## 1 Introduction  
Chlorogenic acid (CGA) is a polyphenol that is present in plants, particularly vegetables, fruits, and some plant seeds [1; 2; 3], such as coffee (\(\sim\)42.4 mg/g dry weight) [4], lettuce (\(\sim\)1.04 mg/g fresh weight) [5], carrot (\(\sim\)0.15 mg/g fresh weight) [6], burdock (\(\sim\)0.48 mg/g dry weight) [7], apple (\(\sim\)2.10 mg/g dry weight) [8], and blueberries (\(\sim\)0.44 mg/g fresh weight) [9]. CGA has been reported to exhibit beneficial activities, including the inhibition of blood glucose elevation [10; 11], the reduction in blood pressure [12; 13], and improvements in cognition [14; 15], as well as anticancer [16] and antioxidant effects [17; 18]. Furthermore, CGA exerts anti-inflammatory [19] and antibacterial effects [20].  
Periodontitis, an inflammatory condition that affects the tissues surrounding teeth, is the main cause of tooth loss in adults and is highly prevalent worldwide [21; 22]. Periodontitis is caused by periodontal bacteria, such as _Porhyromonas gingivalis_ (_P. gingivalis_), _Teponema denticola_ (_T. denticola_), _Tannerella forsythia_ (_T. forythtia_), _Aggregatibacter actinomycetemontans_, and _Prevotella intermedia_[23; 24; 25; 26]. Among these bacteria, _P. gingivalis_, _T. denticola_, and _T. forythia_ are classified as red-complex bacteria because of their close involvement in the onset of periodontitis [27; 28]. Periodontopathic bacteria form biofilms and produce proteolytic enzymes and leukotoxins. Their products induce an inflammatory reaction in the local tissues surrounding teeth. Osteoclasts are then activated and resorb alveolar bone [29].  
A number of local approaches have been adopted against these biological events, such as the administration of antibiotics and surgery. However, each approach has some limitations, such as resistant bacteria and the invasiveness of surgery. Therefore, the use of natural products present in plants may exert beneficial effects against periodontal bacteria and the symptoms of periodontitis.  
CGA has been suggested to prevent bone resorption in periodontitis. [PERSON] et al. investigated the effects of CGA on the receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclast differentiation by inhibiting RANKL signaling in an _in vitro_ study and lipopolysaccharide-induced bone erosion at the femur in an _in vivo_ study [30]. The effects of CGA in an _in vivo_ experimental periodontitis model currently remain unclear, and only a few studies have investigated its pharmacological effects on periodontitis in a ligature-induced experimental periodontitis model [31]. Moreover, limited information is currently available on whether CGA has the ability to restore alveolar bone that had already decreased (or resorbed). Thus, there is no evidence to support the beneficial effects of CGA for patients with periodontitis [32].  
Therefore, the present study examined the inhibitory effects of CGA on the development of alveolar bone loss and its reparative effects on such bone loss. The aim of this study was to confirm the pharmacological effects of CGA on alveolar bone loss in a ligature-induced experimental periodontitis model. This model has a number of advantages over other models in studying periodontal tissue and alveolar bone regeneration, such as the rapid induction of the disease and predictable bone loss [33].