without immediate host response (inflammation). Bacterial products including hyaluronidase, chondroitin sulfatase, proteolytic enzymes, as well as cytotoxins in the form of organic acids, ammonia, hydrogen sulfide and endotoxins (e. g., lipopolysaccharides, LPS) have been demonstrated in periodontal tissues.
In recent years, the conceptual view concerning the etiology of periodontitis has evolved. Early on, it was the bacteria that were viewed as the determining factor. Certain pathogenic microorganisms were shown to be associated with various forms of periodontal disease, as well as the speed of progression. However, the existence and distribution of pathogenic bacteria did not always correlate with the inception and clinical progression of periodontitis. Furthermore, it was demonstrated that the presence of pathogenic bacteria in a periodontal pocket is not necessarily the cause of that pocket; rather, it seemed much more important that the pocket milieu presents a favorable environment for the existence and proliferation of pathogenic organisms. The stage would then be set—like a vicious cycle—for the progression of the disease processes (Mombelli et al. 1991).
Nevertheless, the old adage “no bacteria = no periodontitis” still holds true, but on the other hand it is also a fact that bacteria, including periodontopathic bacteria, do not without exception cause periodontitis.
1 The primary etiologic factor for the existence of periodontitis is pathogenic microorganisms within the subgingival biofilm.
2 The genetically determined non-specific and specific immune responses, as well as systemic syndromes and diseases influence the existence and the clinical course of periodontitis.
3 “Habits” and the patient’s own approach to general health will influence plaque formation and host immune response, both systemically and particularly with regard to oral health.
4 Social circumstances influence the systemic and psychic well being of the patient. Problems in the socioeconomic arena lead to negative stress.
5 Psychic burdens and stress influence the immune status.
In addition to specific microorganisms, diverse host factors are critical for the development of periodontitis from a preexisting gingivitis (cf. Fig. 41, modified from Clarke & Hirsch 1995). Such factors include the immune responses triggered by pathogens, and these are well understood today. Such defense reactions may be disproportional to the insult, resulting in immunopathologic tissue injury.
Recently, however, in addition to the genetically determined immune reactions, a great number of other individual risk factors have been identified, which may be responsible for the initiation and the degree of severity of the clinical course of periodontitis (p. 51).
Of the risk factors listed in Figures 41 and 104, only a few are capable of damaging the periodontium directly (e. g., smoking); of much greater importance is the influence of such factors on the patient’s own immune system. The delicate balance between “attack/destruction” (bacteria) and defense (host response) is disturbed. It is only logical to assume that the most severe, early-onset and aggressive forms of periodontitis will occur when particularly virulent bacteria are present in a weak (immunodeficient) host.
Bacteria are present throughout life in a myriad of sites on and in the human body. The bacteria may be beneficial for the host, or of no consequence (commensal), or injurious. In the oral cavity, over 530 different species of microorganisms have so far been identified; fortunately, for the most part these organisms remain in ecological balance and do not cause disease. Certain facultatively pathogenic (“opportunistic”) bacteria are occasionally observed in high numbers, e. g., in cases of disease (periodontitis, mucosal infection). It remains unclear whether these bacteria alone represent the cause of the diseases, or whether they simply find favorable living conditions in the disease milieu. Non-specific supragingival plaque (mixed flora) will elicit gingivitis within ca. seven days. If the plaque is removed, gingivitis regresses in a short period of time (“reversibility”). On the other hand, for the various forms of periodontitis, especially the aggressive, rapidly-progressing forms, specific bacteria are associated.
The oropharynx is an open ecosystem wherein bacteria are always present; bacteria attempt to colonize in all favorable locations. Most bacteria, however, can only persist after the formation of a biofilm upon desquamation-free surfaces, i. e., hard substances (tooth and root surfaces, restorative materials, implants, prostheses etc.). In the presence of healthy dental and gingival relationships, there is a balance between the additive and retentive mechanisms of biofilms vis-à-vis the abrasive forces that tend to reduce biofilm formation, e. g., self-cleansing by the cheeks and tongue, diet and mechanical oral hygiene measures.
The existence of a biofilm results within a matter of hours or days, in the phases described below (Darveau et al. 1997, Descouts & Aronsson 1999, Costerton et al. 1999).
The establishment and stabilization of bacteria within a biofilm are important not only for the etiology of periodontitis, but also for adjunctive systemic and topical medicinal treatment for periodontitis (p. 287): Biofilm bacteria imbedded within a matrix of extracellular polysaccharides are more than 1,000 times less sensitive to antimicrobials (e. g., antibiotics) than free-floating (“planktonic”) bacteria.
A Association: Through purely physical forces, bacteria associate loosely with the pellicle.
B Adhesion: Because they possess special surface molecules (adhesins) that bind to pellicle receptors, some bacteria become the “primary colonizers,” particularly streptococci and actinomyces. Subsequently, other microorganisms adhere to the primary colonizers.
C Bacterial proliferation ensues.
D Microcolonies are formed. Many streptococci secrete protective extracellular polysaccharides (e. g., dextrans, levans).
E Biofilm (“attached plaque”): Microcolonies form complex groups with metabolic advantages for the constituents.
F Plaque growth—maturation: The biofilm is characterized by a primitive “circulatory system.” The plaque begins to “behave” as a complex organism! Anaerobic organisms increase. Metabolic products and evulsed cell wall constituents (e. g., lipopolysaccharides, vesicles) serve to activate the host immune response (p. 38). Bacteria within the biofilm are protected from phagocytic cells (PMN) and against exogenous bacteriocidal agents.
… and its initial subgingival expansion
The first bacteria that accumulate supragingivally on the tooth surface are mostly gram-positive (Streptococcus sp, Actinomyces sp.). In the course of the following days, gram-negative cocci as well as gram-positive and gram-negative rods and the first filamentous forms begin to colonize (Listgarten et al. 1975, Listgarten 1976). By means of a variety of metabolic products, the bacterial flora provoke the tissue to an increase in exudation and to migration of PMN leukocytes into the sulcus (“leukocyte walls” against the bacteria).
The increase in PMN diapedesis and the flow of sulcus fluid lead to initial disintegration of the junctional epithelium. This makes it possible for bacteria to more easily invade between the tooth and the junctional epithelium, and invade the subgingival area (gingivitis, gingival pocket formation). In the total absence of oral hygiene, plaque formation and an initial host defensive response within gingival tissue occur. With optimum—including interdental—oral hygiene, the formation of biofilm is repeatedly disrupted and gingival health is maintained.
The formation of a plaque biofilm can be enhanced by natural retention factors, which can also render biofilm removal by means of oral hygiene more difficult. These retention factors include:
• Supra- and subgingival calculus
• Cementoenamel junctions and enamel projections
• Furcation entrances and irregularities
• Tooth fissures and grooves
• Cervical and root surface caries
• Crowding of teeth in the arch.
By itself, calculus is not pathogenic. However, its rough surface presents a retention area for vital, pathogenic bacteria. At the microscopic level, the cementoenamel junction is very irregular, and offers retentive roughness. Enamel projections and “pearls” also inhibit soft tissue attachment. Furcation entrances, fissures, etc. are retentive niches for plaque. Carious lesions represent a huge bacterial reservoir. Crowding of teeth reduces self-cleansing and renders oral hygiene more difficult.
Restorative dentistry—from a simple restoration to a full-mouth reconstruction—can do more harm than good to the patient’s oral health if performed improperly! Placing only optimum restorations is synonymous with preventive periodontics (tertiary prevention, p. 198).
Fillings and crowns that appear to be perfect clinically and macroscopically almost always exhibit deficiencies at the margins when viewed microscopically. When margins are located subgingivally, they always present an irritation for the marginal periodontal tissues.
Overhanging margins of restorations and crowns accumulate additional plaque. Gingivitis ensues. The composition of the plaque changes. The number of gram-negative anaerobes (e. g., Porphyromonas gingivalis), the organisms responsible for initiation and progression of periodontitis, increases rapidly (Lang et al. 1983).
Gross iatrogenic irritants such as poorly designed clasps and prosthesis saddles may exert a direct traumatic influence upon periodontal tissues.
Extending apically from the supragingival region, a subgingival plaque biofilm will often form within the existing gingival sulcus/pocket; this was previously called the “adherent” plaque. In addition to gram-positive bacteria such as streptococci, actinomyces, etc., as the probing depth increases so does the number of anaerobic gram-negative bacteria (p. 36).
This subgingival biofilm can also calcify. A dark, hard and difficult to remove calculus (“serum calculus”) accumulates. In addition, the gingival pocket also contains loose agglomerates of non-adherent, often mobile bacteria (with a high concentration of gram-negative anaerobes and spirochetes). In acute phases, periodontopathic bacteria often increase dramatically. These include Actinobacillus actinomycetemcomitans, P. gingivalis, T. forsythensis, spirochetes etc. (pp. 30, 33, 38). Despite these alterations in the subgingival plaque, periodontitis, even in the acute stage, cannot be characterized as a “highly specific” infection because large differences have been reported in the bacterial composition between patients and even within different pocket locations in the same patient (Dzink et al. 1988, Slots & Taubmann 1992, Lindhe 1997).