## 2 The Influence of Different Factors on Oral Microbiome
### Diseases
#### 2.2.3 Periodontal and Peri-Implant Diseases  
Acute and chronic oral infections, including severe gingivitis and periodontitis, are closely linked to changes in the oral microbiome [81; 82]. These conditions can promote the growth of pathogenic bacteria and create a pro-inflammatory environment conducive to disease progression [83]. Gingivitis, an inflammation of the gingiva, is often the result of the accumulation of dental plaque, which harbors pathogenic microorganisms. The shift from a balanced microbial community to one dominated by pathogenic bacteria such as _Porphyomonas gingivis_, _Tannerella forsythia_, and _Troponema denticola_ is a hallmark of gingivitis [84]. This dysbiotic state can trigger an inflammatory response, leading to the clinical signs of gingivitis, including redness, swelling, and bleeding of the gums [85]. Periodontitis, a more severe form of gum disease, extends beyond gingivitis, affecting the supporting structures of the teeth. The progression from gingivitis to periodontitis involves deeper microbial invasion and a more pronounced inflammatory response. Periodontitis is characterized by the destruction of the periodontal ligament and alveolar bone, which can ultimately lead to tooth loss if untreated. The oral microbiome in periodontitis patients shows a significant increase in pathogenic bacteria such as _Aggregatibacter actinomycetemcomitants_ and _Fusobacterium nucleatum_, which contribute to the disease's pathogenicity [83; 86; 87]. The inflammatory environment created by these infections not only exacerbates the local destruction of periodontal tissues but can also have systemic implications. Chronic periodontitis has been linked to numerous systemic conditions such as cardiovascular and neurodegenerative diseases, diabetes, inflammatory bowel disease, autoimmune diseases (e.g., rheumatoid arthritis), chronic renal insufficiency, neoplasms, as well as to fertility and adverse pregnancy outcomes, highlighting the importance of maintaining oral health for overall well-being [88]. The pro-inflammatory cytokines and mediators released during periodontitis can enter the systemic circulation, influencing distant organs and contributing to systemic inflammation [89]. Research indicates a significant association between periodontal disease and an increased risk of developing OPMD and OSCC. A case-control study found that individuals with periodontitis were more likely to have poorly differentiated OSCC compared to those without periodontitis, suggesting a potential link between periodontal disease and OSCC progression [90]. Additionally, a retrospective cohort study by [PERSON] et al. [91] demonstrated that periodontitis and tooth loss are significantly associated with increased OSCC mortality in individuals aged \(\geq\)75 years. Treatment of periodontal diseases involves mechanical removal of dental plaque and tartar, alongside antimicrobial therapies to reduce the bacterial load. Recent advancements in microbiome research suggest that probiotic and prebiotic treatments may also help restore a healthy microbial balance in the oral cavity, providing a novel approach to managing these conditions [92]. Similarly, peri-implant diseases--conditions affecting the tissues surrounding dental implants--are influenced by dysbiosis in the microbiome. Peri-implant health is associated with a balanced microbial community dominated by commensal species, whereas peri-implant mucositis, an early inflammatory condition, shows increased levels of pathogenic bacteria. Key pathogens such as _Fusobacterium nucleatum_, _Prerotella intermedia_, and _Porphyromonas gingivalis_ have been implicated in mucositis, which, if left untreated, may progress to peri-implantitis [93; 94; 95]. Peri-implantitis involves extensive tissue destruction, including alveolar bone loss, and exhibits a microbial profile more dominated by anaerobic Gram-negative bacteria, such as _Troponema denticola_ and _Aggregatibacter actinomycetemcomitants_, akin to periodontitis [96].