Composition for improving periodontal tissue inflammation

Abstract

The purpose of the present invention is to improve periodontal inflammation. It is possible to improve periodontal inflammation by using a periodontal inflammation improving composition that contains plasmalogen extracted from a tissue of an animal such as shellfish, ascidians, and aves.

Description

Technical Field

[0001] The present invention relates to a composition for improving inflammation of periodontal tissues.

Background Art

[0002] Plasmalogen is a kind of phospholipid having an antioxidant action and is one of glycerophospholipids. Plasmalogen is present in all tissues of mammals and accounts for about 18% of the phospholipids in the human body, and is known to be abundant particularly in brain nerves, myocardium, skeletal muscle, leukocytes, and sperm.

[0003] Plasmalogen is known to have an action of promoting neurogenesis, an action of suppressing neuroinflammation, an action of suppressing the accumulation of amyloid-β (Aβ) protein in the brain, etc., and is said to be effective in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, depression, and schizophrenia. For example, it has been reported that the memory function of mild Alzheimer's disease is improved in patients orally administered with scallop-derived purified plasmalogen (see, for example, Non-Patent Document 1).

[0004] On the other hand, periodontal disease is a disease in which chronic inflammation occurs in the periodontal tissues (gums, jawbones, etc.) that support teeth due to periodontal pathogenic bacteria that inhabit dental plaque and tartar, and when the symptoms of this periodontal disease progress, the teeth may even lead to tooth extraction. Many modern Japanese adults suffer from periodontal disease, which is currently the largest cause of tooth extraction in adults. In addition, it has also become known that periodontal disease is associated with systemic diseases such as diabetes, cardiovascular disease, osteoporosis, and low-birth-weight infant birth, and it has been clarified that the treatment and prevention of periodontal disease contribute to the improvement of systemic diseases.

[0005] Periodontal bacteria release various virulence factors, but among them, endotoxins (lipopolysaccharides (LPS)) have a strong inflammatory effect and are one of the major causes of the inflammatory response in periodontal disease. Intercellular adhesion molecule-1 (ICAM-1 / CD54) is a glycoprotein belonging to the immunoglobulin superfamily expressed on the cell surface, and controls the migration and infiltration of leukocytes through adhesion with its ligands, Lymphocyte Function-associated Antigen-1 (LFA-1) and Macrophage-1 antigen (Mac-1). In gums where periodontal disease has progressed, ICAM-1 expression is elevated, and it is thought that ICAM-1 plays an important role in the pathogenesis of periodontitis in the chronic inflammation of periodontitis (see, for example, Non-Patent Document 2). [Prior art documents] [Non-patent literature]

[0006] [Non-Patent Document 1] Fujino T. et al, “Efficacy and Blood Plasmalogen Changes by Oral Administration of Plasmalogen in Patients with Mild Alzheimer's Disease and Mild Cognitive Impairment:A Multicenter,Randomized,Double-blind,Placebo-controlled Trial”EBioMedicine,

[17] (2017)199-205 [Non-Patent Document 2] Kasprzak, A., Surdacka, A., Tomczak, M. & Konkol, M. Role of high endothelial postcapillary venules and selected adhesion molecules in periodontal diseases: A review. J. Periodontal Res. 48, 1-21 (2013). [Disclosure of the Invention] [Problems that the invention aims to solve]

[0007] As mentioned above, various reports have been made regarding plasmalogens, but the effects of plasmalogens on inflammation of periodontal tissue have not been investigated.

[0008] The object of the present invention is to provide a composition that has an excellent effect in improving periodontal tissue inflammation. [Means for solving the problem]

[0009] As a result of diligent research to solve the above problems, the inventors of the present invention have discovered that plasmalogens suppress the expression of ICAM-1, which plays an important role in the pathogenesis of periodontal tissue inflammation (periodontitis), and thereby can improve periodontal tissue inflammation, thus completing the present invention.

[0010] In other words, the present invention is as follows: [1] A composition for improving periodontal tissue inflammation, characterized by containing plasmalogen. [2] The periodontal tissue inflammation improving composition according to [1] above, characterized in that the plasmalogen is a plasmalogen extracted from animal tissue. [3] The periodontal tissue inflammation improving composition according to [1] or [2] above, characterized in that the plasmalogen is an ethanolamine type plasmalogen. [Effects of the Invention]

[0011] The composition of the present invention has an excellent effect in improving periodontal tissue inflammation. [Brief explanation of the drawing]

[0012] [Figure 1] This figure shows the time course of ICAM-1 expression in mouse pancreatic islet microvessel endothelial cells (MS-1) stimulated with liposuction of Porphyromonas gingivalis (Pg) (Pg-LPS). [Figure 2] This figure shows the ICAM-1 expression levels in MS-1 cells stimulated with varying doses of Pg-LPS. [Figure 3] This figure shows the effect of varying concentrations of plasmalogen (Pls) on ICAM-1 expression in MS-1. [Figure 4] This figure shows the effect of varying concentrations of plasmalogen (Pls) on Pg-LPS-induced ICAM-1 expression in MS-1. [Figure 5] This figure shows the flow cytometry results of ICAM-1 expression in MS-1. [Figure 6] This figure shows the time course of TNF-α expression in human monocyte / macrophage cell lines (THP-1 cells) stimulated with Pg-LPS. [Figure 7] This figure shows the TNF-α expression levels in THP-1 cells stimulated with varying doses of Pg-LPS. [Figure 8] This figure shows the effect of varying concentrations of plasmalogen (Pls) on Pg-LPS-induced TNF-α expression in THP-1 cells. [Figure 9] This diagram shows the procedure for ligature ligation on a model mouse. [Figure 10] This is a photograph showing a model mouse after ligature ligation. [Figure 11] This figure shows pre- and post-operative computed tomography (μCT) images of maxillary samples from periodontitis model mice, with and without plasmalogen (Pls) intake.

Mode for Carrying Out the Invention

[0013] The composition for improving periodontal tissue inflammation of the present invention is characterized by containing plasmalogen.

[0014] The composition of the present invention can suppress the expression of ICAM-1, which plays an important role in the pathogenesis of periodontitis, and improve the inflammation (chronic inflammation) of periodontal tissues. Specifically, the inflammatory symptoms are improved by suppressing the expression of ICAM-1 induced by LPS of Porphyromonas gingivalis (P.g.), which is the most important periodontal pathogenic bacterium.

[0015] In addition, the composition of the present invention can suppress the expression of TNF-α, which is a kind of inflammatory cytokine that activates osteoclasts in periodontal tissues, and suppress the bone destruction of periodontal tissues. Specifically, the bone destruction of periodontal tissues is suppressed by suppressing the expression of TNF-α induced by LPS of P.g.

[0016] The improvement of periodontal tissue inflammation in the present invention is a concept including the suppression of the occurrence of inflammation in periodontal tissues such as gingiva (gum), periodontal ligament, etc., and the reduction of the generated inflammatory symptoms. Specifically, for example, the occurrence of swelling, redness, pain, etc. of the gingiva can be prevented, and the generated symptoms can be alleviated and treated.

[0017] That is, the composition of the present invention can also be used as a composition for suppressing ICAM-1 expression, a composition for suppressing TNF-α expression, a composition for anti-inflammation in the oral cavity, a composition for improving alveolar abscess, a composition for improving periodontal disease, a composition for improving gingival swelling, a composition for improving gingival redness, a composition for analgesia of the gingiva, etc.

[0018] The plasmalogen used in this invention is a type of phospholipid with antioxidant properties, and is a type of glycerophospholipid. It is a subclass of glycerophospholipids characterized by having a vinyl ether bond at the sn-1 position of the glycerol backbone, and has been found in high concentrations in the cell membranes of many mammalian tissues. A plasmalogen with a fatty acid ester bond at the sn-2 position is preferred.

[0019] The plasmalogen used in the present invention is not particularly limited as long as it is generally classified as a plasmalogen, but examples include choline-type plasmalogen, ethanolamine-type plasmalogen, inositol-type plasmalogen, and serine-type plasmalogen. Among these, choline-type plasmalogen and ethanolamine-type plasmalogen are preferred, and ethanolamine-type plasmalogen is particularly preferred.

[0020] The plasmalogen of the present invention can be extracted from animal tissue. The animal tissue is not particularly limited as long as it contains plasmalogen, and examples include aquatic animals such as shellfish, sea squirts, sea cucumbers, salmon, saury, and bonito, as well as birds. Among these, shellfish, sea squirts, and birds are preferred, with shellfish being particularly preferred. The part to be used is preferably the edible part. These animal tissues may be cut pieces, but it is preferable to use pulverized material as it allows for more efficient extraction of plasmalogen.

[0021] Examples of shellfish include edible bivalves and gastropods such as scallops, mussels, and abalone, with scallops being particularly preferred. Scallops are edible bivalves belonging to the family Pectinidae, and examples include those belonging to the genera Mizuhopecten and Pecten. Specifically, examples include the Japanese scallop (scientific name: Mizuhopectenyessoensis) and the European scallop (scientific name: Pectenmaximus (Linnaeus)) collected in Europe. Edible parts include the adductor muscle and mantle.

[0022] Sea squirts are edible chordates belonging to the family Halocynthidae, and include species belonging to the genera Halocynthia and Halocynthia. Specifically, these include Halocynthia roretzi and Halocynthia aurantium. The edible part is the flesh (fascia).

[0023] The type of bird used is not particularly limited as long as it is a bird intended for consumption; for example, chickens, silkie chickens, and ducks can be used. The breast meat, which is rich in plasmalogens, is preferred as the edible part.

[0024] Plasmalogens can be extracted using water, organic solvents, or aqueous organic solvents, and it is preferable to use enzymatic treatment in combination. For example, ethanol extraction and hexane extraction can be used, with ethanol extraction being preferred.

[0025] The ethanol extraction method is not particularly limited as long as it uses ethanol (including aqueous ethanol) for extraction. Examples include the methods described in Japanese Patent Publication No. 2019-140919, Japanese Patent Publication No. 2018-130130, Japanese Patent Publication No. 2012-039472, Japanese Patent Publication No. 2010-065167, Japanese Patent Publication No. 2010-063406, etc.

[0026] The hexane extraction method is not particularly limited as long as it uses hexane for extraction. Examples include the methods described in Publication No. 2009-154309 and Publication No. 2008-146942.

[0027] The composition of the present invention can be used as an oral or parenteral preparation. When used as an oral preparation, possible forms include tablets, capsules, powders, granules, liquids, granules, rods, plates, blocks, solids, rounds, pastes, creams, caplets, gels, chewables, sticks, lozenges, and the like. Among these, lozenge and capsule forms are preferred.

[0028] Furthermore, when used as a parenteral agent, specific examples include topical preparations and injections. Topical preparations are not particularly limited as long as they can be applied to periodontal tissue, and their forms include ointments, creams, gels, and liquids. Specifically, examples include ointments, powder toothpaste, paste toothpaste, water-based toothpaste, mouth fresheners, mouth freshening films, mouthwash, and gargles.

[0029] The present invention's composition for improving periodontal tissue inflammation contains plasmalogen and is used to improve periodontal tissue inflammation. As long as it can be distinguished from other products, it is not particularly limited. For example, it can be used as a pharmaceutical (including quasi-drugs), a cosmetic, a functional food such as a Food for Specified Health Uses, a Food with Nutrient Function Claims, or a Food with Function Claims whose efficacy has been approved by a designated institution. For example, any product that displays a statement that it has an effect of improving periodontal tissue inflammation on the product itself, packaging, instructions, or promotional materials is included within the scope of the present invention.

[0030] Specifically, examples include products that display phrases such as "maintain gum firmness," "for those concerned about gum deterioration," "for those concerned about gum color," "gum care," "barrier for gums," "protect gums," "for weakened gums," "periodontal disease prevention," "periodontal disease care," "pyorrhea prevention," and "gingivitis prevention."

[0031] The plasmalogen content in the composition of the present invention may be appropriately included within a range that achieves its effect. Depending on the form, for example, if the plasmalogen is present in a dry mass equivalent of 10% of the total composition of the present invention -10 Preferably, it is 10% by mass or more.-5 It is more preferably % by mass or more, even more preferably 0.1% by mass or more, and particularly preferably 1.0% by mass or more.

[0032] Furthermore, there are no particular restrictions on the amount of plasmalogen taken when the composition of the present invention is an oral preparation, but from the viewpoint of exhibiting the effects of the present invention more significantly, the amount of plasmalogen taken per adult per day is 10 -6 It is preferable to ingest at least μg / day, more preferably at least 1 μg / day, even more preferably at least 500 μg / day, and particularly preferably at least 1000 μg / day. The upper limit is, for example, 20,000 μg / day, and preferably 10,000 μg / day.

[0033] The composition of the present invention can be packaged in one packaging container, or divided into, for example, two or three separate packaging containers, to constitute a one-day supply, so that the daily intake amount is the aforementioned intake amount.

[0034] The compositions of the present invention can be manufactured by known methods, with the addition of other components besides the components of the present invention as needed. Examples of other components besides the components of the present invention include vitamins, minerals, proteins, peptides, amino acids, animal oils, and vegetable oils.

[0035] The present invention will be described in detail below based on examples. [Examples]

[0036] [Example 1] By examining the ICAM-1 gene expression level using mouse pancreatic islet microvessels (MS-1), we confirmed the effect of plasmalogen, the active ingredient of the present invention, on periodontal tissue inflammation.

[0037] [Exam Overview] (Plasmalogen (Pls)) As a plasmalogen, we used one obtained by extracting scallops (scientific name: Mizuhopecten yessoensis) with ethanol and purifying it by HPLC (ethanolamine-type plasmalogen).

[0038] (cell culture) Endothelial cells (MS-1) derived from mouse pancreatic islet microvessels (MS-1) were used. MS-1 cells were cultured in αMEM medium (Thermo Fisher) supplemented with 10% fetal bovine serum. MS-1 cells were seeded in 6-well plates, and the experiment was started when the cells reached confluence.

[0039] MS-1 cells were pretreated with 2% FBS-αMEM supplemented with Pls for 24 hours, and then stimulated with Pg-LPS (in vivogen) at various concentrations. Subsequently, total RNA was recovered, and cells were harvested for flow cytometry.

[0040] (Real-time PCR method) Real-time PCR was used for the analysis of ICAM-1 gene expression in MS-1. RNAeasy mini-kit (Qiagen) was used for total RNA extraction. cDNA was synthesized from 1 μg of total RNA using ReverTraAce® qPCR RT Master Mix (TOYOBO). ICAM-1 expression analysis was performed using THUNDERBIRD® SYBR qPCR Mix (TOYOBO) and StepOnePlus Real Time PCR System (Thermo Fisher).

[0041] As shown in Table 1 below, PCR was performed using specific primers for mouse GAPDH and mouse ICAM-1. Gene expression was calculated as the ICAM-1 / GAPDH ratio, and comparisons were made between experimental groups.

[0042] [Table 1]

[0043] (Flow Cytometry Analysis) The protein-level expression intensity of ICAM-1 on the cell surface was investigated by flow cytometry analysis. Specifically, MS-1 cells were fixed with 4% PFA, blocked with Blocking One-PBS (x5, Nakarai), and stained with anti-mouse CD54 antibody-PE conjugated (Biolegend) and rat IgG isotype control-PE conjugated (BioLegend). Cell surface antigen expression was then examined using FACS Verse (BDbioscience). The data were analyzed using FlowJo software (BDbioscience).

[0044] (statistical analysis) All data were collected after verifying reproducibility by conducting similar experiments at least three times, and representative results were presented graphically. Results are expressed as mean ± standard deviation, and statistical analysis was performed using R software with a significance level of 5%. Analysis of variance was used for comparisons between groups, and if a significant difference was found, Turkey multiple comparison tests were performed as post-hoc tests.

[0045] [Preliminary Examination 1-1] This study investigated whether LPS, a virulence factor of Pg (Pertussis viridis), a representative periodontal pathogen, enhances ICAM-1 gene expression in the vascular endothelial cell line MS-1. Specifically, MS-1 cells were stimulated with 1 μg / ml Pg-LPS, and ICAM-1 gene expression was compared at 0, 2, 6, 10, and 24 hours using Realtime PCR.

[0046] The results are shown in Figure 1. As shown in Figure 1, ICAM-1 gene expression increased from 2 hours after stimulation, peaked at 6 hours, and then decreased.

[0047] [Preliminary Examination 1-2] We investigated the Pg-LPS concentration sufficient to induce ICAM-1 gene expression in MS-1. Specifically, as a dose-response study, we established a control group (no Pg-LPS stimulation) and experimental groups with Pg-LPS concentrations of 0.01 μg / ml, 0.1 μg / ml, and 1 μg / ml, and measured ICAM-1 gene expression levels 6 hours after stimulation in each group.

[0048] The results are shown in Figure 2. As shown in Figure 2, a significant increase in ICAM-1 gene expression was observed with 1 μg / ml Pg-LPS.

[0049] [Preliminary Examination 1-3] We investigated whether Pls affects ICAM-1 gene expression. Specifically, we set up a control group (no Pls) and experimental groups with Pls concentrations of 5 μg / ml, 25 μg / ml, and 125 μg / ml. MS-1 cells were treated with each concentration of Pls, and the ICAM-1 gene expression level was measured after 24 hours.

[0050] The results are shown in Figure 3. As shown in Figure 3, no difference was observed between the control group and the Pls group at any of the Pls concentrations, indicating that Pls alone does not alter ICAM-1 expression levels in MS-1.

[0051] [Example 1-1] We investigated whether Pls affects ICAM-1 expression in MS-1 cells induced by Pg-LPS. Specifically, MS-1 cells were pretreated with various concentrations of Pls, and then stimulated with Pg-LPS in the presence of Pls. The Pg-LPS concentration used for stimulation was 1 μg / ml, and the stimulation time was 6 hours.

[0052] The results are shown in Figure 4. As shown in Figure 4, ICAM-1 gene expression levels were significantly lower in all Pls concentrations compared to the Pg-LPS group. Furthermore, ICAM-1 gene expression levels decreased gradually with increasing Pls concentration, and in the 125 μg / ml Pls + Pg-LPS group, it decreased to the control level.

[0053] [Examples 1-2] To investigate the effect of Pls-mediated suppression of ICAM-1 expression at the protein level, ICAM-1 expression on the surface of MS-1 cells was examined using flow cytometry.

[0054] The results are shown in Figure 5. As shown in Figure 5, the peak of ICAM-1 (CD54)-positive cells shifted to the right in the Pg-LPS-stimulated group compared to the control group. Furthermore, when ICAM-1 expression intensity was quantified using mean fluorescence intensity (MFI), it was 2064±34 in the unstimulated control group, 10726±74 in the Pg-LPS group, and 2085±97 in the Pls+Pg-LPS group. It was observed that the ICAM-1 protein expression level, which increases with the addition of Pg-LPS, was suppressed to a control level by Pls pretreatment.

[0055] [Example 2] By checking the TNF-α gene expression level using a human monocyte / macrophage cell line (THP-1 cells), we confirmed the effect of plasmalogen, the active ingredient of the composition of the present invention, on inflammation of periodontal tissue.

[0056] [Exam Overview] (Plasmalogen (Pls)) The plasmalogen used was an ethanolamine-type plasmalogen extracted and purified using the same method as in Test 1.

[0057] (cell culture) Human monocyte / macrophage cell line THP-1 cells (from RIKEN BioResource Center) were used. The THP-1 cells were cultured in the same manner as in Experiment 1, except that RPMI1640 + 10% FBS was used.

[0058] (Real-time PCR method) TNF-α gene expression analysis in THP-1 cells was performed using the same method as in Experiment 1. The primers used are listed below.

[0059] Human TNFαF: 5'-CCTCTCTCTAATCAGCCCTCTG-3' Human TNFαR: 5'-GAGGACCTGGGAGTAGATGAG-3' Human GAPDH F: 5'-CTCTCTGCTCCTCCTGTTCGAC-3' Human GAPDH R: 5'-TGAGCGATGTGGCTCGGCT-3'

[0060] (statistical analysis) The same method as in Test 1 was used for statistical analysis.

[0061] [Preliminary Examination 2-1] This study investigated whether Pg-LPS enhances TNF-α gene expression in THP-1 cells. Specifically, THP-1 cells were stimulated with 1 μg / ml Pg-LPS, and TNF-α gene expression at 0, 2, 6, 10, and 24 hours was compared using Realtime PCR.

[0062] The results are shown in Figure 6. As shown in Figure 6, TNF-α gene expression levels peaked 2 hours after stimulation and then decreased, but were significantly higher than at 0 hours after stimulation at all times after 2 hours post-stimulation.

[0063] [Preliminary Examination 2-2] We investigated the optimal Pg-LPS concentration to induce TNF-α gene expression in THP-1 cells. Specifically, as a dose-response study, we set up experimental groups with Pg-LPS concentrations of 0 μg / ml, 0.1 μg / ml, 1 μg / ml, and 10 μg / ml, and measured TNF-α gene expression levels 6 hours after stimulation in each group.

[0064] The results are shown in Figure 7. As shown in Figure 7, a significant increase in TNF-α gene expression was observed in the experimental groups receiving 0.1–10 μg / ml.

[0065] [Example 2-1] We investigated whether Pls affects TNF-α gene expression in THP-1 cells induced by Pg-LPS. Specifically, THP-1 cells were pretreated with various concentrations of Pls, and then stimulated with Pg-LPS in the presence of Pls. The Pg-LPS concentration used for stimulation was 1 μg / ml, and the stimulation time was 6 hours.

[0066] The results are shown in Figure 8. As shown in Figure 8, TNF-α gene expression levels were significantly lower in all Pls-treated groups compared to the Pls-untreated group.

[0067] [Example 3] The effect of the composition of the present invention on inflammation of periodontal tissue was confirmed using a mouse model of experimental periodontitis induced by ligature ligation.

[0068] [Exam Overview] (Plasmalogen (Pls)) The plasmalogen used was an ethanolamine-type plasmalogen extracted and purified using the same method as in Test 1.

[0069] (Experimental animals) Six 8-week-old male C57BL / 6N mice (clean water experimental material) were purchased and randomly divided into two groups of three, designated as the control group and the experimental group, depending on whether or not Pls was added to their drinking water. All animals were housed at room temperature of 22±2℃ with a 12-hour light-dark cycle (lights turned on at 8am) and fed solid food. The control group was given normal drinking water, while the experimental group was given water with 10 μg / ml Pls added. Both groups received water orally through ad libitum from the start of rearing until sample collection. The water bottles were changed once a week for both groups. All animal experiment protocols were approved by the Animal Ethics Committee of Osaka Dental University, and efforts were made to minimize animal suffering and the number of animals involved (Approval Number: 20-12001).

[0070] (Experimental periodontitis model using ligature ligation) After a 6-day acclimatization period, all mice underwent ligation to create an experimental periodontitis model. Inhalation anesthesia with isoflurane and intraperitoneal administration of a triple anesthetic mixture (medetomidine, midazolam, and butorphanol) were performed. After anesthesia took effect, 5-0 surgical silk sutures were ligated to the left maxillary molar region according to a previously reported method (Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils (URL:https: / / www.jove.com / video / 59667, doi:10.3791 / 59667)). Specifically, as shown in Figure 9, first, the ligature was passed between M2 and M3 from the palatal side to the buccal side, then between M1 and M2 from the buccal side to the palatal side, surrounding M1, and then again between M1 and M2 from the buccal side to the palatal side. The ligature end that passed between M2 and M3 was then tied to the palatal side, and the knot was placed in the interdental space between M1 and M2. Figure 10 shows the state of surgical sutures tied to the left maxillary molar area.

[0071] After the procedure, the ligature was checked daily, and if any defects such as ligature detachment or loosening were observed, the ligature was immediately re-ligated, and the ligature was maintained in place in the left maxillary molar region for 15 days. On the 15th day after the ligature ligation procedure, all mice were sacrificed, and maxillary samples were collected. The collected samples were fixed in 4% paraformaldehyde for 24 hours, and then immersed in PBS to prevent drying for storage.

[0072] (Analysis using microcomputer tomography) Mouse maxillary samples were scanned using a computed tomography (μCT) scanner (Sky Scan 1275, Bruker). The scanning conditions were under a copper filter, with a tube voltage of 90kV, a tube current of 100μA, and a pixel size of 17.8μm. The obtained scanning data was displayed as volume rendering data using analysis software (CTVOX, Bruker) to observe the presence and degree of alveolar bone resorption (Figure 11). In addition, tomographic image data of the coronal section at the center of the M2 tooth crown was extracted using 2D visualization software (Data Viewer, Bruker), and the straight-line distance from the cementoenamel junction on the buccal side of the M2 tooth to the alveolar bone crest was measured.

[0073] As shown in Figure 11, observation of the teeth and alveolar bone revealed significant alveolar bone resorption in both the control group and the Pls-administered group, indicating experimental progression of periodontitis and destruction of periodontal tissue. The distance from the cementoenamel junction on the M2 buccal side to the alveolar bone crest was 542.823 μm in the periodontal disease-induced area, while it was 365.419 μm in the area where periodontal disease was induced while Pls was administered. These results indicate that the degree of alveolar bone resorption on the M2 buccal side was smaller in mice administered Pls, suggesting that Pls administration suppresses the destruction of periodontal tissue due to periodontal disease.

[0074] [Combination example 1] A liquid formulation (100g) was prepared using the following formula. Scallop extract plasmalogen 0.5mg Glycerin 0.5mg Purified water remainder

[0075] [Combination example 2] Hard capsules were manufactured using the following formulation. Scallop extract plasmalogen 0.5mg Cyclodextrin 3.3mg Amino acids 1.2mg Painex 185.0mg [Industrial applicability]

[0076] The present invention's composition for improving periodontal tissue inflammation can be used as a pharmaceutical product and is industrially useful.

Claims

1. A composition for improving periodontal tissue inflammation, characterized by containing an ethanolamine-type plasmalogen.

2. The composition for improving periodontal tissue inflammation according to claim 1, characterized in that the plasmalogen is a plasmalogen extracted from animal tissue.

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