Which supporting structure is not part of the periodontium

Alveolar mucosa — The area of tissue beyond the mucogingival junction. It seems less firmly attached and redder than the attached gingiva. It is non-keratinized and provides a softer and more flexible area for the movement of the cheeks and lips. Attached gingiva — This tissue is adjacent to the free gingiva and is keratinized and firmly attached to the bone structure. It can range from mm in height. Free gingiva — This tissue is not attached and forms a collar around the tooth.

The trough around the tooth is called the sulcus and its depth is normally mm. It is lined with sulcular epithelium and attached to the tooth at its base by the epithelial attachment. Gingival margin — The border region of the gingiva that touches the tooth. Interdental papillae — The region of gingival tissue that fills the space between adjacent teeth.

In a healthy mouth this is usually knife-edged and fills the interdental space. Muco-gingival junction — The scalloped line that divides the attached gingiva from the alveolar mucosa. Figure Healthy Gingiva. Recent evidence indicates the role of Th17 cells as one main regulator of T cell response and bone resorption in the periodontium [ 70 ]. In addition, Treg cells can limit the progression of periodontal disease without suppressing the immune response.

When chronic gingivitis progresses to periodontitis, there is a shift from T cell dominance to B and plasma cells. Different types of B cells include naive B cells, memory B cells, and antibody-secreting B cells.

Antibodies produced against periodontitis-associated pathogens can be found in saliva and in serum as well [ 32 ]. Finally, periodontitis is a complex disease with a nonlinear character, and its effects on immune response are rather disproportional [ 71 ]. Although knowledge about immune cell functions has considerably increased, it is still difficult to fully understand cellular interactions in periodontal disease pathogenesis due to its multicausal etiology.

The junctional epithelium forms a unique seal between the root surface and gingiva, and its main function is to provide protection to the underlying tissues against the constant exposure of oral microbes and their by-products [ 72 ]. Various molecular factors involved in adhesion, cell—cell interactions, chemotaxis, proinflammatory cytokines, epithelial growth, MMP activation, and antimicrobial peptide production contribute to the function of the junctional epithelium.

If this elegant and well-adapted defense system is overwhelmed by bacterial virulence factors e. It is noteworthy that although gingival inflammation is the precursor of periodontitis and a clinically relevant risk factor for disease progression, not all gingivitis lesions lead to periodontitis [ 73 ].

During periodontal pocket formation, new tissue formation by resident cells keratinocytes, fibroblasts, osteoblasts is suppressed, whereas tissue degradation by neutrophils, macrophages, and osteoclasts is stimulated; thus, the balance between tissue removal and regeneration is disrupted [ 74 ].

Phagocytic cells mainly aim to eliminate invading pathogens by producing and secreting antimicrobial agents, reactive oxygen species, and enzymes. However, abundant tissue concentrations of collagenolytic MMPs and elastase activate the degradation of type I collagen in the connective tissue and periodontal ligament [ 75 ].

During disease, MMP-8 is the major collagenase in periodontal tissues. Irreversible periodontal destruction occurs when the inflammatory cell infiltrate, predominantly containing plasma cells, extends deeper into the connective tissue, leading to tissue damage in periodontal ligament and alveolar bone [ 76 ].

Alveolar bone resorption is the principal pathological characteristic of periodontitis. The activation of osteoclasts, multi-nucleated bone-resorbing cells, is regulated by a cascade of inflammatory proteins cytokines and enzymes MMPs. MMP-1, -8, and are especially involved in alveolar bone destruction by degrading type I collagen the main type of collagen in the periodontium , while two gelatinases MMP-2 and -9 accomplish the degradation of denatured collagen [ 78 ].

Furthermore, MMP-9 assists in osteoclast migration and MMP triggers osteoclast activation, which all facilitate type I collagen degradation. The disease development with fast or slow progress and with stable periods varies among periodontal sites and among individuals. Diagnosis of periodontitis is based on clinical and radiographic information on periodontal attachment and alveolar bone loss. In the current classification system, staging estimates the severity of the disease, while grading aims to estimate the rate of its progression, taking the known risk factors into account [ 10 ].

At the early phase of periodontal disease, the clinical signs and symptoms can be lacking or very mild. When periodontal tissue destruction proceeds, deepened pocket depths with alveolar bone loss result in tooth mobility, drifting, flaring, and finally loss of the affected tooth. In advanced cases, where several teeth are affected, these abnormalities lead to the collapse of the bite function.

The primary goal of periodontal therapy is to reduce the infectious and inflammatory challenge and to halt the progressing tissue destruction. Removal of pathogenic biofilms and suppression of inflammation can discontinue the periodontal tissue degradation; however, only limited regain of lost tissues occurs, depending on the form of tissue defects, systemic health status, and age [ 79 ].

In advanced cases, the active anti-infective treatment phase is often combined with surgery to eliminate residual pockets—with the aim of improving the ecology at periodontal sites—or sometimes with adjunctive systemic antimicrobials to reduce pathogen burden. In smokers, however, the treatment outcome is compromised, which makes smoking cessation an essential part of their periodontal therapy [ 80 , 81 ]. The beneficial influence of quitting may partly be due to decreased pathogen numbers and increased abundance of health-associated commensals in subgingival biofilms [ 82 ].

Although anti-infective treatment reduces total bacterial counts, proportions of periodontal pathogens, as well as the number of sites colonized with pathogens, many of the species return with time [ 83 ]. Therefore, daily oral hygiene of the patient and continuing professional supportive periodontal therapy are necessary to maintain the outcome and strengthen the long-term success of the treatment [ 84 , 85 ]. Moreover, patients with advanced disease and masticatory dysfunction and bite collapse due to severe tooth loss have an obvious need for complex rehabilitation of the bite function as well as esthetic treatment.

After treatment, however, periodontitis patients with prosthodontic reconstructions have still an increased risk for tooth loss, and many patient-related factors such as age, socioeconomic status, non-compliance, and diabetes are associated with abutment tooth loss [ 86 ].

Since untreated periodontitis increases systemic low-grade inflammation, another treatment goal is to improve this condition [ 87 ]. Although intensive mechanical periodontal treatment of patients with severely damaged periodontal tissues can cause an acute systemic inflammatory response and impair endothelial function, this occurs only transiently and, after six months, a significantly improved endothelial function is reached [ 88 ].

Furthermore, periodontal treatment has been shown to reduce atherosclerotic biomarkers e. Periodontal disease is multifactorial and the imbalance between tissue loss and gain can occur due to various reasons, including aggressive infection, uncontrolled chronic inflammation, weakened healing, or all of the above simultaneously. Thus, successful disease management requires an understanding of different elements of the disease at the individual level and the design of personalized treatment modalities, including immunotherapies and modulators of inflammation [ 92 , 93 ].

With the aid of newly developed omics technologies, these novel strategies may become available for clinicians. Conceptualization: E. National Center for Biotechnology Information , U. Journal List J Clin Med v.

J Clin Med. Published online Jul Author information Article notes Copyright and License information Disclaimer. Received Jun 28; Accepted Jul This article has been cited by other articles in PMC. Abstract Periodontitis is an infection-driven inflammatory disease in which the composition of biofilms plays a significant role. Keywords: periodontal disease, alveolar bone loss, gingiva, bacteria, biofilm, immunity, inflammation, smoking.

Introduction Periodontitis is an infection-driven inflammatory disease in tooth-supporting tissues i. Open in a separate window. Figure 1. Pathogenic Biofilms Multispecies biofilm formation and maturation occur on tooth surfaces via intergeneric interactions, where coaggregations occur between different bacterial taxa, and highly diverse bacterial communities are formed at supragingival above the gumline and subgingival below the gumline sites [ 13 , 14 ].

Immunologic Players of the Periodontium Due to the constant interaction with bacteria, immune cells neutrophils, macrophages, and lymphocytes are present in the periodontium to take part in maintaining a healthy equilibrium. Figure 2. Inflammatory Process and Periodontal Tissue Destruction The junctional epithelium forms a unique seal between the root surface and gingiva, and its main function is to provide protection to the underlying tissues against the constant exposure of oral microbes and their by-products [ 72 ].

Periodontal Therapy—Impact on Oral and General Health The primary goal of periodontal therapy is to reduce the infectious and inflammatory challenge and to halt the progressing tissue destruction. Future Considerations Periodontal disease is multifactorial and the imbalance between tissue loss and gain can occur due to various reasons, including aggressive infection, uncontrolled chronic inflammation, weakened healing, or all of the above simultaneously.

Author Contributions Conceptualization: E. Conflicts of Interest The authors declare no conflict of interest. References 1. Eke P. Prevalence of periodontitis in adults in the United States: and Kassebaum N. Global burden of severe periodontitis in — A systematic review and meta-regression. Genco R. Risk factors for periodontal disease.

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Kolenbrander P. Oral multispecies biofilm development and the key role of cell-cell distance. Paster B. Bacterial diversity in human subgingival plaque. Development of oral bacterial flora in young children. Haraldsson G. Clonal persistence of oral Fusobacterium nucleatum in infancy. Gursoy U. Biofilm formation enhances the oxygen tolerance and invasiveness of Fusobacterium nucleatum in an oral mucosa culture model. Mendes R. Hypoxia-induced endothelial cell responses - possible roles during periodontal disease.

Socransky S. Microbial complexes in subgingival plaque. Griffen A. Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing. ISME J. Hajishengallis G. The inflammophilic character of the periodontitis-associated microbiota. Oral Microbiol. Population-based study of salivary carriage of periodontal pathogens in adults. Microbiology of aggressive periodontitis.

Curtis M. Saglie F. Intragingival occurrence of Actinobacillus actinomycetemcomitans and Bacteroides gingivalis in active destructive periodontal lesions. Intracellular replication of fusobacteria requires new actin filament formation of epithelial cells.

Baek K. Complex intratissue microbiota forms biofilms in periodontal lesions. The periodontium consists of those tissues that support the teeth and is divided into a gingival unit and an attachment unit or attachment apparatus. The following is a list of the various parts of the gingival unit:. The gingiva is made up of free and attached gingiva Fig. Composed of very dense mucosa called masticatory mucosa, it has a thick epithelial covering and keratinized cells.

The underlying mucosa is composed of dense collagen fibers Table This type of masticatory mucosa is also found on the hard palate. Masticatory mucosa is well designed to withstand the trauma to which it is subjected in grinding food. The rest of the mouth is lined with a different type of mucosa called lining mucosa. This type makes up the alveolar mucosa. It is thin and freely movable and tears or injures easily. The epithelium covering this lining mucosa is thin and nonkeratinized.

Its mucosa is composed of loose connective tissue and muscle fibers. Free gingiva is the gum tissue that extends from the gingival margin to the base of the gingival sulcus. The attached gingiva extends from the base of this sulcus to the mucogingival junction. Alveolar mucosa is found apical to the mucogingival junction and is contiguous with the rest of the mucous membrane of the cheeks and lips and the floor of the mouth. Free gingiva is usually light pink in color and averages between 0.

The free gingival margin around a fully erupted tooth is located next to the enamel about 0.