Imaging in Periodontology

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© Springer Nature Switzerland AG 2021

K. Orhan (ed.)Ultrasonography in Dentomaxillofacial Diagnostics

14. Ultrasonographic Imaging in Periodontology

Kaan Orhan1   and Revan Birke Koca2

Faculty of Dentistry, Department of Dentomaxillofacial Radiology, Ankara University, Ankara, Turkey

Faculty of Dentistry, Department of Periodontology, University of Kyrenia, Kyrenia, Cyprus

GingivaImagingPeriodontologySoft tissueUltrasonography

14.1 Periodontium

Periodontium is the tissue integrity that surrounds the teeth and consists of four main components. They are gingiva, periodontal ligament, cementum, and alveolar bone. Each of these periodontal components is different, but all of these components function together as a single unit [1]. The main function of the periodontium is to attach the tooth to the alveolar bone and to maintain the integrity of the surface of the masticatory mucosa of the oral cavity.

This chapter first describes periodontium and periodontal diseases; then discusses the usage areas of ultrasonography in periodontology.

14.1.1 Gingiva Anatomy of Gingiva

The gingiva is the part of the masticatory mucosa covering the alveolar process and surrounding the cervical part of the teeth. It consists of an epithelial layer and an underlying layer of connective tissue called lamina propria. The color of the gingiva is coral pink and it has a stippled “orange peel” surface (Fig. 14.1). The gingiva acquires its final shape and texture with the eruption of the teeth. The gingiva is divided anatomically into free gingiva, attached gingiva, and interdental gingiva (Fig. 14.2).

Fig. 14.1

Healthy periodontium

Fig. 14.2

Anatomy of the healthy gingiva

Free Gingiva
The free or marginal gingiva is the most coronal part of the gingiva, coral pink, has a dull surface and a firm consistency. It is clinically about 1 mm wide and forms the soft tissue wall of the gingival sulcus. The free gingival margin is rounded and is located approximately 1.5–2 mm coronal to the cementoenamel junction (CEJ) (Fig. 14.3).

Fig. 14.3

Anatomy of healthy gingiva (a) UHFUS aspect of the gingiva; (b) Schematic exemplification of anatomy

The Attached Gingiva
The attached gingiva is located in the continuation of the free gingiva and is tightly attached to the periosteum underneath. It is separated from the movable alveolar mucosa by the mucogingival border. The distance between the mucogingival border and the gingival sulcus is defined as the width of the attached gingiva and is an important parameter for the health of the periodontium. This width is the largest in the incisor area (3.5–4.5 mm in the maxilla, 3.3–3.9 mm in the mandible), the narrowest in the premolars (1.9 mm in the maxilla, 1.8 mm in the mandible) [2]. The dark red alveolar mucosa (AM) located in the mucogingival junction apical is loosely attached to the periosteum. Alveolar mucosa is seen more reddish than the attached gingiva since it has more blood supply (Fig. 14.4). Therefore, it is mobile unlike the attached gingiva.

Fig. 14.4

Anatomy of the healthy buccal mucosa, (a) UHFUS aspect of the buccal mucosa; (b) Schematic exemplification of anatomy

The Interdental Gingiva

The interdental gingiva is a pyramid or “col” shaped gingiva covering the interproximal space below the contact area of the teeth. It is not seen between the teeth without contact, it becomes flat.

The Gingival Sulcus

The gingival sulcus is a shallow groove with an epithelium lined with a tooth surface on one side and free gingiva on the other. The depth of the gingival sulcus is a parameter in the periodontium health. This depth is measured with the help of a periodontal probe. In healthy gingiva, the depth of the sulcus is between 0–1 mm clinically and an average 1.8 mm histologically [1].

The Gingival Fluid

In the gingiva sulcus, there is the gingival fluid originating from the subgingival gingiva. In the healthy sulcus, although the amount of gingival fluid is very small, during inflammation, the gingival fluid increases and its composition begins to resemble an inflamed exudate.

14.1.2 Periodontal Ligament

Periodontal ligament is a cellular connective tissue rich in vascularization that surrounds the tooth roots and connects the cement to the inner wall of the alveolar bone [3]. It is continuous with the connective tissue of the gingiva and communicates with the alveolar bone through the vascular channels of the bone.

The periodontal ligament is in the shape of an hourglass and is the narrowest at the middle root level. The average width of the periodontal ligament is about 0.2 mm; however, it decreases in dysfunctional teeth, increases in teeth exposed to hyperfunction [1]. Periodontal Ligament Cells

The cells of the periodontal ligament are undifferentiated mesenchymal cells, fibroblasts, osteoblasts, osteoclasts, cementoblasts, epithelial cells, neurovascular elements, and immune system cells [4]. Extracellular Matrix of Periodontal Ligament (ECM)

The periodontal ligament also contains a large amount of ECM that fills the gaps between the fibers and cells. This matrix consists of two main components, such as glycosaminoglycan (hyaluronic acid, proteoglycan, heparan sulfate, dermatan sulfate, chondroitin sulfate) and glycoprotein (fibronectin and laminin) and 70% water [1]. Besides, cells use it for support, water storage, bonding, and intercellular exchange.

14.1.3 Cementum

Cementum is a calcified avascular mesenchymal tissue that covers the root surfaces. Contrary to the bone, the cementum does not contain blood or lymph vessels, has no innervation, moreover it does not have a physiological resorption or remodeling. The cementumt is characterized by continuing to accumulate throughout life. Cementoenamel Junction

There may be three possibilities in cementoenamel combination (Fig. 14.5);

  • About 30%, mine-cementum comes to tip.

  • 60–65%, cement texture covers the enamel.

  • 5–10%, enamel-cement does not combine, dentin tissue remains exposed. In this case, the risk of gingival recession and dentin sensitivity increases.

Fig. 14.5

Schematic exemplification of possibilities in cementoenamel combination Cementum Resorption

In the regions where cementum resorption is active, multinucleus giant cells and mononuclear macrophages are present. Cementum resorption may be caused by local or systemic factors or may be idiopathic. Local conditions that cause cementum resorption include [1];

  • Occlusal trauma

  • Orthodontic movement [5]

  • Teeth pressures outside the dental arch

  • Cysts or tumors

  • Teeth without functional antagonists

  • Impacted teeth

  • Reimplanted teeth

  • Periodontal and periapical diseases

Systemic conditions that predispose the individual to cementum resorption include;

  • Calcium deficiency

  • Vitamin A and Vitamin D deficiency

  • Hypothyroidism [6]

  • Hereditary fibrosis osteodystrophy

  • Paget’s disease

  • Tuberculosis

  • Pneumonia

Cementum resorption (Fig. 14.6) can extend into the dentin and even the pulp under the resorptive process and is asymptomatic. It is not continuous, repair period may begin with newly formed cementum tissue.

Fig. 14.6

Cementum resorption in the sagittal section of CBCT

14.1.4 Alveolar Process

The alveolar process is the portion of the maxilla and mandible that forms and supports the tooth sockets. The alveolar process extends from the basal bone of the jaws and develops in conjunction with eruption of the teeth, gradually disappears when the tooth is lost [1]. Anatomy of Alveolar Process

Alveolar bone proper forms the attachment apparatus of the teeth with the root cementum and periodontal membrane. The main function of the alveolar process is to distribute the masticatory force and other occlusal forces.

The alveolar process consists of the following:

  • Cancellous trabeculae between these two compact layers, supporting alveolar bone

  • Compact bone on the inner wall of the socket called alveolar bone proper, which is called lamina dura on radiographs

  • An external plate of cortical bone formed by Haversian bone canals and compact bone lamellae

The walls of the sockets and the outer walls of the alveolar process are made of cortical bone. The area surrounding the cortical bone walls is occupied by the cancellous bone. Cancellous bone covers most of the interdental septa; however, only a relatively small portion of the buccal and palatal bone walls. Also, the bones of maxilla and mandibula include the basal bone, which is the portion of the jaw located apically but unrelated to the teeth. The cancellous part of the alveolar bone consists of trabeculae surrounding the irregularly shaped bone marrow cavities covered with a thin, flattened endosteal cell layer. Cancellous bone is found mainly in interradicular and interdental spaces. The adult person has more cancellous bones in the maxilla than the mandible.

The bone covering the socket wall usually continues with the compact bone in the lingual and buccal aspects of the alveolar process. In the cheek and lingual aspects of the alveolar process, the thickness of the bone can vary from one area to another. The same is true for teeth. In the incisors and premolar regions, the bone in the buccal directions of the teeth is much thinner than the lingual aspect. In the molar region, the bone is thicker than the buccally and lingually.

A region without bone coverage in the marginal part of the root is called dehiscence. If there is a bone in the most coronal part of the buccal bone, but the defect is found more apically, it is called fenestration. In areas with such deficiencies, the root is covered only with connective tissue attachment and overlying mucosa.


All bone-forming active sites contain osteoblasts. The outer surface of the bone is covered with a layer called the periosteum. This layer consists of an inner layer surrounded by osteoblasts and an outer layer containing dense vascularization, innervation, and collagen fiber. Blood vessels branch extensively and travel through the periosteum. On the inner surface of the bone, that is, in the bone marrow cavity, there is an endosteum with properties similar to the periosteum. Periosteum regulates bone size for life. A change in bone size is the result of periosteal osteoblastic and osteoclastic activity.


Remodeling provides bone shape changes, resistance to forces, repair of wounds, and regulation of calcium and phosphate metabolism in the body. New bone formation and bone destruction in a constant balance constitute the main principle of bone. Remodeling involves coordination between osteoblasts that stimulate new bone formation and osteoclasts that stimulate bone resorption.

In healthy alveolar bone, renewal and remodeling made by osteoblasts are balanced by resorption by osteoclasts. Although the number of osteoblasts decreases with aging, there is no change in the number of osteoclasts. Systemic effects that stimulate bone remodeling are usually caused by hormones such as parathormone, calcitonin, and vitamin D3.

Alveolar bone is constantly renewed depending on functional conditions. The life-long tendency of the teeth to be mesialized requires a continuous remodeling of the alveolar bone.


Bone resorption is associated with osteoclastic activity. These cells are large multi-core cells that specialize in the breakdown of matrices and minerals.

Regulation of bone remodeling is a complex process involving hormones and local factors that act in the form of an autocrine and paracrine on the formation and activity of different bone cells. Bone contains 99% of the body’s calcium ions. Therefore, it is the main source of calcium release when the level of calcium in the blood drops; it is regulated by the parathormone secreted by the parathyroid gland.

Remodeling of the trabecular bone begins with the resorption of bone surface by osteoclasts.

14.2 Periodontal Diagnosis and Prognosis

14.2.1 Classification of Periodontal and Peri-implant Diseases and Conditions

Classification of diseases affecting the gingiva and periodontium provides a universal assessment of diseases in terms of etiology, pathogenesis, clinical symptoms, radiographic symptoms, medical history, and treatment.

Universal features of gingival diseases include clinical signs and symptoms associated with inflammation, the reversibility of diseases by the elimination of the etiology, the presence of bacterial plaque to initiate or exacerbate the disease.

A classification scheme for periodontal and peri-implant diseases and conditions is essential for clinicians to accurately diagnose and treat patients, as well as for scientists to investigate the treatment of etiology, pathogenesis, natural history, and diseases and conditions.

So far, many periodontal disease classifications have been introduced such as 1989, 1993, 1996, and 1999. The Classification of Periodontal and Peri-Implant Diseases and Conditions organized by the World Workshop in 2017 is as follows [7]: Classification of Periodontal and Peri-Implant Diseases and Conditions-2017

  1. A.
    Periodontal Diseases and Conditions

    1. I.
      Periodontal Health, Gingival Diseases and Conditions

      1. 1.
        Periodontal Health and Gingival Health

        1. (a)

          Clinical gingival health on an intact periodontium

        2. (b)
          Clinical gingival health on a reduced periodontium

          1. (1)

            Stable periodontitis patient

          2. (2)

            Non-periodontitis patient

      2. 2.
        Gingivitis–dental biofilm-induced

        1. (a)

          Associated with dental biofilm alone

        2. (b)

          Mediated by systemic or local risk factors

        3. (c)

          Drug-induced gingival enlargement

      3. 3.
        Gingival diseases–non-dental biofilm-induced

        1. (a)

          Genetic/developmental disorders

        2. (b)

          Specific infections

        3. (c)

          Inflammatory and immune conditions

        4. (d)

          Reactive processes

        5. (e)


        6. (f)

          Endocrine, nutritional & metabolic disorders

        7. (g)

          Traumatic lesions

        8. (h)

          Gingival pigmentations

    2. II.
      Forms of Periodontitis

      1. 1.
        Necrotizing Periodontal Diseases

        1. (a)

          Necrotizing Gingivitis

        2. (b)

          Necrotizing Periodontitis

        3. (c)

          Necrotizing Stomatitis

      2. 2.

        Periodontitis as Manifestation of Systemic Diseases

        Classification of these conditions should be based on the primary systemic disease according to the International Statistical Classification of Diseases and Related Health Problems (ICD) codes

      3. 3.

        1. (a)
          Stages: Based on the severity and complexity of management

          1. (1)

            Stage I: Initial periodontitis

          2. (2)

            Stage II: Moderate periodontitis

          3. (3)

            Stage III: Severe periodontitis with potential for additional tooth loss

        2. (b)

          Extent and distribution: localized, generalized; molar-incisor distribution

        3. (c)
          Grades: Evidence or risk of rapid progression, anticipated treatment response

          1. (1)

            Grade A: Slow rate of progression

          2. (2)

            Grade B: Moderate rate of progression

          3. (3)

            Grade C: Rapid rate of progression

    3. III.
      Periodontal Manifestations of Systemic Diseases and Developmental and Acquired Conditions

      1. 1.

        Systemic diseases or conditions affecting the periodontal supporting tissues

      2. 2.
        Other Periodontal conditions

        1. (a)

          Periodontal abscesses

        2. (b)

          Endodontic-periodontal lesions

      3. 3.
        Mucogingival deformities and conditions around teeth

        1. (a)

          Gingival phenotype

        2. (b)

          Gingival/soft tissue recession

        3. (c)

          Lack of gingiva

        4. (d)

          Decreased vestibular depth

        5. (e)

          Aberrant frenum/muscle position

        6. (f)

          Gingival excess

        7. (g)

          Abnormal color

        8. (h)

          Condition of the exposed root surface

      4. 4.
        Traumatic occlusal forces

        1. (a)

          Primary occlusal trauma

        2. (b)

          Secondary occlusal trauma

        3. (c)

          Orthodontic forces

      5. 5.
        Protheses and tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis

        1. (a)

          Localized tooth-related factors

        2. (b)

          Localized dental protheses-related factors

  2. B.
    Peri-Implant Diseases and Conditions

    1. I.

      Peri-implant Health

    2. II.

      Peri-implant Mucositis

    3. III.


    4. IV.

      Peri-implant Soft and Hard Tissue Deficiencies


14.2.2 Definition and Etiology of Periodontal Diseases Plaque-Induced Gingivitis

The onset of gingival diseases occurs in the presence of microbial dental plaque. If the accumulation of microbial dental plaque increases between the tooth and the marginal gingiva, inflammation and classic clinical gingivitis may develop.

Plaque-induced gingivitis is inflammation of the gingiva resulting from bacteria located at the gingival margin. In gingivitis, the inflammatory lesion is confined to the gingiva. However, when the microbial dental plaque is not eliminated, the infection may spread to deeper tissues and periodontitis may develop. This process varies according to the individual’s host response.

Clinical manifestations of gingivitis, bleeding during probing, enlarged gingival contours due to edema or fibrosis are color change to a reddish tone and increased exudate and increased temperature. Clinical attachment levels and radiographic records are needed to establish this diagnosis. Periodontitis

Periodontitis is a common chronic inflammatory disease due to host response caused by subgingival biofilm products characterized by destruction of the periodontal ligament and alveolar bone around the teeth.

Gingivitis precedes periodontitis, but it is clear that not all cases of gingivitis progress to periodontitis. In gingivitis, the inflammatory lesion is confined to the gingiva; however, with periodontitis, the inflammatory processes extend to additionally affect the periodontal ligament and the alveolar bone. The net result of these inflammatory changes is the breakdown of the fibers of the periodontal ligament, resulting in clinical loss of attachment together with resorption of the alveolar bone. Etiology of Periodontal Diseases

Periodontal disease develops as a result of disturbances in the oral microbiota, leading to an immune response of the host thus affecting periodontium protection and support [8]. An understanding of the etiology and pathogenesis of periodontitis is essential for diagnosis and treatment planning.

In some diseases caused by microorganisms such as periodontitis, the symptoms of the disease do not always have to be seen in the presence of a microbial agent. The development of the disease, in addition to the microbial agent, may depend on many additional factors as specific host response, toxic exposures, nutritional deficiencies, systemic status, emotional stress, and social effects.

Alveolar Bone Loss

Alveolar bone destruction can be seen both in clinical examination and radiological examination. Clinical examination is carried out by probing. In the radiological examination, the distance from the interdental area to the crest indicates the level of alveolar bone loss.

The pattern of bone loss also determines the cause of bone loss in some cases. These are also called local factors. These can be grouped under two headings as gingival inflammation and occlusal trauma.

Aug 7, 2022 | Posted by in Oral and Maxillofacial Radiology | Comments Off on Imaging in Periodontology

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