Periodontitis associated with osteomalacia.

Osteomalacia is a metabolic bone disorder characterized by an alternation of bone mineralization, bone pain, increased bone fragility and fractures. A 23-year-old female patient reported with short stature and depressed nasal bridge with oral manifestation showing partial anodontia and periodontitis. This case report attempt to highlights clinical, radiographic, biochemical features of osteomalacia and periodontitis.

INTRODUCTION

Osteomalacia is a disease of bone metabolism, frequently affecting mature skeleton in adults. It is usually a manifestation of deficient intake or malabsorption of vitamin D3. Most patients with osteomalacia experience some degree of bone pain with muscle weakness of varying severity. Radiographic features include pseudofractures occurring most commonly in the ribs, pelvis and rarely in the mandible. This article presents a case of the female patient showing features of periodontitis associated with osteomalacia.

CASE REPORT

The present case report is about a 23-year-old female patient who had reported to the Department of Periodontology with the complaint of difficulty in mastication due to missing teeth. Detailed history of systemic complaints was taken where she reported of continuously experiencing mild pain with her limbs and in the pelvic area. The past dental history revealed that the deciduous teeth had erupted normally and shedding was normal. However, patient had the history of exfoliation of permanent teeth rather than extraction of teeth.

General examination

On general examination, it was observed that she had short stature (height of 119 cm) [Figure 1a] depressed nasal bridge, bow legs and difficulty in walking, climbing stairs.

Figure 1a

Short stature

Intra-oral examination

Intra-oral examination findings revealed that the patient's oral hygiene was fair. Gingiva showed generalized enlargement with bleeding on probing and only 12 teeth were present. The following teeth were present 11, 13, 14, 16, 17, 22, 25, 26, 27, 37, 43 and 47. Full mouth probing depths, mobility and periodontal status were recorded. Deepest pockets were present at mesiobuccal and distobuccal of 16 with mobility. All the teeth showed generalized pocket depth of 5-6 mm with 2-3 mm of recession. There was reduced alveolar ridge in mandible due to exfoliation of teeth [Figure 1b and c].

Figure 1

(b) Buccal view (c) Reduced alveolar ridge in mandible

Investigations

Radiographic findings

A skeletal radiographic investigation was conducted for the patient. Hand-wrist radiographs demonstrated decreased opacity suggesting of poor bone mineralization and sponge like appearance in the X-ray [Figure 2a and b]. Pelvic radiograph showed altered bone mineralization with reduced bone opacity along with pseudo fractures or incomplete fractures in the pelvis [Figure 2c]. Posteroanterior cephalometric projection view showed hypoplastic maxillary sinus [Figure 2d]. An orthopantomogram was done which showed generalized sever bone loss (up to the apex of tooth), impacted lower left second premolar along with thinning of mandibular cortex [Figure 2e]. Lateral view of skull demonstrated increased mandibular angle and maxillary micrognathia, along with thickening of the diploic space when compared with normal [Figure 2f].

Figure 2

(a) (Arrow) wrist radiograph of the patient demonstrating poor bone mineralization with X-ray; (b) Hand radiograph of the patient demonstrating poor bone mineralization with X-ray; (c) Pseudo fractures or incomplete fractures seen in the radiograph of pelvis (arrows); (d) Posteroanterior cephalometric projection demonstrated hypoplastic maxillary sinus; (e) Orthopantomograph of the patient showing impacted premolar (arrow); (f) Lateral view of skull demonstrated increase in angle of mandible and maxillary micrognathia and also demonstrated thickening of the diploic spaces (arrow); (g) Ground section of the tooth shows the paucity of cellular cementum (×10)

Hematological tests

Hematological tests were carried out, all finding were within normal range (hemoglobin, total leukocyte count, platelet count, differential leukocyte count) except an increase in erythrocyte sedimentation rate (25 mm).

Hormonal examination

T3, T4, Thyroid stimulating hormone (TSH), parathyroid hormone (PTH), serum calcium and serum phosphorous level were checked and found to be normal but the level of vitamin D3 was found to be decreased.

Biochemical examination

Bio-chemical tests were carried out which included aspartate aminotransferase, alkaline phosphatase (ALP) level in saliva and in blood. Serum ALP was markedly raised (828.00 U/L).

Examination of ground-section of tooth

Extraction of 16 was done due to severe mobility and was indicated for extraction. Tooth was sent for ground section examination. The result of ground section showed no abnormality regarding dentin and enamel but the paucity of cellular cementum was found, which may indicate developmental deformity in cementogenesis [Figure 2g].

Differential diagnosis

Considering the general examination, intra-oral examination, hormonal, hematological, radiographic, biochemical analysis and ground section of tooth findings the following were considered for differential diagnosis.

Cleidocranial dysplasia

Achondroplasia.

Diagnosis

A diagnosis of osteomalacia is based upon in view of the findings from general examination, intra-oral examination, radiographic, hormonal, hematological and biochemical analysis and ground section of tooth along with consultation of an orthopedic surgeon.

Treatment

Non-surgical therapy was started in the patient, which included full mouth scaling and root planing with detailed oral hygiene instructions. The patient was prescribed chlorhexidine digluconate mouth rinse (0.2%) twice daily.

DISCUSSION

Vitamin D3 is essential for intestinal calcium absorption and plays a central role in maintaining calcium homeostasis and skeletal integrity.[1] The principal (classical) function of vitamin D3 is to maintain serum calcium and phosphate concentration within the physiologically acceptable range. It is well-established that prolonged and severe vitamin D3 deficiency leads to rickets in children and osteomalacia in adults.[2] Rickets is a disorder of mineralization of the bone matrix (osteoid) in growing bone, involving both the growth plate (epiphysis) and newly formed cortical and trabecular bone. It often develops in the early months of life with growth retardation.[3]

Clinical and laboratory manifestations include muscle weakness, tetany, bowing deformity of the long bones, indentation of lower ribs, deformities of the back, bone pain, decreased bone density and abnormal biochemical parameters which includes decreased serum calcium, phosphorus, vitamin D3 and high ALP and PTH. If untreated it may result in permanent dwarfing, gross bowing of the legs and a distorted pelvis which could lead to obstetric complications for females in later life.[4] Rickets, although most commonly seen in infancy, can also occur during the pubertal growth spurt and adolescence. In late or adolescent rickets may cause bowing of legs, muscle weakness, pain in lower limb and back.[4]

The term osteomalacia is generally used to describe the bone disease caused by vitamin D3 deficiency in adults, who no longer have growing bones. Bone pain is a characteristic feature of osteomalacia. However, rickets in children is often accompanied by osteomalacia.[5]

The biochemical features of osteomalacia are similar to those of rickets, with increased serum ALP and PTH values and low calcium, phosphorus and vitamin D3 values in most cases. However, in our case, calcium and serum phosphorus and PTH levels are found to be within normal range but the levels of ALP were found to be increased in serum. The level of vitamin D3 was found to be decreased. The elevation in the level of serum ALP in osteomalacia, rickets and certain other bone diseases is generally attributed to increased osteoblastic activity. The osteoblasts are the cells rich in ALP but sometimes ALP appears to correlate better with the resorption than formation of the bone.[6]

Pseudofractures in osteomalacia appear as radiolucent bands extending into the bones from the cortex, usually at right angles to the periosteal margin. These are partial or complete fractures without displacement, in which callus has been deposited but has failed to calcify, Approximately, one-third of patients have spontaneous fractures,[7] similar types of Pseudo fractures are seen in radiograph of pelvic region in our case.

With regards to periodontitis, in year 1940, Taylor and Day have reported that a 50% incidence of severe periodontitis in a series of 22 Indian women with osteomalacia.[8]

Glickman in the early 1950s considered that there is a role of systemic component in all cases of periodontitis. The nature of the systemic component whether its presence or absence has influence on the severity of periodontal destruction and coined as “bone factors” concept.[9] Although the term “Bone factor” is not in current use, the concept of a role played by systemic defense mechanisms has been validated and studies have indicated such association may exist, but final proof is lacking. However as periodontitis is an inflammatory condition of the supporting structure of tooth (Cementum, Alveolar bone) the severity of periodontitis may aggravate more rapidly due to influence of systemic condition (osteomalacia) on alveolar bone and cementum.

Assessment of periodontal disease activity was carried out by evaluating enzyme level of aspartate aminotransferase and ALP in saliva. Biochemical results showed that level of ALP in saliva was higher than cut-off given for ALP in cases of severe periodontitis by Nomura et al.[10] Level of ALP in blood was much higher than normal level which reflects abnormality in normal cascade of systemic condition.

In patients of osteomalacia, tooth histopathology shows aplasia or hypoplasia of cementum and enlarged pulp chambers.[6] One of the features of ground section of tooth of the patient showed the paucity of cellular cementum. The principal function of cementum is to provide anchorage of the tooth in its alveolus which is accomplished through the collagen fiber bundles of the periodontal ligament whose terminations (Sharpey's fibers) become firmly embedded in cementum during the process of cementogenesis,[11] thus, it could be one of the reason why the exfoliation of permanent teeth occurred in this patient.

CONCLUSION

The present case represents a typical case of periodontitis associated with osteomalacia. It became evident that diagnosis of the disorder in the early stage of life may contribute significantly towards the management of osteomalacia and periodontal disease. By careful observation and investigation, a periodontist may be the first to detect systemic condition associated with periodontitis and/or otherwise serious systemic condition may initiate destruction of periodontal tissue. This case can be a gateway for further research that how systemic condition has influence on the severity of periodontal health and disease.