The Effects Of Systemic Curcumin On Alveolar Bone Loss During An Experimental Periodontitis Model On Rats

Periodontal disease and pregnancy is an important thing for all of us to take into consideration when dealing with clients. When it comes to pregnancy there is a great change occurring in the body, these changes can leave women more susceptible to infections within the body. So it is important for us to have the knowledge as to what we should do to help and teach our patients so they can help prevent periodontal disease as well as treat it to help better their overall health as well as their baby’s health.

read this, about osteoporosis and its effect on the oral cavity. With this paper I hope to

     Periodontal disease is more commonly known as gum disease or gingivitis. This infection is serious enough, that it can lead to tooth loss if left untreated. This chronic infection starts around the tooth and it affects the supporting bone and gums. Periodontal disease can affect anywhere from one tooth to all thirty-two teeth. The disease pathology starts with the plaque that builds up on your teeth everyday.

Treatment of periodontal disease can be broadly divided into two, non-surgical and surgical. Longitudinal comparison between non-surgical and surgical therapy had been studied extensively by groups of researchers, namely the Gothenburg, the Michigan, the Minnesota, the Nebraska, and the Arizona group. There are some heterogeneities between studies from different groups. Some studies focused on single rooted teeth, while others included molars. Majority of the studies are done in a university setting, while the Arizona study was done in private practices.

Periodontal disease can lead you to lose all of your teeth. The mouth is the gateway to the rest of the body; it can be the entering passage between healthy and sick. The moment an infection grows in the mouth, the entire body automatically starts to try to fight it. “…due to significant findings supporting the association between periodontal disease and systemic conditions such as cardiovascular disease, type 2 diabetes mellitus, adverse pregnancy outcomes, and osteoporosis” (Amar and Kim). It has been suggested that the bacteria of this infection may enter the bloodstream and attach themselves to the blood vessels which then increase clot formation. These clots then lower the blood flow to the heart indicating that a heart attack is a common consequence of gum

Figure 7 shows how endocytosis inhibition blocked ALN- induced bone formation in vivo. To examine if endocytotic inhibition affected the ALN-induced bone formation in vivo, DC was added to the ALN solution and put the extracted teeth in the solution and then replanted them. More bone tissue observed in ALN-treated tissue than in PBS-treated tissue on day 7. Adding DC to the ALN solution drastically reduce the ALN-induced increase in ALP-positive cell ratios and the ALN-induced decrease of attached TRAP-positive cells. Part A is a hematoxylin and eosin staining of the mesial and distal root. Part B is bone volume/tissue volume (BV/TV) between the mesial and distal roots of replanted teeth was determined. Part C is ALP staining, the image taken

Chronic periodontitis has been identified as the most prevalent form of periodontitis affecting the adults and occasionally the adolescents and children.(Merin, 2015) This periodontal disease of inflammatory origin is thought to be the result of host immune response against bacterial colonies in the subgingival plaque.(Merin, 2015) In many cases, systemic and environmental factors play a significant role in the disease progression. Common risk factors such as uncontrolled diabetes mellitus and smoking, contribute to periodontal destruction in genetically susceptible individuals by modifying the host’s immune reactions towards periodontal pathogens. Clinically, the diagnosis of chronic periodontitis is made based on the presence of supragingival and subgingival plaque and calculus, signs of gingival inflammation, periodontal attachment loss and radiographic bone loss. Chronic periodontitis can be further classified based on the extent and severity of periodontal destruction. Localised chronic periodontitis is diagnosed when less than 30% of the sites are affected; whereas the generalised form of the disease affects more than 30% of the sites. The severity of the disease is determined by the amount of clinical attachment loss. It is classified as mild, moderate or severe when 1-2mm, 3-4mm or 5mm or more attachment loss is recorded respectively. (Merin, 2015)

Tobacco smoke contains carbon monoxide (CO) which will lower the oxygen(O₂) saturation of haemoglobin in healthy gingiva. Oxygen tension within the pockets was substantially reduced in smokers. This may favour the growth of anaerobic bacteria, even in the shallower pockets 21.The local host response to bacteria, which initiates periodontitis, includes the recruitment of leukocytes and the subsequent release of infiammatory mediators and cytokines such as interleukin (IL-1,6,8,10,12) and tumor necrosis factor (TNF- alpha). Researchers have tried to study a possible relationship between smoking, stress and cytokine production.15 Giannopoulou studied cytokines in the pathogenesis of periodontal

Chronic oral health problems begin with a mouth full of bacteria (Nidcr.nih.gov, 2015). This bacteria combined with mucus and particles begins to cause plaque on teeth, which then can become tartar, and this bacteria causes the body to have an immune response (Nidcr.nih.gov, 2015). The toxic effect produced by bacteria along with the body’s immune system can then cause tooth decay and gum disease (Pace, 2000). These toxins will eventually cause a breakdown of the bone and connective tissue which holds the tooth in place (Nidcr.nih.gov, 2015). The bacteria also cause inflammation of the gums, known as gingivitis (Nidcr.nih.gov, 2015). Gingivitis can then advance to peridonitis (Nidcr.nih.gov, 2015) which is inflammation of the membrane around

These disorders seem to be induced through the disruption of the homeostasis of collagen synthesis and degradation in gingival connective tissues.

Periodontal regeneration is defined histologically as regeneration of the tooth’s supporting tissues, including alveolar bone, periodontal ligament and cementum over a previously diseased root surface2. Great strides are being made to achieve this goal using bone grafts and various other regenerative procedures3. With the exception of blood, bone is the most frequently transplanted tissue in the human body. Virtually every operative day, orthopaedic surgeons, neurosurgeons, craniofacial surgeons and periodontists need to fill bony defects or augment deficient bone. The major types of commonly used bone graft materials include autografts, allografts and alloplasts.

Regeneration has been defined as the reproduction or reconstitution of a lost or injured part to restore the architecture and function of the periodontium. To be considered a regenerative modality, a material or technique must histologically demonstrate that bone, cementum and a functional periodontal ligament (a new attachment apparatus) can be formed on a previously diseased root surface. Bone grafts and their synthetic substitutes have been used in an attempt to gain this therapeutic endpoint. However, among the graft materials to date, only autogenous bone of extraoral or intraoral sources and demineralized freeze dried bone allograft have human histological evidence to include them as regenerative materials. More recently the use of recombinant human bone morphogenetic proteins (BMP)-2 (Ishikawa et al. 1994), enamel matrix derivative (EMD) (Sculean et al. 1999), platelet-rich plasma (PRP) (Anitua et al. 2004), growth factors like platelet-derived growth factor (PDGF) and insulin-like growth factor-1 (IGF-1) (Lynch et al. 1989) and recombinant human basic fibroblast growth factor (bFGF) (Murakami et al. 2003) have been proposed as a source for periodontal regeneration. Initial investigation has demonstrated that anorganic bovine bone matrix supports the attachment and proliferation of osteoblastic cells in vitro (Stephan et al. 1999). Indeed, human histologic studies have concluded that this bone substitute is osteoconductive and incorporated in new bone

Optimal dental health is indicated with the control and prevention of gum disease, gingivitis, bacterial carries, cavities, and periodontal disease (PD). Alternatively, signs of poor oral health can be seen with the accumulation of bacterial pathogens in the area between the tooth and gingiva, known as the gingival sulcus (see Figure 1). PD is a severe condition due to its chronic inflammatory nature that leads to tooth decay and eventual tooth loss. The pathogenesis of PD involves bacterial invasion of the gingival sulcus, which stimulates a host reaction of leukocytes and lymphocytes. This immune response constitutes a progressive, destructive, and inflammatory

With a sample size of 20-30 teeth per study group in mind, Neves et al began by extracting specimens and protecting them by capping with ProRoot Mineral Trioxide Aggregate, Kolspon alone or mixed with either 50 nM BIO or Tideglusib 50 nM. Pulp collection was then performed using the 21G needle, 23 scalpel blade, and 0.6 mm straight tip tweezer. After pulp extraction, the upper molars of the mice were dissected and fixed with PFA 4% and then scanned using a Bruker Skyscan1272 micro-CT scanner. From the scanned images, Neves et al were able to evaluate the injury site and perform mineral analysis. However, Neves et al failed to include any indication that inducing dentin growth may cause complications. Without detailing the possibility of unwanted dentin growth, Neves et al are substantially lowering the potential for Tideglusib as a treatment for caries lesions. As with most treatments, Tideglusib is not immune to the possibility of negative side effects and it is this aspect that minimizes the credibility of the study done by Neves et al.

The association between obesity and periodontitis has been reported in previous studies(32). But, the physiological basis of the causal relationship is not yet understood. However periodontitis and obesity share the same pathogenesis through release of inflammatory cytokines. These cytokines and hormones released from adipose tissues could modulate the response of periodontal tissues to the oral environment(54). Some evidence linking periodontitis with abdominal fats, metabolic disorders and abnormal fat metabolism(54,61)