Ultrastructural studies of infalmmation induced in rats by injection of antigen‐antibody precipitates

Abstract

Single intramucosal injectins of ferritin‐antiferritin into the palate adjacent to the 1st molar produced a dense neutrophil infiltration within perivscular tissue adjacent to the palatal bone. Neutrophil degranulatin related to the phagocytosisi of antigen‐antibody (Ag‐Ab) precipitates occurred during the 1st 24 hours post injection. Rapidly developing bone damage was characterized by periosteal disruption, osteoblast and osteocyte necrosis and occasional swquestration of necrotic bone. Cytoplasmic changes such as dilated endowere observed inosteoblasts within 2 hrs of Ag‐Ab injection. Wound healing with regeneraionof periosteal tissue at the margins of the lesion was observed to begin at 4 days post injection. New bone was formed directly over the older necrotic bone without any intervening bone resorption. Extracellular matrix vesicles were observed adjacent ot newly differentiated bone cells.

Peri-implant Inflammation Defined by the Implant-Abutment Interface

“…Such detrimental tissue destruction as a consequence of inflammation is known to develop in diverse pathophysiological settings. Around teeth with periodontal disease, this has been described as an "extended arm" of gingival inflammation (Waerhaug, 1979), an "effective radius of action" (Garant, 1979), and an "inflammatory front" (Graves and Cochran, 2003). If the host inflammatory response is minimized, bone loss is greatly reduced, e.g., as demonstrated with inhibitors of the pro-inflammatory molecules IL1 and TNF␣ (Assuma et al, 1998).…”

Bone Response to Loaded Implants With Non‐Matching Implant‐Abutment Diameters in the Canine Mandible

“…This spatial location of the inflammation, and its association with bone loss, has been shown to be critical for the bone loss observed in periodontitis. Such a relationship between bone loss and inflammation has been recognized since the 1970s, with concepts such as Waerhaug's 29 “extended arm” of gingival inflammation that could result in osteoclastic bone resorption and Garant's 30 “effective radius of action of locally produced bone resorption stimulators.” These studies and others 31–33 reinforce the importance of the spatial relationship between inflamed connective tissue and the loss of alveolar bone 34 . Thus, these studies suggest that the butt‐joint connection, which places the inflammation directly adjacent to the bone, promotes the osteoclastic resorption of 1.5 to 2.0 mm of bone.…”

A Prospective Multicenter 5‐Year Radiographic Evaluation of Crestal Bone Levels Over Time in 596 Dental Implants Placed in 192 Patients

“…Bacterial products stimulate inflammatory cells to enter the surrounding tissues, and these cells release proinflammatory molecules that recruit more inflammatory cells; osteoclastogenesis and, eventually, bone loss result 29 . Data indicate that the closer this inflammation is located to the alveolar crest, the more bone loss is observed 30–33 …”