Table 2.
Sl No | Author and Year Country | Study Subjects | Parameters Studies | Major Observations |
---|---|---|---|---|
1 | Amar et al. 2007 [50] USA | DIO mice and lean control C57BL/6 mice were infected orally | Oral microbial sampling, inflammatory response, (TNF-alpha, IL-6, and serum amyloid A (SAA). |
Obesity causes immune dysregulation. It also interferes with the ability of the immune system to respond to P. gingivalis infection. Increased alveolar bone loss after bacterial infection was observed in mice with DIO. |
2 | Simch et al. 2008 [57] Brazil |
30 female Wistar rat. Test group (n = 14 rats on cafeteria diet) control group (n = 16 on regular). |
Morphometric analysis of alveolar bone loss by standardized digital photographs (software Image Tool 3.0). | No statistically significant differences between alveolar bone loss of test animals and controls. Progression of alveolar bone loss in rats not influenced by obesity. |
3 | Tomofuji et al. 2009 [59] Japan |
28 rats. The obese Zucker rats (n = 14) lean littermates (n = 14) | 8-hydroxydeoxyguanosine, ratio of reduced/oxidized glutathione, serum level of reactive oxygen metabolites, gingival gene-expression pattern. |
Obese rats had higher levels of gingival 8-hydroxydeoxyguanosine. There was also a decreased ratio of reduced/oxidized glutathione with increasing serum reactive oxygen metabolites. No significant differences in the degree of alveolar bone loss between lean and obese rats Gene expressions related to a capacity for xenobiotic detoxification were downregulated in obese rats. |
4 | Verzeletti et al. 2012 [58] Brazil | 24 female Wistar rats cafeteria diet (n = 13) regular diet (n = 11) |
Body weight, Morphometric registration of alveolar bone loss. |
Alveolar bone loss was not statistically different between obese and non-obese group |
5 | Brandelero et al. 2012 [61] Brazil |
20 newborn male Wistar rats MSG group (n = 10) Control group (n-10) |
Radiographic analyses of alveolar bone resorption, Tumor Necrosis Factor α (TNFα), Gene expression in gingival tissue. | The alveolar bone resorption was 44% lower in MSG-obese rats compared with control rats. Hypothalamic obesity may produce a protective effect against periodontal disease |
6 | Cavagni et al. 2013 [52] Brazil | 28 Wistar rats. Control group (n = 10) Test group (cafeteria diet: n = 10) | Morphometric analysis of standard digital photographs, Mean alveolar bone loss. | Animals in the test group showed 20 sites with spontaneous periodontal disease, whereas in control animals, only 8 sites exhibited periodontal breakdown. Obesity increases the occurrence of spontaneous periodontal disease in Wistar rats. |
7 | Cavagni et al. 2016 [51] Brazil |
60 male Wistar rats. Control group (n = 15) periodontitis (n = 15) obesity/hyperlipidemia (n = 15) obesity/hyperlipidemia plus periodontitis (n = 15). |
Body weight and Lee index, Serum glucose and cholesterol/ triglycerides, alveolar bone loss (micro CT), Serum tumor necrosis factor (TNF)-α, Interleukin (IL)-1β. |
Groups exposed to CAF exhibited higher ABL in the sides without ligature. No differences were observed among groups for IL-1β and TNF-α. Obesity and hyperlipidemia modulate the host response to challenges in the periodontium, increasing the expression of periodontal breakdown. |
8 | Muluke et al. 2016 [53] USA |
Four-week-old male C57BL/6 mice (n = 10 per group) high-fat diet (HFD) normal caloric diet |
percentage fat, serum inflammation (TNF-α, OC, CTX, P1NP markers | Alveolar bone loss was significantly greater in obese animals. Osteoclasts also showed an augmented inflammatory response to P. gingivalis in obese animals. High-fat diet was more important than obesity in affecting alveolar bone loss. |
9 | Zuza et al. 2018 [54] Brazil |
48 adult Wistar rats High fat diet group (n = 24) Normal diet group (n = 24) |
Histopathological, histometric, and immunohistochemical analyses. TRAP, RANKL, OPG via immunolabeling. | Histology shows that inflammation lasted longer in obese rats. Obesity induced by a high-fat diet caused more severe local inflammatory response and alveolar bone loss. |
10 | Damanaki et al. 2018 [55] Germany | 12 C57BL/6 mice Younger lean mice (n = 4) Older lean mice (n = 4) Younger obese mice (n = 4) |
IL-6, COX-2, visfatin and adiponectin in gingival samples (real-time PCR) | Alveolar bone loss was significantly lower in the older mice as compared to the younger animals. Gingival COX-2 and visfatin expressions were higher in the obese versus lean mice and in the older versus younger mice |
11 | Damanaki et al. 2021 [56] Germany |
15 Wistar rats High-fat diet (n = 15) Normal diet (n = 15) |
Histomorphometry to assess healing, TRAP staining and immuno-histochemistry for RUNX2 and osteopontin. | Spontaneous bone healing in periodontal defects is affected by obesity even in the presence of regeneration-promoting molecules like EMD. |
12 | Lopes et al. 2022 [60] Brazil |
16 Holtzman rats were ligature-induced periodontitis (n = 8). Obesity plus ligature-induced periodontitis (O.P.) (n = 8) |
Body weight, adipose tissue weight, and blood test, Bone loss (micro-CT and histologic analyses), Proteome analysis from the periodontal ligament tissues (PDL), Immunohistochemistry for spondin1, vinculin, and TRAP. | Histologically, it was found that obesity did not significantly affect bone loss resulting from periodontitis. Obesity affects the proteome of PDL submitted to experimental periodontitis. |