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The periodontium is a connective tissue consisting of four components: cementum, the periodontal ligament (PDL), alveolar bone, and gingival tissue (see Image. Periodontium Anatomy).[1] This topic details the histological and embryological structure and origin of this tissue, as well as the function, clinical significance, and pathophysiology of some of the periodontal diseases.

Understanding the structure and histology of the periodontium is clinically significant to the discussion of wound healing, drugs and environmental factors affecting it, periodontal diseases, and overall health risk factors. Lamina propria of gingiva regenerates more readily due to fiber differentiation after wounding, compared to the alveolar bone, which relies on osteocyte, bone marrow cells, endosteum cells, and osteogenic cells of periosteum, which occupy different compartments.[1] Histopathology of periodontal diseases is described in 4 stages: Initially, the gingival crevicular fluid amount is increased due to vascular changes in response to the initial insult. At this benign stage, polymorphonuclear neutrophils are attracted to the lesion site, and T lymphocytes are responsible for fibroblasts. The early lesion is characterized by redness. At this stage, PMNs clear and breakdown the collagen fibers, which increases the previously made space for infiltrates. At this stage, the established lesion is dominated by B cells and leukocyte aggregation. This initiates the lesion side transformation by changing the junctional and sulcular epithelium into an extremely vulnerable epithelium called the pocket epithelium. This is apparent as bleeding upon gentle gingival manipulation. An advanced lesion characterized as loss of gingival fibers and alveolar bone is caused by the migration of biofilm into the pocket and creating an environment for anaerobic bacterias' proliferation.[9] Gingivitis is an initial response to combat the first insult to the periodontium. As the name suggests, it is an inflammation of the gingiva, a component of the periodontium resulting from the accumulation of microbial plaque near the gingival sulcus. Gingivitis has a delayed appearance in children with a predominance of T lymphocyte infiltrates.[10] Most cases are transient, non-progressive, and reversible. However, it can progress to Periodontitis.

Gingivitis is an initial response to combat the first insult to the periodontium. As the name suggests, it is an inflammation of the gingiva, a component of the periodontium resulting from the accumulation of microbial plaque near the gingival sulcus. Gingivitis has a delayed appearance in children with a predominance of T lymphocyte infiltrates.[10] Most cases are transient, non-progressive, and reversible. However, it can progress to Periodontitis. Periodontitis is the inflammation of the periodontium, which extends to the jawbone and is irreversible (see Image. Periodontitis). The pathophysiology of periodontitis is explained by the replacement and remodeling of previously normal alveolar bone, especially the spongy bone, which can happen in healthy individuals due to chronic inflammation. White blood cells are active during inflammation, and osteoclast lineage is related to WBC. As a result, osteoblast is inhibited without reducing the rate of osteoclasts. It is observed on a radiograph as a reduced opacity of the alveolar crest.[11] Hyper-cementosis is thought to be due to growth factor disturbances in conditions such as acromegaly, gigantism, or Paget’s disease. Cementoblasts are located within the PDL and can undergo remodeling and repair. Excessive cementoblast deposition can cause hyper-cementosis. This can cause concrescence, which is the adherence of two teeth together by the roots (hence, a radiograph is needed before tooth extraction). This rare finding has been seen in patients with systemic lupus erythematosus.[12] Cementicle is a condition in which masses of acellular cementum appear in abnormal locations due to the disruption of the oppositional growth of cementum. This condition happens mostly in the elderly and appears as psammoma body-like calcifications. The process is thought to develop due to the encounter of cementoblasts with thrombus lodged in a nearby capillary.[13][14] Mesial drift: Also known as physiological drift, this refers to the migration of teeth in a mesial direction caused by the asymmetrical remodeling of alveolar bone tissue. Two major concepts are believed to cause this drift: First, unbalanced bone remodeling of 2 adjacent teeth. Second, remodeling due to occlusal forces leads to an imbalance of acellular cementum. This asymmetrical remodeling causes tooth movement.[15]

Mesial drift: Also known as physiological drift, this refers to the migration of teeth in a mesial direction caused by the asymmetrical remodeling of alveolar bone tissue. Two major concepts are believed to cause this drift: First, unbalanced bone remodeling of 2 adjacent teeth. Second, remodeling due to occlusal forces leads to an imbalance of acellular cementum. This asymmetrical remodeling causes tooth movement.[15] Peri-implantitis is due to the failure to create the junction between the implant and the oral mucosa, leaving the underlying connective tissue exposed to the permanent oral microbiome and creating chronic inflammation of gingival and bone tissue.[11] Knowledge of histology helped to demonstrate that coating the peri-implant pocket with hyaluronic acid gel reduces inflammation in peri-implantitis by improving the connection between the core and recipients’ connective tissue through reducing inflammation.[16] Widening of PDL space: with occlusal/orthodontic trauma, the fibroblast in PDL responds by increasing its activity and leads to the widening of PDL, as the neighboring tissue is lost. This can be seen on a radiograph and can be accompanied by bone loss or hyper-cementosis. Certain medications, such as bisphosphonate, are used to manage rheumatoid arthritis, osteoporosis, osteogenesis imperfecta, and multiple myeloma.[4] can cause PDL widening. In contrast, conditions that affect bone health, such as radiation-induced bone defects, reduce the force and also cause a widening of the PDL space. Infection, inflammation, and malignancy can also cause PDL widening.