Abstract: Periodontal disease affects the majority of the population and is the second most common dental disease worldwide. Infection arises from plaque that is formed when starches and sugars in food interact with the bacteria normally found in the mouth. Plaque can lead to tarter and eventually can result to severe irritation and inflammation of the gingivitis. Ongoing inflammation creates pockets that accumulate with bacteria, resulting in the recession of the periodontium and the progressive loss of alveolar bone. A potential target for inhibiting bone resorption is the protein Developmental Endothelial Locus-1 (Del-1). Del-1 is able to function as an anti-inflammatory by blocking excessive immune cell infiltration into the periodontium
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Periodontitis, meaning “inflammation around the tooth”, is a serious gum infection that damages the soft tissue and bone that supports the tooth. The infection arises from plaque, a sticky biofilm that is formed by bacteria on the teeth resulting from saliva and food scraps. Brushing and flossing the teeth can remove plaque but plaque re-forms quickly, usually within 24 hours. Plaque that stays on the teeth longer than two to three days can harden under the gumline into tartar. Tartar is difficult to remove and acts as a reservoir for bacteria. If plaque and tartar remain on the teeth for an extended period of time, irritation and inflammation of the gum surrounding the teeth occurs; this is called gingivitis. Ongoing inflammation eventually causes pockets to develop between the gums and teeth that will fill with plaque, tarter, and bacteria. This periodontal pocket is located in the area where the gum tissue is attached to the tooth structure. Over time, the pockets become deeper and more bacteria accumulates, resulting in loss of tissue surrounding and supporting the teeth, called the periodontium, and the progressive loss of alveolar bone …show more content…
Microbial pathogens elicit a host immune response and the reaction of the host’s immune-inflammatory system is responsible for most of the destruction found in alveolar bone. Inflammation from the gingiva spreads along the outer periosteal surface of the bone and penetrates into the marrow spaces, which is the spongy, red tissue that fills bone cavities and is the source of red and white blood cells. After inflammation reaches the bone, it spreads into the marrow spaces and multinuclear osteoclasts and mononuclear phagocytes increase in number. Resorption proceeds from within these marrow spaces, causing a thinning of the surrounding bony trabeculae and enlargement of the marrow spaces. This is followed by destruction of the bone and a reduction in bone height. Targeting bone resorption and controlling unwanted inflammatory responses would provide the initial approach for treatments to preserve alveolar bone
Periodontitis, meaning “inflammation around the tooth”, is a serious gum infection that damages the soft tissue and bone that supports the tooth. The infection arises from plaque, a sticky biofilm that is formed by bacteria on the teeth resulting from saliva and food scraps. Brushing and flossing the teeth can remove plaque but plaque re-forms quickly, usually within 24 hours. Plaque that stays on the teeth longer than two to three days can harden under the gumline into tartar. Tartar is difficult to remove and acts as a reservoir for bacteria. If plaque and tartar remain on the teeth for an extended period of time, irritation and inflammation of the gum surrounding the teeth occurs; this is called gingivitis. Ongoing inflammation eventually causes pockets to develop between the gums and teeth that will fill with plaque, tarter, and bacteria. This periodontal pocket is located in the area where the gum tissue is attached to the tooth structure. Over time, the pockets become deeper and more bacteria accumulates, resulting in loss of tissue surrounding and supporting the teeth, called the periodontium, and the progressive loss of alveolar bone …show more content…
Microbial pathogens elicit a host immune response and the reaction of the host’s immune-inflammatory system is responsible for most of the destruction found in alveolar bone. Inflammation from the gingiva spreads along the outer periosteal surface of the bone and penetrates into the marrow spaces, which is the spongy, red tissue that fills bone cavities and is the source of red and white blood cells. After inflammation reaches the bone, it spreads into the marrow spaces and multinuclear osteoclasts and mononuclear phagocytes increase in number. Resorption proceeds from within these marrow spaces, causing a thinning of the surrounding bony trabeculae and enlargement of the marrow spaces. This is followed by destruction of the bone and a reduction in bone height. Targeting bone resorption and controlling unwanted inflammatory responses would provide the initial approach for treatments to preserve alveolar bone