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Periodontal Disease and the Bite
Dentist North Carolina Charlotte NC 

 Periodontitis Bite Dentist Charlotte NC North Carolina Holistic Biological Biocompatible 


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Although periodontitis is caused by bacterial infection on the roots of the teeth, it is made worse when the bite or occlusion is unbalanced. This is another example of how how important the bite is in preventing or promoting dental disease. The fact that an unbalanced bite promotes periodontal disease is yet another reason why I am constantly educating my Charlotte North Carolina area patient about the importance of getting the bite properly balance.

The following diagram shows the structures of the tissue around the tooth. 

Histomorphometric Landmarks: GM= gingival margin, aS= apical extension of sulcus, aJE= apical extension of junctional epithelium, IAI=implant abutment interface, BC= bone contact. SD= sulcus depth, JE= junctional epithelium, CTC=connective tissue contact. BW=biologic width = SD+JE+CTC. From the cementum collagen fibers project laterally into the gingiva 



The gingival epithelium facing the tooth is divided into the sulcular (unattached) and junctional (attached) epithelia and is nonkeratinized. The gingival epithelium facing the oral cavity is keratinized and displays numerous rete pegs (extensions of stratified squamous epithelium into the underlying lamina propria): 


The following is from: 


Host parasite reaction between bacterial plaque and host inflammatory response is the cause of pocket depth and attachemnt loss. The presence of traumatic occlusion can accelerate the damage when periodontitis proceeds apically into the periodontal ligament space. 


The first reaction to increased occlusal loading is increased vascularity in the periodontal ligament space. No changes are seen in gingival tissues. 

Normal periodontal ligament with normal occlusal forces showing dense collagen fibers attached to bone and cementum with minimal vascularity: 


With excessive occlusal loading the collagen fibers lose their connection between cementum and bone, and blood vessels proliferate: 

This initial increased vascularity results in a more compressible periodontal ligament and increased clinical mobility. Changes in the apical periodontal ligament vascular patterns can also result in increased vasodilation of the pulp with increased sensitivity and pain to hot and cold stimuli secondary to traumatic occlusion. 


In traumatic occlusion, after the initial change of increased vascularity, there is a stimulation of osteoclasts which cause bone loss and a widened periodontal ligament space. This also increases tooth mobility: 

Further effects of traumatic occlusion ae seen with loss of density of collagen and absence of a functional fiber arrangement. 

High powered view. No collagen fibers adjacent to bone and loss of functional support of the periodontium: 


Advanced traumatic occlusion with minimal periodontal ligament tissue. An advancing plaque induced periodontitis can rapidly spread apically in this situation:

Periodontal ligament tissues can respond with traumatic occlusion changes when normal periodontium is affected by increased occlusal loading due to bruxing, clenching or a high restoration. These changes are called pirmary occlusal trauma or primary trauma from occlusion. In teeth with bone loss due to periodontal disease previously well tolerated occlusal loading can become traumatic and cause changes in the periodontal ligamnet tissues. These changes are called secondary occlusal trauma or secondary trauma from occlusion. 

Region of crestal bone showing intrabony defect due to plaque. This is blending with traumatic occlusion: 


Apical part of plaque induced periodontitis: 


Traumatic occlusion changes deep in periodontal ligament: 


Radiograph of lower molar with traumatic occlusion. Widened periodontal ligament space on mesial all the way arounf the apex with beginning bone loss in furcation (arrows): 


There is also thickened lamina dura (bone next to tooth)(arrows) and this tooth has increased mobility: 


First molar has traumatic occlusion causing the bone loss in the furca. Clinically there is no pocket depth nor periodontitis in the furcation and so the diagnosis is traumatic occlusion and the treatment is occlusal adjustment to reduc occlusal loading: