title: Periodontal disease: linking the primary inflammation to bone loss.
abstract: Periodontal disease (PD), or periodontitis, is defined as a bacterially induced disease of the tooth-supporting (periodontal) tissues. It is characterized by inflammation and bone loss; therefore understanding how they are linked would help to address the most efficacious therapeutic approach. Bacterial infection is the primary etiology but is not sufficient to induce the disease initiation or progression. Indeed, bacteria-derived factors stimulate a local inflammatory reaction and activation of the innate immune system. The innate response involves the recognition of microbial components by host cells, and this event is mediated by toll-like receptors (TLRs) expressed by resident cells and leukocytes. Activation of these cells leads to the release of proinflammatory cytokines and recruitment of phagocytes and lymphocytes. Activation of T and B cells initiates the adaptive immunity with Th1 Th2 Th17 Treg response and antibodies production respectively. In this inflammatory scenario, cytokines involved in bone regulation and maintenance have considerable relevance because tissue destruction is believed to be the consequence of host inflammatory response to the bacterial challenge. In the present review, we summarize host factors including cell populations, cytokines, and mechanisms involved in the destruction of the supporting tissues of the tooth and discuss treatment perspectives based on this knowledge.
authors.affiliation: Department of Basic Medical Sciences, Neurosciences and Sense Organs, Section of Human Anatomy and Histology "R. Amprino", University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy. adridibenedetto@libero.it
authors.forename: Adriana
authors.initials: A
authors.lastname: Di Benedetto
authors.forename: Isabella
authors.initials: I
authors.lastname: Gigante
authors.forename: Silvia
authors.initials: S
authors.lastname: Colucci
authors.forename: Maria
authors.initials: M
authors.lastname: Grano
mesh_terms: D056704:Adaptive Immunity; D016301:Alveolar Bone Loss / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D001424:Bacterial Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D015870:Gene Expression; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D010586:Phagocytes / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines; D051193:Toll-Like Receptors